Hubs2503 Lecture Notes

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Hubs2503-lecture-notes
Clinical Exercise Physiology (University of Newcastle (Australia))
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HUBS2503 CLINICAL EXERCISE PHYSIOLOGY NOTES
LECTURE 1: INTRODUCTION TO EXERCISE PHYSIOLOGY
Definitions
 Physical activity: Any bodily movement produced by skeletal muscles that requires energy
expenditure.
 Exercise: Physical activity that is planned, structured, repetitive and designed to sustain or
improve health or fitness.
 Physical inactivity: Doing insufficient physical activity to meet the level of regular physical
activity recommended in national guidelines (or to maintain health).
o 4th leading risk factor for global death (after high BP, smoking, high blood glucose).
o Major contributor to premature death (< 60).
o Major contributor to non-communicable diseases.
 Australia led the way in creating exercise recommendations, developing the national
physical activity guidelines in 1999.
 PA and exercise are principal interventions for primary and secondary disease prevention.
Overweight & Obesity

 Causes: Inappropriate diet & insufficient energy expenditure.
 Treatment: ↓ energy intake and ↑ energy expenditure (i.e. ↑ PA).
 68% of men and 55% of women overweight or obese in Australia (AIHW 2010).
 >80% of hospital patients OWT or Obese.
The Inflammation theory of disease

 Many chronic diseases associated with persistent low grade (chronic) inflammation marked
by elevated circulating levels of proinflammatory cytokines observed (IL-6, TNFα, CRP).
 Obesity-related conditions show this profile.
 Exercise has been shown to reduce this inflammation and thus reduce the risk of
atherosclerosis, NIDDM, tumour growth and neurodegeneration.
Exercise responses
 Pattern of change in physiological variables seen during a single
bout of exercise or PA.
 Often described as the acute response to exercise. E.g.
relationship of running velocity and energy expenditure.
Training Responses
 Changes in body that occur as a result of regular exercise
(training). E.g. Lactate levels pre/post training intervention.
 DO NOT confuse with exercise responses.

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Mode of exercise
 The type of activity being performed.
 Many different classifications;
o Static vs dynamic (muscle action)
o Endurance vs sprint (aerobic vs anaerobic)
o Cardio-respiratory vs resistance
o Activity specific (walking vs cycling vs swimming)
o Sport specific (netball vs rugby league vs soccer)
Exercise intensity
 How hard is the exercise?
 What is the workload or work rate? (e.g. running speed, power output)
 Is it submaximal or maximal?
o Maximal exercise is the highest level that can be performed (Greatest load/Longest
duration). May be determined by a progressive exercise test to maximum (failure or end
point) and is influenced by motivation.
o Submaximal exercise may be described by a set workload – E.g. Heart rate or treadmill
speed.
 Absolute submaximal workload is a precise quantifiable level – E.g. 5 kg weight
lifted 10 times – Load is same for everyone.
 Relative submaximal workload is a workload relative to maximum capability – E.g.
% of that individual’s maximum capacity – Load varies for different individuals.
 May be reported precisely (quantitative) or subjectively (qualitative).
 Relative intensity depends on what a person is capable of doing (relative to their fitness).
 Descriptors of relative intensity;
o Low or light < 55% of VO2max
o Moderate 55-69% of VO2max
o Hard or heavy 70-89% of VO2max
o Very hard or heavy 90-99% of VO2max
o Maximal 100% of VO2max
o Supramaximal > 100% of VO2max
 Generally exercise of high intensity is of short duration, and exercise of low intensity is of
longer duration.
Exercise models
 Used to examine physiological responses.
 They are activities maintained at the same level for a period of time.
 Low-moderate intensity submaximal aerobic – Rhythmic, continuous, 30-69% of VO2max.
 Moderate-vigorous intensity submaximal aerobic
o Rhythmic, continuous, 55-89% of VO2max
o Some anaerobic contribution at higher intensities
 Incremental aerobic exercise to maximum
o Progressive (graded) exercise tests (e.g. the beep test).
o Start at a low intensity. Progresses in steady increments to exhaustion.
o Increments in workload often called stages.
o Pattern of workload changes called protocol.
o Stages commonly 2 or 3 min.
 Static exercise
o Muscle contracts and develops tension.
o Muscle does not produce movement (muscle fibres ~ same length).

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o Also called isometric.

o Maximal force a muscle can exert is maximal voluntary contraction (MVC).
o Often performed at % of MVC level – Duration usually short (2-10 minutes).
 Dynamic resistance exercise
o Muscle produces force so movement occurs – Workload usually constant.
o Number of repetitions determines duration.
o Higher loads, less repetitions and vice versa.
o Maximal load that can be lifted only once is a 1repetition maximum (1-RM).
 Short duration - high intensity
o Near maximal efforts (or supramaximal).
o Usually anaerobic
o Duration <1 s to 3 min typical
o E.g. Jumps, throws, sprints, short cycle tests
LECTURE 2: PRE-EXERCISE SCREENING

Sudden death & Exercise
 Under 35 years of age
 ~ 50 sudden cardiac deaths per year in Sydney in people aged 35 or younger.
 More males (5-20x) than females.
 About 67% due to structural abnormality.
 About 33% due to electrical abnormality.
 Frequently genetic or congenital conditions.
 Usually asymptomatic
 Other cause is Commotio Cordis – blow to chest.
 Over 35 years of age- Usually due to coronary artery disease (CAD).
 Males >> females even with CAD.
 ~ 70% of sudden deaths occur during or shortly after exercise.
 Underlying condition predisposes to problems associated with exercise- If any family history
of sudden death should get evaluated, especially if involved in sport.
 Fitness does not provide protection. Any symptoms (e.g. fainting) should be investigated.
 Regular exercise reduces risk factors for most (but not all) forms of heart disease.
 Not exercising regularly increases risk of many CV diseases.
Purpose of pre-exercise screening

 Identify individuals with risk factors and symptoms requiring medical evaluation prior to
exercise.
 Identify individuals with conditions requiring medically supervised exercise testing and
programs.
 Identify and exclude individuals with contraindications to exercise.
 Identify individuals with special needs for safe fitness testing and exercising (e.g. pregnancy).
Types of pre-exercise screening

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Screening questionnaires
 Should assess the following:
o Personal history of diseases and illnesses
o Family history of disease
o Surgical history
o Past and present health behaviours (smoking, physical activity)
o Current use of drugs/medications
o History of signs or symptoms of C-P disease
 Examples commonly used include;
o ACSM Health History Questionnaire
o ACSM Exercise Screening Questionnaire
o Australian adult pre-exercise screening tool- classifies people into 3 broad categories;
 High risk
 Medical clearance recommended before any testing, change to or new
exercise program.
 Moderate risk
 Can begin a low-moderate intensity exercise program WITHOUT medical
clearance.
 Can undertake a low-moderate intensity submaximal aerobic fitness test
WITHOUT medical clearance.
 DOES need medical clearance before beginning a vigorous exercise
program or vigorous aerobic fitness test.
 Low risk
 DOES NOT need medical clearance before beginning any exercise program
or vigorous aerobic fitness test.
 Fitness professionals need to use professional judgement.
 If in doubt, refer patient for medical follow up.

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ESSA Screening tool

 Stage 1 - compulsory (determines who is at high risk). 7 questions.
o Does the client have known medical conditions that should be checked out e.g. CV,
cerebrovascular, respiratory or metabolic disease?
o Any signs or symptoms of major CV, cerebrovascular, respiratory or metabolic disease?
o Any other condition that you think requires a medical opinion?
Signs & symptoms of cardiopulmonary disease

 Pain in chest or surrounds
 Shortness of breath
 Dizziness or syncope
 Dyspnoea (especially at night)
 Ankle oedema
 Palpitations or tachycardia
 Claudication with exercise
 Heart murmur
 Undue fatigue
Other serious conditions

 Serious musculoskeletal conditions (arthritis, back pain, osteoporosis) or bone fractures.
 History of blood clots.
 Recent substantial weight loss without trying.
 Epilepsy
 Rheumatic fever
 Latter stages of pregnancy or history of problems in pregnancy.
 Psychiatric conditions
 Undiagnosed symptoms of indigestion.
 Regular use of prescribed or OTC drugs.
 Any other chronic medical condition affecting ability to exercise.
Stages 2 and 3 – Risk factor assessment

 Optional (determines who is at moderate or low risk).
 Age and gender (males > 45 years & Female > 55 years at risk). NOTE: Females with
premature menopause and NOT on oestrogen replacement therapy are at risk at a younger
age.
 Family history of heart disease (only risk factor if in close M relative at <55 or F relative <65).
 Smoking status (current & past smokers within 6 months at risk).
 Physical activity status (+ 1 risk <150min mod intensity PA weekly. -1 risk >150mins).
 Height, weight, BMI* (BMI >30 or waist >94cm M or >80cm F = risk factor).

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 Blood pressure (risk if on antihypertensive meds, SBP 140 or DBP 90).

 Cholesterol (Total Chol >5.2 , TGs >1.7, LDLs >1.7, HDL <1. -1 risk if HDL >1.55).
 Blood sugar (fasting blood glucose >5.5= risk).
 If < 2 risk factors – LOW risk
 If > 2 risk factors – Moderate risk
 If many risk factors – use professional judgement or refer for medical screening.
Functional movement screening

 Form of musculoskeletal screening.
 Functional assessments of strength, mobility (flexibility), and stability.
 Application is for sport (sports specific).
 E.g. deep squat, hurdle step, in line lunge, shoulder mobility, active straight leg raise, trunk
stability push-up, rotary stability.
LECTURE 3: STRESS TESTING

 Graded eXercise testing (GXT) is also called exercise stress testing.
 Not a new concept (1846). Often the first choice for evaluating CV function- but not perfect
at detecting CV disorders.
What does a GXT involve?

 10 electrodes are placed around the chest & exercise.
 Mason-Likar system of electrode placement- 10 electrodes used to produce
12 signals (leads). 6 electrodes (V1-6) placed around chest. 4 electrodes
originally placed on limbs (rest) and moved to trunk for exercise testing –
Right Leg lead is ground.
 Signals from 10 electrodes are combined to form 12 combinations (called
leads). The 12 leads provide views of the heart from different positions;
o 6 limb leads provide information in the frontal plane (I, II, III, AVR, AVL, AVF).
o 6 chest leads provide information in the horizontal plane (V1, V2, V3, V4, V5,
V6).
Pre-GXT instructions
 Wear comfortable clothing & footwear during test.
 No food at least 2h before test.
 Avoid cigarettes, alcohol, caffeine, many OTC/herbal medications. Doctor to inform
regarding other medications.
 Tester should be aware of reason for the test & patient history.
 Ensure consent form is signed, prepare skin for electrode placement.
What does the test measure?

 HR, BP, RPE (rated perceived exertion) and ECG (12 lead).
 These are measured at rest (standing & supine), during the GXT, and after the GXT.
 May be performed using treadmill, cycle ergometer, lifting tasks etc.

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GXT protocols
 Usually conducted on treadmills. Variety of protocols but most commonly used is the “Bruce
protocol”- designed for and programmed into many treadmills. Large amount of normative
data on diverse populations.
 Bruce protocol stages last 3 mins with gradient increasing by 2% each stage.
 Limitations of the Bruce protocol include;
o Relatively large increments in workload with each stage.
o Long (3 min) stages at some workloads problematic re walk or run.
o Steepness may lead to premature leg fatigue (vs C-R limitations).
 Overall Bruce is okay if subject is not frail, does not have extremely low Functional Capacity
and can handle gradient orthopedically.
 The tests are always progressive, but the speed at which they progress and the level at
which they start varies.
 Alternate treadmill protocols include;
o Balke-Ware or Naughton (1-2 minute stages & Increments 1 MET or less).
o Ramp protocols are becoming increasing popular and have been shown to be
tolerated better by patients. It involves very small increments every 10-15s.
Cycle tests
 Good alternative if weight bearing or gait problematic (or TM not working!).
 Functional capacity often 5-20% less than TM-not regular activity for most.
 Electrically braked cycles preferred- Cadence not critical and ramp protocols possible.
 Most cycles mechanically braked – 15-25 W increments usual. Cadence critical for workload
determination.
Arm ergometer protocols

 Protocol should use small (<25 W) load increases.
 Recommended when:
o Severe lower-limb orthopaedic problems
o Lower extremity amputation
o Peripheral vascular disease

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o Neurological disorders
o Myocardial symptoms present with upper body activity only
o Return to work after MI involves extensive upper body activity
Effort/symptom rating scales

 Borg’s Rating of Perceived Effort (RPE) scales.
 OMNI Rating of Perceived Effort scales.
 In addition to Borg’s Rating of Perceived Effort (RPE) scales may use ratings of:
o Chest pain
o Dyspnoea
o Claudication
What is a normal GXT response?

 No indications of ischemia (e.g. ST depression).
 Normal haemodynamics (HR and BP responses).
 No signs of dysrhythmias on ECG.
 Reach acceptable workload (MET level) on GXT.
Reasons for stopping a GXT

 Sign or symptom-limited
o Absolute indications
o Relative indications.
 Reach predetermined submaximal level.
 Maximal level of exertion reached.
 Morbidity and mortality with GXTs rare.
 Important that tests are symptom-limited.
Value of GXTs
 Non-invasive
 Relatively cost effective
 Good diagnostic value if patient has multiple CV risk factors/symptoms.
 Less diagnostic value if: < 40 years of age and/or apparently healthy.
Indications of GXTs
 Evaluate possible cardiac disease- rule it out/evaluate symptoms/pre-exercise program
screening.
 Evaluate existing cardiac disease- severity, prognosis after MI, estimate disease progression.
o Allows stratification of risk associated with physical activity.
 Evaluate effectiveness of surgical procedures (e.g. pacemaker, angioplasty).
 Evaluate effectiveness of pharmacological therapy.
 Evaluate functional capacity for;
o Safe return to work
o ADLs
o Participation in leisure activities
o Entry to cardiac rehabilitation program
o Entry to other exercise program
 Cardiologist is not always present during test but always reviews and interprets ECG and
other measurement data.

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 Medical supervision should be present or nearby during the exercise test- Cardiologist
presence desirable for high risk patients.
Analysis of ECG traces

 Determine any abnormality in rate, rhythm, axis or hypertrophy.
 Determine shape of the wave and each of the segments/waves.
 ST-segment changes (V5 is most diagnostic)
o ST depression suggests subendocardial ischemia- Angina symptoms confirmatory.
o ST elevation during exercise- Possible transmural ischemia or coronary artery spasm.
 May also indicate more complex abnormalities
 T-wave changes- should be reported. Interpretation depends on other indicators.
 R-wave changes- – Depend on relative intensity of exercise. R-wave changes alone rarely
indicative of CAD.
 Dysrhythmias (arrhythmias) often appear suddenly during exercise test. Not all
dysrhythmias problematic, although may be life threatening. 3 main types of abnormalities;
o Supraventricular dysrhythmias
o Ventricular dysrhythmias
o High-grade conduction abnormalities (blocks).
Whats new in stress testing?

 Nuclear (thallium) cardiac imaging
o Images taken at rest and after exercise
o Dark areas show regions of low blood flow
o Also provides indications of structural abnormalities e.g. hypertrophy
 Increasingly combined with CT scanning
o If can’t exercise, use drugs (e.g. dobutamine) to stimulate changes in demand for blood flow
while imaging.
LECTURE 4: EXERCISE TRAINING

 Performed to cause biological adaptations that influence performance in specific tasks.
o Improve fitness
o Maintain fitness
o Delay declines in fitness
 Also sometimes referred to as conditioning or ‘work hardening’.

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The 4 principles of exercise training
 Overload
o Must OVERLOAD the body system relative to normal to get a response – i.e. must do more
than you normally do to provide the stimulus for adaptation (Higher load, more frequent,
longer duration).
o Training must be PROGRESSIVE to continue to get a response – must continue to increase
load, frequency, duration.
 Specificity
o Responses are specific to the characteristics of training performed e.g. responses to
endurance training different to sprint or resistance training.
o SAID principle- Specific Adaptions to Imposed Demand.
o Critical principle for getting desired responses from a training program.
o In muscles responses are specific to which muscles, energy systems, movement
patterns are used and therefore adaption is very specific to the activity/demand.
o In cardiac & respiratory tissues, responses generalise for aerobic training.
 Responsiveness
o Refers to the capacity to respond to/improve from exercise training.
o This is determined by;
 Genetics (genetic impact ~25-30% in humans)
 Recovery (must be adequate to prevent overtraining, injury, fatigue).
 Nutrition (e.g. CHO + protein supplement shown to be more beneficial for post
exercise glycogen recovery than just CHO supplementation).
 Health status (Directly affects capacity to respond. Programs must be individualised
to best target areas of weakness, optimise progressions, and make the best use of
therapist time).
 Reversibility
o Adaptions are transient and reversible.
o Detraining (deconditioning) describes the loss of physical capacity with inactivity –
E.g. immobilisation, bed rest, general sedentary behaviour.
o “Use it or lose it”- deconditioning happens far more rapidly than conditioning back
to previous level- some training benefits lost faster than others depending on level
of inactivity.
o After 10 week training program, most benefits lost after 4-8 weeks inactivity.
o Rapid detraining with bed rest- 20d bed rest, decreased VO2max 25%.
o Most rapid detraining in space (microgravity - gravity provides loading).
Factors influencing training responses

 FITT- Frequency, intensity, time, & type.
 Total volume (dose) = frequency, intensity, & duration.
 Frequency
o Usually number of training sessions per week.
o Minimum of twice a week to produce a response.
o Rarely benefit to more than 5 times a week.
o Frequent training more beneficial if intensity or duration lower - Important for contributing
for weight loss.
o Excess frequency may compromise recovery.

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 Intensity
o Threshold intensity for most effects.
o Relative intensity determines individual’s benefits.
o Intensity a challenge for group/team training- what is hard may be easy for another.
o Training zones: %VO2max for aerobic training (% HRmax, RPE, Lactate threshold).
o Higher intensity may produce faster adaptations.
o Longer duration offsets much of lower intensity over long term.
 Duration
o Large influence on quantity of training – Longer sessions = more training.
o Minimum duration for response influenced by;
 Intensity (more intense, shorter session).
 Fitness of individual (less fit, get response with shorter duration).
o A study in swimmers compared the effects of training for 1.5h twice a day to training 1.5h
once daily and found training twice per day offered nil additional benefit to performance.
Aims of exercise training

 To improve performance;
o Intensity most important variable
o Balance frequency/duration to allow recovery
o For novices, at least 3 times a week, moderate intensity, short duration.
o Increase duration, then intensity.
 To maintain performance;
o Need less training
o Maintain intensity
o Reduce frequency to 2 x week- reducing to once a week slows rate of detraining.
 To regain performance;
o If use same training program response is no faster or greater response the second time.
o Most people train harder than originally because they know what they can achieve.

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Types of training
 Continuous training
o Used for aerobic/endurance training
o Can be described as long slow distance (LSD) –
o Steady, paced, prolonged (> 20 min). Moderate-
high intensity.
o Relatively comfortable.
o Fartlek (speed play)- Blend of continuous and interval. It involves higher and lower intensity
segments in continuous activity and uses varied terrain (hills). Used most often for cross
country. Intensity usually individualised and based on RPE.
 Interval training
o Alternating periods of physical activity and relief.
o Can be used for aerobic, anaerobic and resistance training.
o Activity phase: seconds to minutes, intensity usually high (HIIT: High Intensity Interval
Training).
o Relief phase: active or passive, seconds to minutes.
o Alternating exercise and rest intervals – Ideal for metabolic (energy system) conditioning.
o Wide variety of effects based on;
 Intensity of interval
 Duration of interval
 Active or passive rest
 Duration of rest
 Number of repetitions (and sets).
o Developed for cardiac rehabilitation, now used more widely in sports training.
o Advantages:
 Provide high intensity that is better tolerated.
 Great way to initiate training when low fitness.
 Provide variety to training.
 Great for team sport applications
 Primary training approach for anaerobic conditioning. E.g. 100m sprinters – near max
intensity, long rest OR 50m sprints alternated with short rest – Use to increase lactate
tolerance.
o Clinical use;
 15, 30 or 60s work intervals to initiate programs.
 Rest provides recovery in order to resist fatigue.
 Can initiate with long rest, gradually reduce.
 Aerobic/endurance training
o Interval e.g. 5min Work: 5min Relief x 4
o Continuous (most widely used)- Shorter duration usually higher intensity.
o Fartlek – mostly used for cross country running.
o Mode of exercise may include jogging, cycling, swimming or a combination.
o Freq: Minimum 3 x week – Maximum 5 x week (except competitive athletes or walking).
o Intensity:
 60-75% of aerobic capacity (VO2max)
 70-85% of HRmax (140-170 bpm -20 yr old)
 RPE (Borg scale) of 13 (/20): somewhat hard
o Duration: Minimum of 15-20 min (unless very low fitness) –Maximum of 45 min (unless
walking or competitive athlete).
o Recommendations influenced by health status- individualisation important.

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 Resistance training
o Repetitious exercises using body weight or external resistance.
o Can use exercises using most large muscle groups or specific small muscle groups.
o Only became community wide exercise in last 20 years.
o Can be used to produce wide range of effects – Strength, power, endurance, hypertrophy.
o Outcomes affected by variables including;
 Exercise selection and order (Large muscle groups first).
 Exercise intensity – Influences repetitions
 Number of sets and length of rest
 Frequency of training
 Training volume
o Must determine which muscle groups to train.
o Multi-joint exercises (e.g. Power cleans, dead lifts, squats)
 Good strength transfer to many sports
 Usually form core of athlete program
o Body part (single joint) exercises (e.g. Knee extensions, triceps pushdowns) – Good for injury
prevention & rehabilitation.
o Intensity and reps determined by training goal (e.g. strength ↑ load, ↓ reps, ↑ rest. More
sets (volume) for hypertrophy).
o Usually fewer sessions per week if whole body exercise.
o Usually more sessions per week if only specific body parts per session- Don’t usually train
one body part more than 2-3 times per week.
o Current guidelines recommend 2 x week for health.
 Circuit training
o Originally form of resistance training.
o Often designed to get general fitness benefits.
o Often uses resistance exercises at lower intensities.
o Short intervals (30-60 s) of varying activities
 Perform a circuit (8-10 activities) then repeat 2-3 times
o Usually little rest between activities.
o Can be modified for a variety of goals e.g strength, aerobic fitness.
o Usually reasonable benefits & time effective.
o Enormous potential for clinical use – Can use a variety of everyday activities repeated for
short periods then progress to different activity.
o Combine interval training and/or short bouts of continuous training into a circuit- Improves
exercise tolerance and resistance to fatigue.
 Other training programs

o Other types of training improve other aspects of performance e.g. skill, flexibility, balance,
plyometrics.
o Weight loss
 Most important factor is consistency.
 Any exercise that expends energy will contribute- resistance training low energy expenditure,
endurance training higher energy expenditure.
 Can expend energy faster (work harder) if more fit (tolerate higher intensity).
 Most overweight people have low fitness so need long duration.
 Frequency- Minimum of 3 x week (Currently recommend daily activity).
 Intensity: Any sustainable intensity.
 Duration: Can be cumulative; 1 hour per day if walking or shorter if increased intensity.
 Exercise is not a quick way to lose weight- It is effective over the long term and it is effective
at maintaining weight.

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LECTURE 5: TYPES OF PHYSICAL FITNESS, FITNESS TESTING, AND PA GUIDELINES

What is physical fitness?
 Indication of ability to perform physical activity.
 Ability to perform muscular work satisfactorily (WHO).
 Ability to carry out daily tasks with vigour and alertness, without undue fatigue, to enjoy
leisure pursuits, to meet unforeseen emergencies, and resist hypokinetic diseases.
 PF varies with habitual physical activity levels and is influenced by genetics which impacts on
the capacity to respond to training.
Hypokinetic diseases
 Diseases caused by OR associated with a lack of physical activity.
 Includes Type II diabetes, obesity, CV disease, some cancers, osteoporosis, back problems,
depression.
 Associated with low levels of health related physical fitness.
Types of physical fitness
Health-related physical fitness

 Associated with some aspect of good health or disease prevention.
 Has 3 core components;
o Cardiorespiratory (aerobic) fitness
 Indicates the capacity of the body to deliver oxygen to tissues and remove
metabolites (e.g. CO2).
 Higher levels reduce risk of CV disease, Type 2 diabetes, some cancers, and
depression.
 CRF compromised by presence of respiratory or CV disease.
 CRF compromised by inability to activate skeletal muscle (e.g. stroke, MS, SCI).
o Musculoskeletal fitness
 Strength, muscle endurance, flexibility.
 Influences posture and balance.
 Contributes to capacity to live independently, reduce falls & ↓ back pain.
 Compromised by bone/joint diseases and neuromuscular diseases.
o Body composition
 Excess body fat is main issue for most of the population – Associated with Type 2
diabetes, CV disease, some cancers.
 Lack of muscle mass and low bone density main issues for frail elderly.
 Sports performance generally requires higher levels of muscle and lower levels of
fat compared to the general population.
Sport specific physical fitness

 Associated with superior sports performance- what is good enough for health may not be
good enough to be competitive in sport).
 It is health related physical fitness + sports specific components:
o Energy provision (aerobic, anaerobic).
o Motor performance components (strength, power, endurance, speed, agility, balance,
coordination, reaction time).
o Body structure and composition.

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Occupational fitness
 Certain level of fitness required for entering/undertaking some occupations.
 It is health related fitness + specific occupational components.
 Depends on occupation – Common for military, police, firefighters etc.
 Controversial to introduce to new industries.
Physical fitness testing

 Why test?
o Assess health status
o Assess fitness for work or employment
o Assess for sports needs
o Identify strengths and weaknesses
o Assist in setting training goals
o Influence training program design
o Provide motivation for exercise
o Monitor training program effects
o Monitor rehabilitation
 Components of a good fitness test (SVORS)
o Specificity – test assesses a specific known component of fitness.
o Validity – test measures the component of fitness that is claimed.
o Objectivity – same result is obtained regardless of who conducts the test.
o Reliability – same result is obtained if the test is repeated within a few days.
 Considerations regarding fitness tests
o Does it only test 1 thing? The best tests only assess a single fitness component.
o Is technical competence required? – If the fitness task is unfamiliar or complex, then prior
exposure to the activity may be needed i.e. familiarisation – May require skill on part of
assessor to explain task.
o Does the participant understand what is required? – Failure to perform the task correctly
will influence the results.
o Is the test well standardised? – The test needs to be conducted exactly the same by all
assessors to be justified in comparing results; established protocol should be used.
o Time of day – May influence results. Should be consistent if measuring before and after
intervention.
o Environmental conditions – Will conditions on the day (temperature, humidity, wind velocity
and direction) influence the results?
o Sensitivity – If assessing changes to training, test should be able to detect changes in fitness.
o Nutrition and hydration – Clear instructions should be provided re what/when to eat and
drink.
o Medications – Should be known and directions provided e.g. bring asthma medications, etc.
o Fitness test results usually interpreted by comparison to benchmark values based on age and
gender.
Fitness testing in children

 Recent emphasis on HRPF components particularly CRF and body composition.
 Decreased emphasis on traditional motor performance PF (skill competency).
 Unintended consequence has been decreased motor skills, decreased PA competence &
decreased enjoyment associated with PA for kids.
 Beep test of CRF most common.
 Muscle endurance tests more common than strength tests (push ups, sit ups).
 Flexibility – sit and reach most common.

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 Stork stand for balance.

 Body composition – not commonly assessed until recently (BMI z-score).
Fitness tests for the general population

 Submaximal CRF tests most common.
 Muscle endurance tests more common than strength tests (push ups, sit ups).
 Flexibility – sit and reach most common.
 Body composition – bio-impedance becoming most common.
 Body size – BMI
Fitness tests for the sporting population

 Enormous variation used depending on sport.
 Maximal strength and power widely assessed in athletes.
 Anaerobic tests, speed, and agility usually only assessed in sporting groups.
Fitness tests for the older or clinical populations

 Common examples include; 2MWT, 10 m walk speed, STS, TUG, chair sit and reach, BBS.
 Tests of walking speed useful as speed correlates with community ambulation.
Safety of fitness testing

 Influenced by genetics & medical history.
 Risk greater in sedentary or low active population.
 Maximal effort tests have greater risk than submaximal tests – However maximal tests are
more informative.
 Risk higher when environmental extremes.
Risk of regular exercise

 Major risk is usually injury- most injuries are minor e.g. blisters with weight lifting.
 Most exercise injuries heal without medical intervention.
 Serious injury is usually very activity specific.
Sedentary Environmental Death Syndrome (SEDS)

 Risk of premature death.
 Risk high due to low PA- contributes to increased health-care costs.
 Related to multiple medical conditions e.g. ↑ BP, TGs, cholesterol, glucose, NIDDM, MI, CHF,
obesity, falls, vertebral & femoral fractures.
Importance of regular exercise for those with disease risks

 Genetic predisposition (family history) and lifestyle are main predictors of disease risk.
 Exercise patterns are a component of lifestyle risk.
 Genetic predisposition mostly increases the need for appropriate exercise patterns- it is
rarely a valid excuse not to exercise!
Physical fitness vs Physical activity

 PF varies with habitual physical activity levels.
 PF easier to measure than PA.

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 PF measures are often used as proxy indicators of regular physical activity levels.
 Pedometers and accelerometers have improved the capacity to measure PA.
Physical activity recommendations

 0-5 yr olds- Move and play every day. As much activity as possible. Limit inactivity to <1h.
 5-17 yr olds- More is better- up to several hours daily. At least 60 minutes of moderate to
vigorous PA every day. Variety of aerobic training, with resistance training at least 3
days/week. Limit inactivity <2h.
 18-64 yr olds- Be active on most, preferably all, days of the week. Accumulate 150-300
minutes (2.5-5 h) of moderate intensity PA or 75-150 min (1.25-2.5 h) of vigorous PA or
equivalent combination each week. Muscle strengthening activities on at least 2 days a
week. Minimise prolonged sitting.
 64+ yrs- do some form of physical activity regardless of age, weight, diseases etc. Should be
active every day in as many ways as possible and accumulate at least 30 mins of moderate
intensity PA on most, preferably all, days. Should perform at level that is comfortable for
them.
What intensity am I exercising at?

 If you can talk and sing without puffing at all, you’re exercising at a low level.
 If you can talk comfortably, but not sing, you’re doing moderate-intensity activity.
 If you can’t say more than a few words without gasping for breath, this is vigorous-intensity.
LECTURE 6- SKELETAL MUSCLE & EXERCISE
 Skeletal muscle is the tissue that must be activated for exercise as therapy.
 Skeletal muscle is the major energy consuming tissue in body.
 Skeletal muscle responds to activity & inactivity.
 Largest organ in the body. ~42% of healthy male body weight and ~36% of healthy
female body weight.
 Highly compartmentalised tissue.
 3 roles- force, movement, and metabolism.
 Skeletal muscle density = 1.06 kg/L. Adipose
tissue = 0.92 kg/L. So muscle ~ 15% denser
than fat.
 Resting energy expenditure (REE) per day;
o Skeletal muscle - 54.4
kJ/kg (13.0 kcal/kg)
o Adipose tissue – 18.8 kJ/kg (4.5 kcal/kg)
o Bone - 9.6 kJ/kg (2.3 kcal/kg)
o Therefore muscle mass has a big
influence on REE
 Muscle fibres are embedded in a collagen
matrix (fibrous connective tissue).
 At ends of muscles, the collagen matrix forms the tendon.

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Muscle fibre types

 Muscle fibres vary in many characteristics and properties.
 Human skeletal muscle fibres are heterogeneous both within and between muscles.
 Classifications of muscle fibres:
o Morphology- Red/white; Large/small; capillary density.
o Contractility- Speed; Force; Fatigability.
o Metabolism (histochemistry/biochemistry) – Oxidative vs Glycolytic; Myosin ATPase.
 2 main fibre types:
o Type I – dominant in aerobic activities.
o Type II – 3 subtypes – dominant in anaerobic activities.
 These types differ in;
o Type of motor neuron innervation
o Type of myosin heavy chain
o Reliance on aerobic or anaerobic metabolism
 Major fibre type characteristics;
o Type I : Slow, Oxidative
o Type IIA: Moderately Fast, Oxidative, Glycolytic
o Type IIX: Fast, Mod-oxidative, Glycolytic
o Type IIB: Fast, Glycolytic
 The enzyme myosin ATPase catalyses the hydrolysis of ATP and provides the energy
required for actomyosin contraction. Through this it controls the rate of contraction.
 Myosin heavy chains are the motor protein of muscle thick filaments that determine
specific muscle properties. They are genetic markers.
Type I fibres
 Slow twitch (Slow ATPase, Ca2+ handling, shortening speed).
 Aerobic metabolism- many & large mitochondria.
 Fatigue-resistant
 Produces lower forces
 Fibre-diameter depends more on usage than fibre type but;
o Smallest fibres in inactive people.
o Larger in endurance athletes.
o Least capacity to increase size with training.
 High capillary density (up to 5-7 capillaries per fibre).
 Red colour (high myoglobin content) - aids diffusion of oxygen into fibre.
Type IIA fibres

 Fast twitch- Fast ATPase, Ca2+ handling, shortening speed.
 Mod-FAST, mod fatigue-resistance.
 Reddish colour;
o Moderate myoglobin/oxidative capacity.
o High glycolytic capacity /anaerobic metabolism.
 Capillary density – Up to 3-5 capillaries per fibre.
 Fibre diameter depends on usage

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o Moderate size in sedentary people

o Larger in exercise-trained
 Moderate force
Type IIX fibres

 Fast twitch (Fast ATPase, Ca2+ handling, shortening speed).
 Fast, fatigable.
 Light colour;
o Some myoglobin/mod-oxidative
o Highly glycolytic
 Lowest capillary density (3-4 capillaries per fibre).
 Fibre diameter depends on usage;
o Larger fibres
o Largest in power athletes
 High force
Type IIB fibres

 Fast twitch (Fast ATPase, Ca2+ handling, shortening speed).
 Fast, highly fatigable.
 White colour (little myoglobin/low oxidative- high glycolytic).
 Lowest capillary density (3-4 cap per fibre).
 Fibre diameter depends on usage;
o Largest in power athletes
o Potential to be largest fibres
 Highest force
Muscle fibre type profiles

 Large variations among humans.
 Most people ~ 50% Type I and 50% Type II in major muscles.
 Endurance athletes more Type I, power athletes more Type II.
 Not all muscles in a person have the same fibre type composition.
Muscle force/tension
 At the sarcomere level muscle fibres generate tension through actin-myosin cross
bridge cycling.
 While under tension a muscle fibre may shorten, lengthen or stay the same.
 Contraction is used generically for all conditions of tensions OR to describe
shortening.

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Determinants of muscle force
 Anatomical-physiological
o Size of fibres
 Fibres contain variable quantities of myofibrils.
 More myofibrils, more sarcomeres and more force.
 More myofibrils increase the cross sectional area (diameter) of fibres i.e.
‘thicker’ fibres are stronger.
 Anabolic steroids increase the size of fibres.
o Cross sectional area

 Larger muscles produce more force than smaller muscles.
 Muscle size explains gender differences in
strength.
 Anabolic hormones influence muscle size.
 What is the strongest bone in the body?
 On external object – Masseter (short).
 On bone – quadriceps femoris or gluteus
maximus.
 In women – myometrial layer of uterus
during childbirth
 External muscles of eye – relative to
weight of eye ball.
 Tongue – but 8 muscles!
o Sarcomere length
 Muscle fibres generate force through actinmyosin cross bridges.
 Extent of cross-bridge overlap and attachments influence muscle force.
 Optimal overlap gives greatest force (length tension relationship).
 Usually lower force at extremes of ROM.

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o Muscle fibre length

 Few mm- 30cm (Ratio of fibre length to muscle length 0.2-0.6).
 Limited by spread of signal from neuromuscular junction.
 Shorter fibres are usually stronger (force at a shorter length).
 Longer fibres can shorten faster (higher peak velocity; may be more
powerful but not as much force).
o Muscle architecture
 Organisation of fibres in a muscle is called ‘architecture’ (fibre alignment).
 Arrangement of fibres is described relative to the axis of force.
 Many types of arrangement but for convenience described as 4 types;
 Parallel – fibres parallel to force generating axis (also called fusiform).
 Unipennate – single angle.
 Multipennate –More than one angle. Pennated fibres oriented at an angle
relative to force-generating axis – Angle usually varies between 0 and 300.
 Circular – fibres arranged around an opening or recess.
 Influences total physiological cross-sectional area (PCSA) of muscles.

 Pennation increases fibre packing and results in greater PCSA.
 Increased PCSA results in higher force at the same muscle length and at the
same velocity.
 Influences length of muscles.
 Alters velocity characteristics of muscles.
 Parallel muscles shorten faster – Fibres typically longer.
o Shortening velocity
1. Muscle force is proportional to physiologic cross-
sectional area (PCSA).
2. Muscle shortening velocity is proportional to muscle
fibre length
3. When a muscle shortens quickly it has less time for the
cross-bridges to attach – so force decreases.

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o Fibre type & myosin isoform

 Type II fibres produce more force and greater power at the same velocity.
 Type II fibres can produce more force and power at higher velocities.
 Neurological
o Size of neural drive to muscle to contract i.e. Size & number of motor units
recruited.
o Skeletal muscle is slave to the somatic nervous system.
o Recruitment of muscle:
 Recruit muscle fibres by recruiting motor units (motor unit = group of fibres
supplied by 1 motor neuron).
 All muscle fibres in a motor unit are same.
 Recruit combinations of motor units best suited to task.
 Recruitment pattern (which nerves, which fibres) changes with:
 Force required
 Duration of activity
 Availability of energy
 Fatigue of fibres
 Categories of motor units:
 S - Slow twitch; low tension; fatigue resistant (~Type I fibres).
 FR - fast twitch; moderate force; fatigue resistant (~Type IIA fibres).
 FF - fast twitch; high force; highly fatigable (~Type IIB fibres).
 More motor units = more force.
 Larger motor units = more force.
 Number of fibres per motor unit varies- small motor units are used for fine
motor control, large ones for gross locomotor control.
 Size varies with muscle group;
 Eye- 10 fibres/motor unit
 Finger- 300 fibres/motor unit
 Gastrocnemius- 2000 fibres/motor unit
 Number of fibres per motor unit usually varies with motor unit type;
 S motor units- Smaller number of fibres, smaller increments in force.
 FF motor units- Larger number of fibres, larger increments in force.

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o Recruitment patterns (usage)

 Motor units with Type I fibres- low-moderate force, long duration, many every day
activities, usually small motor units.
 Motor units with Type IIA fibres- higher force, higher speed, moderate/long
duration, Medium sized motor units.
 Motor units with Type IIB fibres- high force, high speed, short duration, large motor
units.
The ‘Size principle’

 Type & number of motor units recruited varies as increase force requirements do (exercise
intensity).
 S (Type I) – lower thresholds for activation so recruited first for light/moderate intensity
activities.
Synchronous vs asynchronous
 Synchronous recruitment of motor units produces maximal forces in the highly trained e.g.
weight lifters.
 Asynchronous recruitment of S/FR motor units allows cycling of motor units for good fatigue
resistance e.g. continuous running.
 Mechanical
o Influence of angle of lever, moment arm length, and joint capability.
o Has effect on sarcomere overlap, therefore force varies through ROM.
o Force highest where most of the recruited fibres are at their optimum sarcomere
length.
 Other factors affecting skeletal muscle force;

o Adrenaline (beta 2 receptors)
o Limbic inputs (slapping face, smelling salts etc.).

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LECTURE 7: ASSESSMENT OF MUSCULAR FITNESS
 Testing muscle performance

o Strength
o Power
o Muscle endurance
o Flexibility
o Posture
 Muscle strength
o Strength – capacity to develop force.
o Maximal strength
 Amount of force a muscle group can exert against a resistance in one
maximal effort.
 Strength is important for health, occupational and sports fitness.
o Types of strength testing

 Isometrically (commonly used clinically, sometimes sport. Muscle held at
fixed length. Force matches load).
 Concentrically (active shortening. Force overcomes resistance).
 Eccentrically (active lengthening. Force doesn’t overcome resistance but
decelerates limb/object).
 Isokinetically (aka isovelocity. Contraction velocity constant but force varies-
uses machine to vary force).
 Isotonically (tension in the muscle stays the same despite a change in
muscle length during concentric contraction).
 Isoinertially (commonly used in sport, sometimes clinically).
o Contractions with constant force (tension) or speed (velocity) are often used
to understand muscle properties. “Iso”= same).
o Testing is specific to:
 Muscle/s used
 Joint angle (isometric, isokinetic)

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 Velocity dependent (less force at higher velocities).
 Muscle performance assessment considerations

o Warm up improves performance.
o Standardise warm up for repeat tests.
o Need to determine number of trials and rest intervals.
o Often a minimum of 3 min rest between trials.
o Often allow 3 trials.
 Isometric strength test devices

o Cable tensiometer – force is deflection on a dial.
o Load cell – force shown as change in voltage.
o Simple Strain gauge dynamometers – E.g. handgrip.
o Maximal effort exerted over 3-4 s.

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 Advantages of isometic tests

o Widely used standard tests.
o High reliability (repeatable results).
o Develop more force during an isometric than concentric contraction – Good
indication of maximum force.
o High margin of safety.
 Limitation of isometric tests

o Force measured at one joint angle only;
 Not necessarily represent strength at other joint angles.
 Could develop specific joint positions for particular situations.
o Often poor relationships with sports performance and training effects.
 Isoinertial strength tests

o Load is constant
o Common activities used for athletes or resistance-trained individuals (e.g.
bench press, military press, squat, power clean, leg press).
o Have concentric and eccentric components.
 Progressive isoinertial testing

o Progressively increase load to failure- Seek 1 RM= Maximal strength.
o 3 RM, 5 RM, 10 RM;
 Used to estimate 1 RM (extrapolate)
 Greater margin of safety
 Less accurate
 Recommended for testing of novices (may
lack skill to perform activity).
o Safety considerations crucial (particulary with
novices). Requires quality instruction,
insistence on good form, spotters, rack supports etc.
o Testing novices with isoinertial tests may not be appropriate until a level of
skill is acquired.
o Better to use alternative tests or NOT test than risk injury.
o Novice athletes may be able to be familiarised quickly with good instruction.
o Ideally have some idea of athlete’s performance before testing.
o Lifts progressively heavier with smaller increments until failure.
o Ideally only 3-4 lifts to 1 RM.
o Allow (5) min rest between attempts.
o Good reliability with experienced subjects-poor with novices.
 Strength field test

o 7 stage abdominal strength test;
 Progressive test (1 rep per stage)
 Strict adherence to Pass/Fail criteria essential.

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 Isokinetic tests
o Involve a dynamometer connected to a motor.
o Subject exerts force as hard & fast as possible against level arm.
o Performed on devices where velocity of movement can be fixed (constant) –
e.g. Cybex, Kin-Com, Biodex, Humac Norm.
o If velocity is zero, tests isometric force.
o Usually repeat test over number of velocities (slow to fast).
o Develop a force velocity profile. Velocity is recorded in degrees per second.
o More powerful individuals produce greater torque at higher velocities (more
explosive).
o Provide a good means of standardising conditions.
o Excellent reliability at lower velocities (to 1200/s).
o Less reliable at faster velocities? (recommend more repetitions).
o Advantages;
 Force record through full ROM
 Use to identify variations in force eg point of weakness (injury recovery
evaluation).
 Most tests unilateral - compare R & L limb forces.
 Compare agonist & antagonist muscles.
 Compare concentric & eccentric movements.
 Profile indicates if not making consistent effort (injury fraud?).
o Limitations;
 Best measurements (accuracy and reliability) obtained at lower velocities-
most relevance to sport at higher velocities.
 Expensive
Power increases with velocity of movement

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 Strength vs Power
o Strength and power are not the same capacities.
o Are relationships between strength and power.
o Maximum strength influences power.
o High power output is mostly important for sports performance.
o Power athletes must be able to generate high forces rapidly.
o Power = force x distance relative to time.
o High values from high force and/or short time.
 Power testing
o Are short duration explosive effort tests.
o Also indicative of anaerobic energy systems as power depends most on these
energy systems.
o Examples of performance tests for power include; vertical jump, standing
long jump, margaria-Kalamen stair run, peak power output on 10 s cycle test.
 Strength endurance
o A stronger muscle usually has greater local muscle endurance than a weaker
muscle performing the same work.
o This is because stronger muscle performs everyday activities at a lower % of
max capacity.
o Greater strength, less fatigue likely with everyday activities.
o Ability to maintain force without fatigue.
o Tests of muscle endurance;
 Sustained isometric force eg at % of MVC e.g. wall squat, plank etc.
 Repetitions of muscle action;
 Repetitions of activity in set time
 Number of repetitions to fatigue (e.g. curl ups, push ups etc).
 Torque decrements in isokinetic tests of repetitions (monitor decline in
force)
o Absolute muscle endurance- number of repetitions with set load eg 50kg or
body weight.
o Relative muscle endurance- number of repetitions at set % of individual’s 1
RM.
o Reliabilty of strength endurace tests;
 Usually lower than strength tests.
 Improved by ensuring correct form on every repetition (incorrect = end).
 Improved if set rate of repetitions.
 May be more reliable if isometric endurance.
 Often poor with novices.

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 Flexibility
o ROM about a joint or group of joints.
o Affected by;
 Joint structure
 Length and distensibility of muscles, tendons and ligaments.
 Soft tissue impediments.
 Physical activity level - more active > less active.
 Environmental conditions – warming increases distensibility of tissues.
 Ability to relax muscles.
 Presence of muscle soreness – adds stiffness.
 Pain tolerance
o Asessing flexbility;
 Visual ratings (risk of bias)- often used in field assessments. Comparisons to
diagram criteria e.g. ACSM common field tests , flexibility Screening Test,
healthy back tests.
 Measured ROM- field tests e.g. sit & reach, ROM using
goniometer/inclinometer.
LECTURE 8: NEUROMUSCULAR ADAPTIONS TO EXERCISE TRAINING

 Evidnce for adaptions comes from 2 types of studies;
o Cross-sectional studies comparing trained and untrained individuals (can’t eliminate
individual differences).
o Longitudinal (intervention) studies comparing the same individuals before and after
training (provide the strongest evidence).
Goals of neuromuscular training

 Enhance musculoskeletal health (fitness, QoL, independent living, worl,
rehabilitation).
 Improve sports performance (leisure to elite. Weightlifting and powerlifting
specifically).
 Change body aesthetics.
Neuromuscular adaptations
 Muscular health benefits
o Develop appropriate muscle mass for health (e.g. for functional activities,
metabolic health).
o Countermeasure to muscle atrophy & weakness (E.g. sarcopenia, N-M
disorders, stroke, frailty, following immobilisation, injury, bedrest).
o Enhance muscle metabolism (e.g. diabetes management and prevention).
o Improve muscle performance (strength, endurance, power, flexibility,
posture, running efficiency).
 Change body aesthetics.

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Influences on neuromuscular adaptations with exercise training

 Initial fitness level & genes (responsivness).
 Training program used (specificity & overload).
o Greatest with resistance training (especially High-Resistance Strength
Training (HRST), modest with circuit training, less with endurance training).
Strengh training equipment

 Free weights and barbells- Resistance constant, movement speed varies through
ROM.
 Cam devices, pulley systems- Resistance constant, movement speed varies through
ROM.
 Isokinetic devices- Movement speed constant, resistance varies through ROM.
Increases in strength with training

 ~ everyone can adapt.
 ~30% increases in children & adolescents with
resistance training.
 25-30% increases typical with resistance training
(young adults + 6 mo training).
 Larger increases with inactive adults.
 Large increases in elderly with resistance training
(Fiatorone et al JAMA 263:3029, 1990).
 Similar relative increases (% change) in M & F.
 Neural changes occur early in the program, muscular
components contribute more greatly as time
progresses (neural vs morphological changes). 90% of
strength gained within the 1st 2 weeks of training is
attributed to neural changes.
Neural contributions to changes in muscle force

 Change motor unit recruitment patterns
o Greater efficiency & specificity of recruitment.
o Improvements in motor skills.
 Change motor unit synchronisation
o Increase synchronisation for maximal & near efforts
o Decrease synchronisation for submaximal activity
 Decrease central inhibition for voluntary efforts
o Concept of ‘central reserve’
o Agonist activation may be non-maximal pre-training.
o Test by superimposing electrical stimulation.
 Increase inhibition of Golgi tendon organ input
o May contribute to change in coordination of contributions from agonists,
antagonists & stabilisers.
o Somewhat speculative

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Evidence for neural changes in muscle force

 Rate of change in strength is much greater than can be accounted for by changes in
muscle size.
 Increase in dynamic strength > isometric – Suggests motor skill/learning effects (ie
neural).
 Crossover effects (Train one leg, can get improvements in other leg- can be valuable
in rehabilitation).
 Imaginary training- found that after few weeks had made substantial strength gains.
Morphological changes
 Muscle force increases with increases in muscle size.
 Whole muscle increases in size.
 After ~8 weeks training, increases in strength track with muscle size.
 Size increases continue for at least 12 months in most studies.
 Eventually a limit to further increases.

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 The magnitude of the muscle size changes depends on;

o Muscle group (UL changes more than LL. Diff androgen receptor density?).
o Selective area (not all parts of muscle loaded evenly)
o Fibre type (Type II fibres more capacity to increase & decrease in size in short term)
o Age (less in children & elderly)
o Gender (LL increases M~F, UL increases M>F- androgen receptor diff? Strength may
increase more % in F).
o Training variables (FITT)
Mechanisms of muscle size changes

 Fibre hypertrophy
o Clear evidence for.
o Increase in size of fibres
o Increase myofibril size & number (myofibril proliferation, ↑ protein synthesis).
 Fibre Hyperplasia
o Evidence less clear- verdict uncertain.
o May get some hyperplasia (more fibres).
o Never a large or rapid contribution.
o May take extreme conditions.
 Fibre length
o Evidence unclear
o May get some increase
o May result from eccentric loading- difficult to establish.
Flexibility & muscle length

 One cause of limited flexibility (ie, range of motion around a joint) is lack of length in
muscle.
 Insertion of more sarcomeres in fusiform muscles could increase muscle length.
 Training strategies to increase muscle length & flexibility;
o Stretching
o Eccentric training
 Loss of elasticity contributes to reduced flexibility (e.g. Aging, disuse or limited use, lack of
use through full ROM or loading).
 Improvements in flexibility with training may be due to changes in
elastic properties of muscle.
Myofibrils & myonuclei

 Skeletal muscle cells are multinucleated.
 Fibre myofibril content is proportional to myonuclei.
o Type II fibres ~ 2X myobrils per nucleus of Type I fibres.
o To increase myofibril content, need to increase number of
nuclei.

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Muscle memory after

de-training
Satellite cells & myonuclei

 Satellite cells are source of more nuclei.
 Exercise loading stimulates satellite cells to undergo mitosis - 1 daughter cell
becomes new nuclei & allows cell to increase in size.
Other morphological changes

 Change in fibre type
o NO major changes re Type I / Type II
o Possible subtle changes in myosin heavy chain (MHC) composition - usually early in
training program.
o Many metabolic changes.
 No evidence of changes in cross-bridge density.
 Changes in tendons or connective tissues
o Tendon stiffness – YES
o Tendon hypertrophy - YES but slow
o Proportion of connective tissue to muscle ~same.
o Change in connective tissue organisation? Unclear
 Changes in muscle architecture
o Angle of pennation (AoP).
o Optimum AoP for strength calculated to be ~ 45°.
o AoP usually < 45° in untrained (suboptimal).
o May increase to 45° with HRST.

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Summary of timing differences

o Neural changes occur rapidly.
o Hypertrophy changes continue over longer time frames.
o Anabolic hormones (steroids) increase hypertrophy when combined with training.
o Changes are fibre type (& motor unit type) specific.
o Changes are training dependent.
o For training to be most effective for strength or size changes it needs to be
progressive (continue to overload).
o Training needs to vary to maintain a stimulus.
Periodisation
 Method of varying training to optimise strength performance.
 Conceptually balance between training volume and training intensity.
 Current debate between linear vs undulating periodisation – Evidence unclear that one is
superior.

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LECTURE 9: SKELETAL MUSCLE: INJURY, SORENESS, CRAMPS, & AGEING
Sources of skeletal muscle problems

 Damage to muscle fibres.
 Damage to tendons.
 Damage to myotendinous junction.
 Damage to tendon attachment to bone.
 Spasm (sustained contraction) due to nerve activation or irritation.
Muscle Soreness
 Acute (during activity)
o Not usually associated with tissue damage.
o Associated with production of lactic acid (associated with higher intensity activity).
o May produce a burning sensation.
o Recovery rapid after stopping activity.
o Fastest recovery obtained with low intensity dynamic activity.
 Delayed onset (24-72 hours after activity)

o Occurs 24-72 hours after unaccustomed physical
activity (work, leisure, vacation, sport).
o Common when start a new exercise program.
o Associated with eccentric muscle actions.
o Associated with damage to muscle fibres &
inflammation (Mild strain injury).
o Soreness can be severe.
o Muscles often swollen and stiff- produces some
weakness and inaccuracy of movement until
soreness resolves.
o Soreness is greatest performing eccentric tasks.
o Usually resolves in 2-3 days.
o Provides lasting protection for ~ 6 weeks.
o To avoid/minimise;
 Use modest loads, especially eccentrically
– No negative reps!
 Limit downhill running and increase
slowly.
 Especially important with older people
o Little benefit to using NSAIDs- some evidence
that supressing inflammatory response
compromises the adaptation. May be better
to use analgesics.

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 Sustained (injury-related)
o Muscle or associated tissue injured.
o May involve fibres &/or connective tissues.
o Often due to over exertion or poor mechanics.
o May feel soreness immediately.
o May take time to heal.
o Requires some rest for recovery.
o Sprain – ligament or joint capsule.
o Strain – muscle &/or tendon.
Markers of muscle damage

 Levels of creatine kinase (CK), myoglobin and Troponin I elevated in blood indicates muscle
fibre membrane damage.
 CK also elevated with myocardial infarction.
 Different enzyme isozymes in heart vs skeletal muscle.
 Elevated with both DOMS and muscle strain injuries.
 Also changes in sarcoplasmic reticulum (SR) and Ca2+ regulation.
Markers of connective tissue damage

 Levels of metabolite hydroxyproline elevated in urine.
 Usually only elevated with severe DOMS or strain injury.
Muscle Regeneration
 Role of satellite cells;
o Type of muscle stem cells that sit between basal lamina and sarcolemma.
o Stimulated and proliferate when cells substantially damaged (i.e. when not in
contact with sarcolemma).
 Process may take up to 6 months in humans depending on level of damage.

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Steps in regeneration:
1. Damage to muscle fibres.
2. Cell infiltration & inflammation responses.
3. Degenerative dismantling of damaged cell.
4. Proliferation of satellite cells.
5. Form myotubes then filled with new myofibrils.
Muscle changes with disuse

 Atrophy - decrease in muscle fibre size (cross-sectional area).
o Results in loss of force (weakness).
o Occurs in all disuse models.
o Mostly due to loss of mechanical ‘loading’ rather than loss of neural activation,
therefore loading necessary to prevent atrophy.
o Effects of bed rest (microgravity);
 Greater atrophy in antigravity muscles.
 Greater atrophy in type II fibres.
 Disuse models;
o Sedentary behaviour (pain states more extreme).
o Immobilisation of body segment(s).
o Bed rest (microgravity).
o Aging.
o Denervation
o Represent range of adaptive changes.
o More extreme the disuse (duration, level of inactivity), the more extreme the
changes and atrophy.
The effect of aging

 Gradual loss of FT fibres – Leads to relative increase in Type I fibres
from ~50% to ~60% of fibres (due to greater atrophy in FT fibres).
 Reduced capacity to activate muscle- loss of motor units.
 Mostly evident after 70 years of age.
 Lose ~ 3-5% muscle mass per decade after age 40 y.
 Exacerbated by inflammatory conditions (COPD, arthritis, cardiac
failure, venous ulceration).
 Contributes to falls, & risk of T2Diabetes, hypertension & CAD.
 Strength declines progressively with age in sedentary individuals.
 Strength can be well maintained with training to at least 60 years of
age.
 Power output declines with age even with training (loss of FT fibres)-
most sports performance depends on power output,

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Role of exercise in ageing

 Greater maintenance of muscle mass (influence on metabolism and T2D risk).
 Greater maintenance of mobility.
 Greater capacity to live independently (QOL).
 Reduced risk of multiple ‘lifestyle’ diseases.
 Recommendations;
o Daily activity
o Range of activities
o Strength and strength endurance important
o Maintenance of range of motion important
o Resistance training very effective
o Water based activities useful especially if balance poor or mobility limited.
Muscle Cramps
 Cause or causes not yet known (difficult to provoke experimentally so research has
been hampered).
 Triggered by nerve activity
o No cramp without nerve activity.
o Unclear whether nerve signal originates locally or in CNS.
o May be due to mechanical irritation or ischaemia of small nerve bundles.
 Only occur with muscle in shortened position.
 Acute treatment;
o Stretch/place in lengthened position.
o Promote blood flow (heat and/or massage).
 Incidence increases with;
o Fatigue
o Dehydration &/or electrolyte imbalance
o Reduced blood flow

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o Hypothyroidism
o Pregnancy
o Genetic component
Stitch (ETAP)
 Exercise-induced transient abdominal pain (ETAP)
 Often described as a cramping sensation.
 Many theories about the source of the pain.
 Characteristics are not consistent with skeletal muscle cramp (especially of
diaphragm).
 Characteristics are consistent with irritation of parietal peritoneum;
o Somatic pain (not visceral).
o Area of sensation
o Referred pain to shoulder tip
o Aggravated by GIT loading (food, water ingestion).
o Exercise may alter lymphatic flow influencing peritoneal fluid content.
 Prevention;
o Don’t eat or drink before exercise if prone to ETAP.
o Limit fluid intake volume during exercise.
o Consider tonicity of fluids.
o Decreases with age!
Recovery after exercise

 Ice baths (cryotherapy)
o Some evidence improves recovery after intense or prolonged exercise but not
conclusive.
o Unclear if contrast (cold/hot) better.
o Unclear if optimal controls used in studies.
o Optimal temperature and duration not determined (<15°?).
 Role of cool down;
o Prevent sudden decrease in venous return.
o Provide good blood flow for reduction/removal of muscle metabolites.
o Provide some restoration of muscle energy stores.
o Contribute to reduced inflammation
LECTURE 10: NEUROMUSCULAR DISORDERS & EXERCISE AGEING

 Symptoms of neuromuscular problems
o Difficulty moving, breathing, swallowing.
o Fatigue
o Weakness
o Muscle atrophy
o Loss of coordination
o Cramps
o Stiffness & pain

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 Exercise has 2 main roles in relation to neuromuscular disorders;

o To assess/monitor function
o As intervention/therapy
 Goals of exercise programs

o Improve QoL and social functioning.
o Prolong ambulation and independent living.
o Minimise secondary comorbidities.
o Limit physical deformity.
 Exercise program characteristics

o Challenging and enjoyable.
o Achievable and rewarding.
o Personalised (individualised).
o RPE monitored (if feasible).
o Use objective assessments.
o May not stress-test pre-program
o Cycle often better than treadmill.
o Walking tests better than cycle-more functional.
o Medications may influence test results.\
 Progressive neuromuscular disorders

o N-M function gradually declines – E.g. MS, Parkinson’s, MN disease.
o Ideally in good N-M shape when diagnosed.
o Early intervention probably beneficial.
o Train both affected and unaffected regions.
o Concerns over exacerbation of symptoms.
Multiple Sclerosis (MS)

 Fatigue is a key symptom of MS- assess with Modified Fatigue Impact Scale.
 Post-exercise fatigue can be overwhelming.
 Evidence supports use of exercise in MS.
 Exercise can improve strength, capacity to perform ADLs and mobility.
 Exercise MAY NOT reduce fatigue.
 Regular exercise may reduce post-PA fatigue.
 No evidence exercise is harmful to those with MS.
 Some concerns with heat load in MS – Water temperature may be a barrier to aquatic
exercise – Cool showers before and after exercise (YFSS).\
 Bladder dysfunction may discourage MS sufferers from appropriate hydration for exercise.
 Sensory deficits and coordination problems may limit scope of activities recommended.
 Evidence does not yet support any particular type of exercise as superior.
 Exercise ability often limited by spasticity- antispasmodic drugs commonly used in MS.
 Maximal strength reduced in MS.

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 Often benefit from strength (resistance) training prior to aerobic conditioning.

 Rate of adaptations to RT may be much slower than in healthy people.
 Circuit training may be beneficial with adequate rest.
 Balance should be assessed (e.g. BBS) as may be impaired and influences safety of exercise.
 Aerobic fitness is impaired in MS- proportional to level of disability.
 Maximal aerobic fitness and submaximal exercise tolerance both affected.
 Cardiovascular responses to submaximal exercise usually normal in MS.
 Exercise prescription for MS is consistent with exercise for aging populations.
 Some PA on most days of the week.
 Aerobic: walking, cycling, water or chair aerobics, weight-supported treadmill.
o 30 min (or 3x 10min); 3 d/wk; mod intensity – Cool environment (warm pools can be a
problem).
 RT: machines, circuits, therabands, pilates
o 2d/wk; 8-15 reps @60-80% 1RM; rest between sets important.
 Stretching: ROM, yoga, tai chi – 1-2/d recommended; hold stretches 30-60s.
 Potential benefits;
o Maintain independence and QoL.
o Increase CRF and decrease risk of CAD.
o Improve strength and strength balance.
o Reduce spasticity.
o Increase ROM
o Increase balance
 Non-progressive neuromuscular disorders

o E.g. stroke, SCI, spina bifida, CP
o Most effects incomplete.
o Exercise can maximise use of both affected and unaffected areas.
o Training effects are specific e.g. ADL improvements specific and should be considered in
activity choices.
Stroke
 ~20% die (immediately or within 1 year).
 ~30% recover reasonably.
 ~50% have some permanent disability.
 Potential roles for exercise:
o Assist in motor recovery.
o Contribute to brain plasticity for recovery.
o Prevent secondary stroke or CVD.
 Challenges for exercise:
o Fatigue
o Paralysis/weakness
o Poor balance (falls risk)
o Reduced ROM
 Assessing fitness post-stroke;
o Walking tests – Speed: 10m fastest walk and usual walk.
o Endurance: 6 Minute Walk Test (30m walkway) - turning agility often limited, compromises
performance on 6MWT.
o Shuttle walk test (new use in stroke) – Walk test analogous to the Beep test – 10m walkway
means much turning.

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o Progressive exercise tests- cycle ergometer testing preferred.

o Ramp protocol with 10W increments.
o Treadmill tests only for most well recovered or safety harness available.
 Within 3 months post stroke survivors have very low VO2 max readings- very aerobically
unfit (10.7ml/o2/kg/min). Remains poor even 3 months post-stroke.
 Values <18 ml/02/kg/min suggest difficulty with ADLs and living independently.
 Unilateral strength testing;
o Assess and compare limb performances.
o Shown to be reliable after stroke.
o Spasticity can compromise hemiparetic side.
 Body composition;
o Important to assess for CVD risk.
o Waist circumference important indicator.
 Exercise for stroke;
o Early emphasis is disability rehab- other aspects of fitness often ignored.
o More stroke survivors die of other CVD events than second stroke.
o Capacity to benefit from exercise can last for years.
o Pre-exercise screening should include CVD risk, not just any disability.
 Aerobic exercise;
o Aerobic fitness can improve 10-20%- improves ADL tolerance, QoL, CVD risk.
o Warm up and cool down important.
o Build up to 30-60 min/d most days of week.
o Moderate intensity recommended initially – improvements better if higher intensity.
o Can be difficult to use HR for intensity if on beta-blockers.
o Ideally BP response to exercise monitored initially (RPP max recommended 20,000).
o Modality depends on participant ability and preferences.
 Resistance training;
o No clear guidelines for stroke.
o Functional exercises recommended.
o Pragmatic approach usually used – Lower loads, more repetitions (monitor BP and RPE).
o Improvements may occur with light loads initially.
o For addressing disability – as many repetitions as can be tolerated.
 Flexibility training;
o Goals to increase ROM and prevent joint contractures.
o Hold stretches with mild tension for 15-30 s (no pain).
o Focus stretching on ‘tight’ muscle groups.
o Stretch at end of sessions (when warm).
o May include stretches during RT (between sets).
 Other options;
o Community groups
o Home-based therapy
o Restraint/mirror therapy
 Considerations for exercise and stroke;
o Heart rate is not always a reliable guide.
o Fatigue is most likely to limit intensity.
o RPE may be compromised if cognitive deficits – We have found limited ability in most > 60y.
o Interval training potentially ideal- allows intermittent higher intensity activity and recovery
from fatigue.
o Trunk stability- important for lifting and carrying tasks.

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Spinal cord injury

 Exercise program for unaffected muscles.
 Program dependent on extent of body effected and level of SCI.
 Autonomic disturbances can compromise training capacity.
 Thermoregulation an issue.
 Use only portion of HHR when exercising.
 FES – functional electrical stimulation useful for metabolic health & body comp. Also useful
in mobility training.
Traumatic neuromuscular disorders

 Many questions about use of exercise for NM disorders unanswered.
 How soon? – If CV recovery any guide, earlier better.
 But stroke, not immediately!
 What type? – Functional tasks probably most beneficial – at least initially.
 Maximising affected mm - restrict use of unaffected mm (i.e. restraint therapy) – E.g.
smile/mirror training; put good arm in sling, etc.
 Maximising less affected muscle

o Increase wheelchair independence- add extra weight to chair (specific resistance
training).
o Increase upper body strength and endurance for SCI and spina bifida.
o Increase mm on other side of body with stroke.
o Capacity to increase fitness of unaffected mm should not be different to normal-
strategies should be as similar as possible to normal training.
o Conventional relationship between RPE and HR may not hold in many N-M
disorders.
 Effects of denervation
o Gradual conversion of contraction speeds to be more like F than S.
o Requires extreme disuse for this to happen.
o Has implications for neural control on reinnervation developments.
o Neuromuscular fatigue;
 Due to:
 altered neural activation OR
 altered muscle metabolism
 Potential locations of source of fatigue;
 CNS (Brain, spinal cord)
 PNS
 N-M junction
 Muscle fibre (membrane, SR, actin-myosin)
 In healthy humans, fatigue is usually muscular.
 In disease, most fatigue is initially due to neural changes.
 CNS and fatigue

o Reduced neural activation within CNS.
o Reduced neural activation due to feedback to CNS- may contribute to perceptions.
o Failure of signal from CNS to PNS e.g. spinal cord injury.

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 PNS to muscle
o Reduced activation of alpha motor neurons e.g. motor neuron disease.
o Reduced transmission of action potential in alpha motor neurons e.g. multiple
sclerosis.
o Reduced Ach release e.g. myasthenia gravis.
o Reduced response to Ach.
 Acute neuromuscular fatigue

o Local contractile failure in muscle
 Lack of blood flow.
 Lack of oxygen
 Nutrient fatigue or substrate depletion (Depletion of creatine phosphate or
depletion of glycogen).
 Increased metabolites
 Altered Ca2 + signalling
 Mostly associated with energy production (energy supply fatigue).
 Tools for monitoring fatigue

o Perception of effort – Subjective rating of effort.
o Endurance time – Ability to continue task.
o Contraction intensity – Ability to maintain force.
 Exercise prescription >65 years
Exercise testing
o May not stress-test pre-program.
o Cycle often better than treadmill.
o Are walking tests better than cycle? - Yes more functional.
o Medications may influence test results.
Aerobic
o Frequency: 5 d/wk min
o Intensity: 5-6/10 for mod; 7-8/10 for vig
o Time: 30-60 min mod/d in bouts of >10min OR 20-30 min vig/d (or combination).
o Type: walking most common if possible or aquatic, cycling etc.
Strength training
o Freq: 2 or more d/wk.
o Intensity: 5-6/10 for mod; 7-8/10 for vig.
o Type: Progressive; major muscle groups; 10-15 reps; 8-10 exercises/session.
Flexibility
o Freq: 2 or more d/wk
o Intensity: 5-6/10
o Type: Static not ballistic- sustained stretches.

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Balance
o Falls prevention
o Freq: 2-3 d/wk
o Type: e.g. Tai chi
 Balance (change base of support)
 Agility (change direction of movement)
 Proprioceptive (eg eyes closed; surface)
Walking speed
o Faster walking speeds suggest better QoL.
o May require changes in stride length or stride rate.
o Slow maximum walking speed increases ambulatory risk (e.g. crossing road) and
independence.
Community based programs

o E.g. Heart moves, active over 50s
LECTURE 11: ENERGY SYSTEMS 1

 ATP
o Adenosine triphosphate
o Energy currency of the body.
o Food energy converted to ATP for energy supply.
o Exercise increases demand for ATP.
 3 energy systems
o Phosphate- immediate supply, short duration.
o Lactate- quick supply, short term OR supplements
rate of supply of aerobic system.
o Aerobic- slower supply, long term.

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 All 3 energy systems are present in skeletal muscle.

 Energy systems work together to optimise ATP production.
 Energy systems can operate singularly or collectively.
 Energy system classifications

o Anaerobic (nonaerobic; oxygen independent)
 Adenylate kinase reactions
 Phosphate
 Lactate
o Aerobic (oxygen dependent)
The phosphate system

 Substrate is creatine Phosphate.
 Chemical process is phosphorylation.
 Enzyme is creatine kinase.
 Not oxygen dependent (anaerobic/nonaerobic).
 Does not involve co-enzymes.
 Regulated by ATP:ADP ratio- equilibrium reaction.

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 Initiation of physical activity.

 Sudden increase in activity level (e.g. getting up from chair, running upstairs).
 For very high intensity tasks (weights, sprints, high jump).
 If maximal effort or task only lasts 10-15 seconds.
Lactate system
 Multi-step (10 step) chemical process.
 Provides ATP quickly.
 Second fastest source of ATP.
 Much greater ATP capacity than phosphate system.
 Located in cytoplasm of cells.
 Chemical process is glycolysis.
 Substrates are glucose OR glycogen.
 Results in production of pyruvic acid.
 May result in formation of lactic acid.
 Involves co-enzymes (NADH) - important regulators of lactic
acid production.
 Not oxygen dependent (anaerobic/nonaerobic).
 Key enzymes;
o Phosphofructokinase (PFK) - glycolysis regulator.
o Lactate dehydrogenase (LDH) - lactate synthesis regulator.
 End product of glycolysis is pyruvic acid- 2 fates for pyruvic acid.
o Aerobic use in Krebs cycle (slow glycolysis)
o Conversion to lactic acid (lactate) (fast glycolysis).
 When does pyruvate get converted to lactate?
o Large and rapid demand for ATP – produce lactate (fast glycolysis).
o When pyruvate production exceeds Krebs cycle capacity to use pyruvate due to:
 Low aerobic ATP synthesis capacity
 High intensity activity
o Other unmet demand for ATP.
o Recruitment of fast twitch muscle fibres;
 Increased glycolysis
 Less capacity to use pyruvate aerobically
o Low oxygen levels in tissues
 Lack of oxygen in blood (altitude, respiratory disease, anaemia)
 Reduced blood flow to muscle (e.g. isometric exercise, CV disease)
 Provides energy during high intensity activity that lasts longer than 10 seconds.
 Supplements aerobic ATP supply during higher intensity PA (including aerobic activities).
 Very small quantities of lactate are produced continuously (even at rest) but blood lactate
levels don’t rise as the lactate doesn’t accumulate above a threshold in muscle.
 Intensity at which the lactate system contributes substantially to ATP production depends
on fitness level of person.
 Occurs at lower intensities (workloads) in less fit people.
 Blood lactate accumulates doing everyday tasks in people with low levels of aerobic fitness
or compromised CV/Respiratory systems.
 Blood lactate only accumulates during high intensity activities in those with high levels of
aerobic fitness.

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 Tolerance of blood lactate accumulation varies with training – High in rowers and middle
distance runners. May be relatively high in chronic disease states.
Aerobic system
 Multi-step chemical process.
 Slowest source of ATP.
 Supplies largest amount of ATP.
 Usual substrates are carbohydrates or fatty acids.
 Can also use amino acids.
 Oxygen dependent.
 Occurs in mitochondria of cells.
 Involves co-enzymes.
 Initial steps differ for carbohydrates and fats- later steps are the same.
 Common entry point is Acetyl-CoA- can be entry point for amino acids too.
 3 main chemical processes are;
o Beta-oxidation (lipids only)
o Citric acid (Krebs, TCA) cycle
o Oxidative phosphorylation (in ETC - electron transport chain).
o Coenzymes in ATP synthesis- NADH & FADH2

 Produced by glycolysis, beta-oxidation & citric acid cycle.
 Transfer protons (H+) to ETC (electron transport chain).
 Co-regulators of key enzymes – Play role in most ATP synthesis.
o Electron transport (respiratory) chain
 Co-enzymes oxidised (electrons removed & transferred to oxygen).
 Water and ATP produced.
 Oxygen used in final step of process – Number of steps involve cytochromes.

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o Aerobic ATP synthesis

 ATP synthesis involves the catabolism of substrates;
 Carbohydrates - glucose, glycogen or glycerol
 Fatty acids
 Amino acids
Catabolism of carbohydrates
o Pyruvate (from glycolysis) to Acetyl Co-A.
o Acetyl Co-A through Citric acid cycle- Small amount of ATP produced, co-enzymes
(NADH & FADH2) produced.
o Co-enzymes transfer H+ to ETC- Plus O2 in ETC, large quantities of ATP produced.
Catabolism of lipids (FAs)

o Beta-oxidation- produces Acetyl Co-A & co-enzymes.
o Acetyl Co-A to Citric acid cycle- small amount of ATP produced, co-enzymes (NADH &
FADH2) produced.
o Co-enzymes transfer H+ to ETC- Plus O2 in ETC, large quantities of ATP produced.
Catabolism of protein
o Not usually used for energy during exercise (important in energy restriction).
o Amino acids may be deaminated to form;
 Pyruvate
 Acetyl co-A
 Intermediates of citric acid cycle.
o Metabolism then follows the path of this substrate
 Energy from the aerobic system.

o Provides most energy at rest and during low to moderate intensity physical activity.
o Provides energy for most everyday tasks in healthy people.
o Provides energy for all prolonged activities.
o Provides most energy for endurance sports activities.

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LECTURE 12: ENERGY SYSTEMS 2

 What determines which energy systems you use?
o Task- How fast you need the ATP (rate) and how long you need it for
(duration).
o Energy system capacity- How well your energy systems can provide ATP
(fitness).
o Oxygen availability (environmental/health).
 What happens during recovery from exercise?

o Small surplus of ATP produced aerobically.
 Small amount of ATP stored as ATP.
 Some ATP used to regenerate CP
stores (replenish the Phosphate
system).

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 What happens to lactate during recovery from

exercise?
o In skeletal muscle - lactate converted back to
pyruvate and used aerobically.
o From blood - transported to cardiac muscle,
converted to pyruvate and used aerobically.
o From blood - transported to liver and converted back
to glucose via Cori cycle.
o Conversion of lactate to glucose only occurs in liver-
everywhere else can only convert it back to
pyruvate.
o Conversion of lactate to pyruvate in muscle is greater
if low intensity aerobic activity performed (warm-
down/cool-down).
o Lactate (like glucose) is NOT excreted by kidneys in
healthy individuals- may be excreted in people with
some metabolic disorders (e.g. diabetes).
 Regulators of ATP synthesis
Local
o ratio of ATP:ADP – ACUTE (ATP high, produce less)
o ratio of coenzymes (eg NADH:NAD+) – ACUTE (NADH high produce lactate, ATP
aerobically).
o substrate levels* - DIET (Low levels, less ATP)
o enzyme activity levels* (Higher levels, more ATP)
o number and size of mitochondria* (More mitochondria, more/faster potential ATP).
Neural/hormonal
o Release of adrenaline (epinephrine) → more ATP.
Hormonal
o Thryroid hormones, cortisol, adrenaline, growth hormone, glucagon.
o Cortisol & adrenaline released to greater extent with more prolonged exercise and
increases availability of substrates to produce ATP.
 Energy provision and fatigue

o Fatigue is a feature of many medical conditions as well as low fitness levels.
o Fatigue is often a consequence of limited ability to provide energy.
o Energy systems are highly adaptive and respond to patterns of regular activation
(training or conditioning) or inactivity.
o Fatigue may result from;
 Low ATP and CP stores in muscle (Diet, inactivity)
 Low glycogen stores in muscle (Diet, inactivity)
 Low enzyme activity levels (Inactivity)
 Low lactate tolerance (Inactivity)
 Limited mitochondria (Inactivity)
 Limited ability to provide O2 (Health status, inactivity, environment)

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 Assessment of energy systems

o Only the aerobic system can be measured directly and precisely – Even then, indirect
tests are often used.
o Other energy systems are assessed indirectly- rely on maximal efforts, duration of
activity is the key indicator of relationship to a particular energy system.
o Alactic power and capacity (Energy from ATP-PC ie stores & phosphate system).
o Anaerobic power and capacity (Energy from both phosphate and lactate systems).
o Power – peak output (rate of use).
o Capacity – total output over time.
o Maximal effort exercise is used to assess the anaerobic energy systems.
o For maximal activities lasting 1-2 seconds energy is primarily from ATP stores in
muscle.
o For maximal activities lasting 3-6 seconds energy from ATP-PC system (ATP stores &
PC).
o Power output in these types of tests is used to assess alactic anaerobic power.
o Tests of alactic power;
 1, 3, 5 RM strength tests
 Vertical jump
 Standing broad jump
 Short sprints – 40 m or 40 yd dash
 25 m swim
 Margaria-Kalamen stair run
o Total work performed during maximal exercise of ~ 10 s duration provides a measure
of alactic capacity ie the total work that can be performed by the ATP-PC system
operating maximally and continuously.
o If values are obtained for each second throughout a 10 s test, the peak 1 s value
indicates peak alactic power.
 Tests of alactic power and capacity

o 10 s cycle test
 Pedal all out for 10 s – Peak power output obtained indicates peak alactic power
(Absolute (W) and relative (W/kg) values reported).
 Total work performed in the 10 s indicates the capacity of the alactic system.
o 100 m sprint
 Time for 100m indicates alactic capacity.
 If measure split times (5 or 10 m intervals) can determine peak velocity and peak
acceleration as indicators of alactic power.
o Wingate test
 30 s maximal cycle test
 Provides an indication of peak power output (alactic power) (Usually occurs in first 5
s of test).
 Provides a measure of anaerobic capacity.
 Energy from ATP-PC & glycolytic systems.
 Average power output over the 30 s is an index of total work performed in 30 s (ie
the capacity to provide this source of energy).

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 Anaerobic capacity lab tests

o AIS (1991) Anaerobic treadmill test
 Designed to assess middle distance runners.
 10% grade and 18kph (M) or 16kph (F).
 Time to exhaustion measured.
 Duration provides indication of energy system capabilities and limitations.
 Better scores indicate better lactate system.
 Post-test blood lactates provide an indication of lactate contribution and lactate
tolerance.
o Cunningham and Faulkner (1969)
 Females: 11.3 kph and 20% grade, Males: 12.9 kph and 20% grade.
o AIS Runners Test (2000)
 20 or 22 kph and 4% grade
 Consider specificity in selecting test – Track vs cross-country vs other sports.
 Anaerobic capacity field test

o 300 m shuttle run test
 20 m x 15 shuttles at maximal effort
o Basketball line drill anaerobic test
 Modification of an agility training drill
 Good specificity for testing basketball players.
 Anaerobic power & capacity summary

o Peak anaerobic power is always peak alactic power.
o No reliable mechanism to assess peak lactic power.
o Alactic capacity is typically based on total work (or average power output) over ~10 s.
o Anaerobic capacity measured ~30s-3min
 Shorter time - alactic:lactic ~ equal.
 Moderate time - mostly lactic
 Longer time - little alactic & more aerobic
o Measurement of blood lactate indicates use.
 Tests of peak aerobic power

o Range of different approaches.
o Direct measurement of VO2max.
o Indirect tests;
 Progressive tests to predict VO2max
 Maximal work for time or distance performances
as indicators of aerobic capacity.
 Submaximal tests as indicators of aerobic
capacity.
o V02 max measures- Oxygen consumption (VO2) &
carbon dioxide (VCO2) production measured throughout test.
o Oxygen consumption (VO2) measured throughout test.
o Involves progressive exercise test to exhaustion.
o Performed on an ergometer – Treadmill, cycle, rower, etc.
o Values reported in absolute (mL of O2/min) or relative (to body weight ie mL of O2/kg/
min) units.

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 Criteria for determination of Vo2 max

o VO2 levels off with an increase in workload.
o Reach age-predicted (220-age) maximum heart rate (+ 10 beats/min).
o R value > 1.10 or 1.15 (R = VCO2/VO2) – Indicates H+ buffering due to anaerobic
contribution to energy supply.
 buring fat r= <1
 burn carbs r=1
 Anaerobic r=>1.1/1.5
o Appearance of voluntary exhaustion.
 Progressive tests to determine Vo2 max

o Tests usually conducted on ergometers.
o Subject exercises progressively to exhaustion.
o VO2 not measured- VO2max predicted on basis of last workload attained.
o Precise control of workload essential.
o Assumes average efficiency.
o Multistage Shuttle Run Test (Beep), progressive Step Test, progressive cycle
tests, 7 stage swim test.

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 Time for distance or distance for time tests

o Time to cover required distance.
o Distance covered in fixed time – Cooper’s 12 min run.
o Require maximal effort.
o Reasonable predictors of VO2max.
 Submaximal aerobic tests

o Results are partly workload based.
o Heavy reliance on heart rate responses.
o Examples; Queen’s College Step Test, PWC170 cycle test, YMCA cycle test.
o Less accurate than maximal tests.
 Predictive aerobic tests

o OK for assessing general population- high margin of safety, submax.
o Most sensitive in ‘average’ ranges.
o Lack precision for athletes or low fit.
o Athletes not usually in ‘average’ range.
o May also lack precision for the least fit.
 Energy systems in children

o Lower ATP-PC stores (vs adults).
o Lower oxygen deficits in children.
o Lower peak blood lactate levels.
o Lactate levels rise at similar relative intensities of exercise.
o Anaerobic performances lower than adults.
o Aerobic capacities also lower in children.
o No major pre-pubertal gender differences.
 Energy systems & gender

o Female values < male.
o Partly due to smaller muscle mass.
o Lower total ATP & PC stores.
o Lower peak lactate levels in females.
o Anaerobic performance only slightly less in females when account for muscle
mass differences.
o Aerobic performance also slightly less in females (less muscle, smaller heart).
 Energy system & ageing

o Anaerobic performance;
 Peaks ~ 30 y of age
 Declines steadily to ~ age 60
 Declines faster after ~ age 60
o These declines with aging are typically greater in females than males.
o Aerobic performance – Peaks ~ age 30-40 y

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LECTURE 13: METABOLISM
 Sum of all the chemical reactions in the body.

 ANABOLISM - synthesis reactions (Energy storage, tissue building or maintenance).
 CATABOLISM - breakdown reactions (energy provision, tissue breakdown).
 Catabolism
o Catabolic reactions release energy.
o Exercise is catabolic - substrates are broken down to provide energy.
o Most energy is converted to heat (all except external physical work).
 Calorimetry
o Process of measuring heat energy (production).
o Takes place in a calorimeter (chamber).
o Energy to raise 1L of water 10C is a kilocalorie.
o Human calorimetry;
 Used to measure human metabolism.
 Valid measure in the absence of external
work or physical activity (ie valid at rest).
 Can measure exercise metabolism if
energy used for physical work converted
to heat.
 Can be used to determine metabolic
rates.
 Metabolic rate is heat production
relative to time.

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o Exercise calorimetry; heat production equivalent of energy used during

exercise.
 Direct calorimetry
 Measurement of heat production in a metabolic chamber.
 Physical work converted to heat energy.
 Metabolic chambers rare.
 Indirect calorimetry
 Measurement of oxygen consumption (VO2).
 Relationship between amount of heat produced (in chamber) and amount
of oxygen used (measured) 1 L of O2 ~ 21 kJ (5 kcal).
 Heat energy varies slightly with the substrate used with O2 (above is with
CHO).
 Fat produces slightly less heat than CHO.
 1 kcal = 4.18 kJ.
 2 types;
Closed circuit indirect
o Breathe in and out of a closed chamber.
o Chamber contains 100% O2 at start.
o CO2 an issue – absorbed by soda lime.
Open circuit
o Breathe room air (wearing mask)
o Short term, energy is provided both aerobically and anaerobically.

o Long term, anaerobic energy stores are replenished aerobically.
o Therefore, measurement of oxygen consumption is a valid measure of
metabolism over time or in the absence of anaerobic energy provision.
 Are you using fat or carbohydrate to provide aerobic ATP?

o Know O2 and CO2 concentrations in ambient air – O2 20.9%; CO2 0.03%.
o Measure O2 and CO2 concentrations in expired air – O2 range ~15-20%; CO2
range ~2-5%.
o Determine VO2 used and VCO2 produced.
o Calculate ratio of carbon dioxide produced (VCO2) to oxygen used (VO2) R =
VCO2 /VO2.
o R is respiratory exchange ratio (approximation of cell respiration).
o Reflects cellular respiratory quotient.
o As substrate changes, VCO2 and VO2 relationship changes.
o If R = 0.70 using ~ 100% fats.
o R = 0.85 using mixture of fats & CHO.
o R = 1.00 using ~ 100% CHO.
o Used to determine types of exercise that burn fat.
o If R > 1.0 indicates buffering of acid (H+).
 Substrate use at rest

o Energy source is primarily aerobic.
o Substrates are fats and CHO.

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o Influenced by:
 Content of last food intake
 Time since last food intake (longer- more fat).
o More CHO in meal, use more CHO as substrate.
o Fat is main substrate during overnight sleep.
 Substrate use during exercise

o Intensity is major determinant.
o Low intensity exercise uses mostly fat.
o Higher intensity exercise uses more CHO.
o Fitness level influences the intensity of exercise that burns fat vs CHO.
o Less fit people burn more CHO at a lower intensity, high fit people burn more
fat at a higher intensity.
o Longer duration exercise uses more fat – longer duration exercise is usually
of lower intensity.
o If intensity initially high, intensity usually decreases as glycogen stores
depleted (fatigue or decrease intensity).
o Fitness level influences the intensity of sustainable long duration exercise –
fitter can work harder and still burn fat.
 Oxygen deficit/debt
o At the onset of exercise, the aerobic system takes time to increase ATP
production.
o Initially, ATP from ATP stores & PC system.
o A measure of the ATP not provided aerobically is oxygen deficit.
o Gray area is exercise oxygen consumption.
o Green area is O2 deficit - ATP from ATP-PC (ie not aerobic).
o During recovery from exercise, excess oxygen is consumed relative to current
need for ATP.
o Yellow on Fig 7.8 termed oxygen debt (ie recovery O2 use) or EPOC (Excess
Post-exercise Oxygen Consumption).
o Initially EPOC thought to equal oxygen debt (debt repaid deficit) but EPOC
too large.
o Fast component- reflects requirements to replenish ATP-PC system.
o Slow component- reflects elevated body temperature and thermogenic
hormone effects on metabolism, cardiovascular & respiratory systems.
o Contributed to idea of post-exercise fat burning but;
 Large EPOC is associated with higher intensity or long duration exercise (fit
people).
 Most overweight people can’t perform this level of exercise (i.e. only get
small EPOC).

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 Energy use in cardiac muscle

o At rest - aerobic system (both fats and CHO used as substrates).
o Submaximal exercise primarily aerobic (fats at lower intensities; CHO at
higher intensities).
o Higher intensity exercise – Lactate system contributes increasingly (more
CHO).
o Lactate converted to pyruvate & used aerobically during recovery from
exercise- can take up lactate from blood.
 Metabolic effects of exercise training

o E – Endurance (continuous) training.
o S – sprint/interval training
o R - Resistance training.
o CR - circuit resistance training
o Dependent on FITT.
o Effects on substrate levels;
 Increase ATP & PC stores in muscle with sprint & resistance training.
 Increase is greater with an increase in muscle mass (hypertrophy).

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 Muscle glycogen stores- Increase with E, S, R, CR.

 Increase GLUT-4 transporter numbers- Increases insulin independent
glucose uptake Liver glycogen stores. Increase with E, S, CR
 Increase intramuscular lipid stores- Increase with E.
o Effects on substrate use;
 ATP-PC turnover – Increases (S & CR).
 Glycogen & glucose use;
 Decreases during submaximal exercise (E & CR).
 Glycogen sparing (E).
 Increase gluconeogenesis (synthesis of new glucose) during prolonged
activities (E).
 Fats;
 Increased mobilisation from adipose (E & CR).
 Increased FFAs in plasma (E).
 Increased use of FFAs in muscle (E & S).
 Increased lipid use during submaximal exercise (E & CR).
 Leads to sparing of glycogen (important in long distance endurance events
and for reducing fatigue).
 Protein
 Increased use of branched chain AAs (E).
 Increased gluconeogenesis from alanine (E).
 Occurs most during very long duration activities.
o Changes in muscle fibre mitochondria with aerobic training;
 Increased size & number (E & CR, S/I).
 Specific to muscles & fibres used – See mostly in Type I and IIa fibres.
 Achieved with higher intensity OR longer duration training.
 Increases capacity to use pyruvate aerobically.
 Contributes to increases in VO2max.
o Changes in muscle fibre mitochondria with resistance training;
 Mitochondria – Decreased size (R), Decreased density especially with
hypertrophy of Type II fibres (R).
o Changes in muscle enzyme activities;
 Creatine kinase & myokinase – Increase (R & S).
 Glycolytic enzymes – Variable effects (not all respond).
 May increase glycogen phosphorylase (E).
 Increase PFK (E, S, R & CR).
 Change in LDH activity (isoform) (E, S CR)- lactate dehydrogenase.
 Decrease affinity for pyruvate to change to lactate (E).
 Increase activity of most TCA cycle & ETC enzymes (E, CR, S & possibly R).
 Cardiac malateaspartate shuttle – Increases (E & CR) i.e. heart metabolism
becomes more aerobic.
 Increased activities of many enzymes involved in beta-oxidation - Results in
increased use of FFAs (Contributes to glycogen sparing).
o Changes in use of oxygen;
 Increased myoglobin in muscle fibres (E, S/I).
 Increases rate of diffusion of O2 into muscle.
 Increased storage of O2 in muscle – Myoglobin content can increase by 75-
80% (E).

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 Decreased O2 deficit at onset of exercise – Faster increase in O2 uptake;

less PC depletion.
 Little or no change in VO2 (oxygen use) during same submaximal exercise (E,
CR).
 May increase efficiency (less O2 used).
 Lower VE & HR (less O2 used).
 Increase in VO2max (E, S/I & CR).
o Changes in lactate accumulation;
 Decreased muscle & blood lactate with submaximal exercise (E, S, CR & R).
 Absolute & relative workloads.
 Higher workloads for lactate thresholds (E, S CR, & R).
 Higher lactate at maximal exercise if maximal exercise capacity increases (E,
S & R).
 Higher lactate capacity
 Higher lactate tolerance
 Increased muscle buffering capacity
LECTURE 14: BODY COMPOSITION

 Anthropometry
o Study of body structure & composition.
 Height (stature)
 Weight (mass)
 Body lengths, breadths and circumferences
 Somatotypes (body types)
 Body composition (fat, muscle, bone)
 Relationships to health & sport
 Somatotypes
o Classification of body types referenced to 3 scales;

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o Calculated from body structure measurements.

o Used to provide a score on each somatotype scale.
o Most people are combinations of the three rather than a single somatotype.
o Data can be plotted on a somatochart or somatomap.
 Relationship to health
o Endomorphs – Shortest life span – Prone to CV diseases.
o Mesomorphs – Cope best with physical work.
o Ectomorphs – Longest living.
o Mesomorphs have least postural deficits.
o Ectomorphs have the most problems – Vertebral column problems common
e.g. poked head, round shoulders, kyphosis, lordosis & scoliosis.
o Endomorphs have more leg deformities – partly weight dependent eg Knock
knees, flat feet, everted feet.
 Models of body composition

o Models vary from 2 compartment (fat mass vs fat free mass) to multi-
compartment models.
o 3 main components: muscle, bone, fat.
 Body composition analysis

o Historically a fat focus (more fat = greater risk of ill health).
o Current interest in bone health (osteoporosis risks).
o Growing interest in muscle maintenance.
o Direct measurements only from cadavers.
o Indirect measurements;
 Hydrostatic (underwater) weighing

 Gold standard
 Also called densitometry or underwater weighing.
 Based on effects of body density on weight measured in water – Fat
is less dense than muscle.
 Influenced by: Residual lung volume, hydration, bone density.
 Skinfold thicknesses plus formulas

 Constant tension calipers used to measure subcutaneous skinfold
thicknesses at multiple sites on body.
 Reliable (with experienced assessor).
 Cost effective (though not inexpensive).
 Provide information about fat mass & distribution of fat.
 Do not need to be converted to % body fat to be useful.
 Best in leaner populations.
 Can be converted to % body fat due to associations between
subcutaneous fat, internal (visceral) fat, and whole body density.

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 Conversion formulas are population specific – Vary with age,

gender, ethnicity, physical activity status.
 Usually not practical in more obese populations.
 Girth measurements plus formulas

 Circumference measurements of six
body sites obtained.
 % body fat prediction equations used
to convert measurements to % BF.
 Equations are age & gender specific.
 Reliable but not valid with many
population groups (Can’t tell fat from
muscle).
 Not reliable in highly trained, very
thin or fat, some ethnic groups.
 Electrical impedance
 Less resistance to current flow through
tissue with high water & electrolyte
content (eg muscle 70% H2O; fat 10%
H2O).
 Fat decreases current flow.
 Person connected to electrodes & small electrical current
introduced.
 Results sensitive to person’s hydration status & skin temperature.
 Many of the new ‘Body fat scales’ currently on market use this
method.
 Often:
o Overestimate fat in athletes.
o Underestimate fat in obese
o Some give you BMI as % fat!
 Cheap models single frequency models, expensive ones multi-
frequency devices.
 Imaging techniques
 Many of the imaging procedures have been used to assess body
composition (research).
 Includes: – Untrasound, X ray, CT, MRI & DEXA – All have some
merit. DEXA- most frequently used.
 Provide more accurate idea of visceral and subcutaneous fat
together.
 Very expensive.

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 Air densitometry
 Procedure analogous to hydrostatic weighing – Uses air
displacement & body mass.
 Suggested to be new reference method.
 Reliable but validity still questioned.

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 Reference values
o Storage fat – Mostly subcutaneous.

 Energy stores: M ~12%; F ~15% BW
o Essential fat – 3% of BW for M & F (4-7%)
 Bone marrow, nerves, heart, lungs, liver, spleen, etc
 5-9% gender-specific fat for females
 Stored in breasts, pelvis, buttocks & thighs.
 Adipocytes
o Specialised connective tissue.
o Lipid storage cells
o Number and size of fat cells varies.
o Influenced by food intake & activity levels.
o Genetics influences where located.
o Increase adipocytes by both hypertrophy & hyperplasia.
o Obese individuals have larger & more.

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 Fat cells when losing weight

o Decrease cell size
o Don’t lose numbers*
 Increases vulnerability to regain weight.
 Do have fat cell turnover ~ 10% pa
o Gaining more fat cells in childhood predisposes to
long-term fatness.
LECTURE 15: OBESITY

 Obesity is a state of having excess body fat relative to
that optimal for good health.
 ~ 67% Males overweight or obese.
 ~ 54% Females overweight or obese.
 Female rates are increasing, especially in <35y age
group.
 Childhood obesity rising rapidly.
 Contributing factors
o Genetic
 But this hasn’t suddenly changed.
 Thrifty gene theory and interaction with new environment.
o Environment
 Diet
 Lack of exercise
 Fidget factor- time spent in physical activity after age 6 is proportional to %
body fat.
 Sitting time
 Loss of physical work and transport.
 Inactive leisure time choices.
 ‘Obsegenic environment’- sedentary, stressful, over-abundance of food,
food centred social occasions.

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 Infuences on fat gain

o Maternal weight gain in pregnancy – > 18 kg get fatter baby (more fat cells).
o Gestational diabetes – Fatter baby.
o Breast feeding & slow exposure to solid food – Tends to decrease baby fatness.
o If fat as child, 3 x risk as adult.
o If parents obese, 3 x risk as adult.
o Most obesity creeping (slow gain) – Previously evident at age 40 y, increasingly
evident at age 30 y.
 Health hazards of excess fat

o CV diseases: CAD, stroke, hypertension.
o Type II diabetes.
o Hyperlipidemia
o Sleep disorders
o Gall bladder disease
o Many cancers
o Pulmonary dysfunction, asthma.
o Increased risk with surgery & anaesthesia.
o Aggravated osteoarthritis, gout, low back pain.
o Mood disorders – depression, anxiety.
o Infertility, erectile dysfunction, pregnancy complications.
o Fatty liver disease.
 Obesity (survival) paradox

o BMI 25-30 may be optimal over 65y.
o Mortality/morbidity may be reduced in some diseases if higher BMI in older age –
Eg hemodialysis patients; COPD.
o Rationale – more severe illness, more loss of body weight (and muscle mass).
o Benefits ~lost when BMI >35.
o So don’t recommend weight loss when loss of appetite associated with disease.
 Determining overweight & obesity

o % body fat (BEST) – rarely used (M: >20%; F: >30%) .
o Weight for height tables – Use pre 1980 data for
reference standards.
o Body mass index (BMI).
o Waist circumference.
o Hip circumference.
o Waist:hip ratio.
o Waist:height ratio.
o Reasonable general guides.
o Can’t distinguish between large fat mass or large
muscle mass.
o Acceptable in population studies and clinical populations.
o Use with caution or in conjunction with body fat analysis in active populations.
o BMI better when combined with waist (& hip) measurements or waist:hip ratio for
individuals.

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o BMI;
 Weight / Height2 (kg/m2).
 Widely used in epidemiology studies – Developed for this purpose.
 U-shaped relationship to health.
 Varies with ethnicity.
 An overweight BMI may not reflect fat mass for athletes with larger muscle
mass.
o BMI for age in children;

 Underweight: < 5th percentile.
 At risk of Overweight: 85th-95th percentile.
 Overweight: > 95th percentile.
 Waist circumference

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 Abdominal height
o Measure of visceral obesity.
o Healthy < 25cm.
o Increased risk of CVD & T2D > 30cm.
o In men, increased risk of dementia after 30 years > 25cm.
 Waist to hip ratio

o Measure waist at naval and hips around largest point of buttocks.
o At risk: WHO M > 0.90 F > 0.85.
o Desirable: M < 0.85 F < 0.75.
o WHO suggests W:H is a better predictor in older people (>75 y) than waist or
BMI.
o Waist= insulin. Visceral adiposity.
o Hip= leptin. Subcutaneous adiposity.
 Overweight vs overfat
o Overweight is not always overfat.
o Excess weight may be due to fat or muscle- important to distinguish this (eg
athletes).
o Anyone with higher BMI is overweight- may be some adverse health effects
of overweight but many adverse health effects of overfat.
o Overfat & obese is where excess weight is fat.
 Crude method is BMI plus waist girth.
 Better method is determination of % body fat.
o Normal BMI may mask being overfat.
o If lack muscle, then BMI <25 may not be appropriate cut off e.g. inactive
populations.
o Strong pressure to lower BMI cut-off to 23 for inactive populations.
 Treatment- diet & exercise

o Diet and exercise important for prevention of overweight & obesity.
o Diet and exercise important for maintenance of weight loss.
o Weight-loss NOT the only benefit of exercise.
o Pathogenesis: Strong evidence lack of PA contributes to increased risk of
obesity.
o Symptoms: Strong evidence lack of PA increases & regular PA decreases
obesity.
o Physical fitness or strength: Strong evidence higher PA level influences PF in
obese.
o Quality of life: Strong evidence higher PA level influences QoL of obese.
o Type of exercise most beneficial:
 Large amounts of mod intensity aerobic exercise.
 Combine with moderate amounts of strength training (at least 30 min daily).

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 To lose weight, must create energy deficit (this usually requires at least 60
min daily to be substantial).
o Effects on body weight inconsistent.
o Decreases body fat mass (% body fat).
o Decreases abdominal fat mass.
o Counteracts loss of muscle mass associated with dieting for weight loss.
o Prevents weight gain.
LECTURE 16: ENERGY BALANCE
 Energy imbalance
o Failure to achieve energy balance contributes to many disease states.
o If energy balance is neutral, body weight is maintained.
o If energy balance is positive, body weight (and usually adipose tissue)
increases.
o If energy balance is negative, body weight decreases.
o If energy input = energy output then in energy balance.
o Energy input = food intake
o Energy output = energy expenditure
 Total daily energy expenditure (TDEE)

o TDEE - Can be determined accurately from studies using double-labelled
water (DLW)– Expensive & impractical (except for research).
o DLW isotope based method to estimate total daily energy expenditure.
o Heavy water: – 2H (deuterium) and 18O (oxygen).
o Urine samples collected and assayed to determine rate of loss of isotopes.

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o Provides TDEE over days.

o TDEE - Usually calculated (estimated).
 Calculations based on knowledge obtained from measurements of
metabolism.
 Lot of assumptions can lead to inaccuracies.
o TDEE has 3 components;
 Resting metabolic rate
 Sleeping metabolism
 Basal metabolism
 Arousal metabolism
 Resting metabolic rate (RMR) can be measured under standardised
OR nonstandardised conditions.
 Resting metabolic rate is not necessarily Basal Metabolic Rate
(BMR).
 Basal metabolic rate is measured under specific standardised
conditions.
 Basal metabolic rate is the minimal energy needed in the awake
state.
 Basal metabolic rate measurement conditions;
o After a 12 hour fast
o After a restful night’s sleep
o Awake for 30-60 minutes and resting
o No exercise since waking
o Environment: (Temperature ~ 25oC, Barometric Pressure ~
sea level, Humidity ~ 50%).
 Metabolic rates reported relative to body surface area (kJ/m2 /h).
Usually used at rest. Body surface area affects rate at which heat is
lost from the body.
 Can be reported relative to body weight (kJ/kg/min) – usually used
during exercise.
 Thermic effect of feeding & other influences
 Thermic effect of physical activity
 Influences on metabolic rate

o Thyroid hormones – Higher levels increase RMR
o Gender – M > F
o Fat-free (lean) body mass – Higher with more skeletal muscle.
o Protein turnover – Higher with more protein turnover (growth).
o Age (decreases with age)
o Pregnancy & lactation (rates elevated)
o Climate (cold vs heat- cold and heat ↑ rate. Comfortable keeps ~constant).
o Fever (temp & rate ↑)
o Nutritional status (starving- ↓ rate)
o Health status

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 Effect of feeding on TDEE

o DIT - Diet-Induced Thermogenesis
 Obligatory thermogenesis (SDA) – Energy required for digesting, absorbing
and assimilating food.
 Facultative thermogenesis – Thermic effects of activating sympathetic
nervous system.
o DIT usually peaks ~ 1 hr after eating.
o Influenced by nutrient content of food – Usually greater with higher protein
content.
o Overweight people often have lower DIT than normal weight people.
o Elite endurance athletes may also have lower DIT than normal (reduced
Energy Availability).
 Physical activity components of TDEE

o Occupational (increasingly low)
o ADLs
o Sport and recreation (exercise)
o PA has potential to have greatest impact on TDEE.
o Most people can sustain PA levels 5 X RMR (5 METs).
o Most people should be able to sustain PA levels 10 X RMR.
o Elite endurance athletes able to sustain PA levels 20 X RMR.
o Endurance athletes may have TDEE double normal person due to training.
o Intensity of activity
o Duration of activity
o Amount of muscle mass activated
o Weight-bearing activity (moving body mass costs more energy)
o Efficiency (economy of movement)
o METs- metabolic equivalents of tasks
o 1 MET = resting energy expenditure.
o 1 MET ~ 3.5 mLO2/kg/min (2.5-4.5).
o Can describe PA or exercise in terms of METs ie as multiples of resting energy
expenditure.
o Usually by measurement of oxygen consumption- used to develop energy
expenditure tables.
o Tables assume no variation between people in efficiency at performing
physical tasks.
o Minutes of activity doing tasks used to estimate total daily energy
expenditure (assumes efficiency doesn’t change over time).
 Terms relating to food intake

o Hunger – Amount (quantity) of food sought.
o Appetite – Type of food sought.
o Satiation – Loss of interest in food.
o Anorexia – Absence of any desire for food.

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 Role of the hypothalamus

o Centre of food intake regulation.
o Contains 2 sets of food regulatory centres;
Lateral hypothalamus (R&L)

 Feeding (hunger/appetite) centres.
 If stimulated; increases hunger, increases appetite, increases salivation (via
parasympathetic NS).
 If damaged or destroyed – lose desire for food.
Ventromedial hypothalamus (R&L)

 Satiation centres
 If stimulated- satiated (loss of hunger/appetite).
 If damaged or destroyed- Voracious eating (can result in obesity), may be
factor in poor eating control with some genetic disorders (Prader-Willi
Syndrome).
 Regulators of food intake

o Inputs to hypothalamus
 Both short term and long term regulators.
 In short term, energy balance is ‘poor’
 In long term, energy balance is ‘good’
o Signals from energy stores
 Leptin, adiponectin & resistin from adipose.
 Insulin levels re blood glucose
 Signals from gastrointestinal tract (GIT) – chemical or mechanical
 CCK (cholecystokinin) -SAT
 Glucagon-like peptide 1 –SAT
 Peptide YY3-36 – SAT
 Ghrelin - AS
 (SAT – satiety, AS - Appetite stimulate)
o Neuronal influences from the GIT – Gastric distension (mechanoreceptors).
o Neuropeptides in the brain;
 Neuropeptide Y (NPY) - AS
 Agouti gene-related peptide - AS
 Orexins - AS
 Melanocortins – SAT
 Alpha-melanocortin-SH – SAT
o Psychosocial factors have variable effects;
 Smell, taste and texture of food.
 Stress, anxiety, depression, boredom
 Food availability
o Food reward (palatability/hedonism) – Food centres in brain adjacent to
addiction brain sites (proposed links to ‘food addiction’).

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o Leptin:
 Hormone secreted by adipose tissue.
 Only discovered in 1990s – breakthrough.
 Role in long term energy balance.
 Blood levels reflect TG (triglyceride) stores in adipose tissue ie more
fat stores, higher blood leptin levels.
 Binds to receptors in ventromedial hypothalamus (satiety).
 Triggers onset of puberty (when fat stores sufficient to maintain
pregnancy?).
 May influence reproductive hormones & fertility.
 Influences immune function.
 Suppresses appetite.
 Increases metabolic rate (via SNS).
 Inhibits NPY (neuropeptide Y) secretion- action increases appetite &
decreases SNS effects on metabolic rate.
 In mice, mutated ob gene produces LOW leptin levels and excessive
obesity.
 In humans, obese usually have excessively HIGH leptin levels- suggests
alteration in leptin receptors.
 Short term food intake regulators

o Gastric distention
 Main role is regulating gastric emptying.
 Once thought very important in limiting food intake-now thought to play a
more minor role.
 Role increases with gastric surgery.
o Blood glucose and insulin levels
 Increased glucose absorption increases blood glucose levels and stimulates
insulin release.
 Elevated blood glucose & insulin levels thought to influence satiation.
 Low blood glucose levels stimulate appetite.
 NOTE – low cell glucose levels also stimulate appetite
o CCK (cholecystokinin) secretion
 Increased secretion from duodenum when food in small intestine.
 Signals presence of nutrients still to be absorbed.
 Contributes to satiation.
 Stimulated by fats & proteins.
o Orexins
 Released from lateral hypothalamus when blood glucose levels low.
 Stimulate appetite.
o Takes some time (mins to hours) to exert effects.

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 Loss of appetite and anorexia

o Drugs
 Appetite suppressants (Amphetamines)
 Drug induced aversions such as with chemotherapy drugs.
o Diseases associated with cachetin – E.g. renal failure, cancer, tuberculosis.
o Psychiatric conditions – E.g. Anorexia nervosa.
o Most people cannot voluntarily control hunger or severely restrict food
intake except over very short time frames.
o Characteristics of anorexia nervosa (probably genetic disorder with triggers)
are absence of hunger and progressive aversion to increasing range of foods.
o Chemotherapy may produce food aversion.
o Anorexia common in older populations.
 Protein metabolism
o Protein breakdown metabolic products are anorexic modulators.
o Characteristic of low energy intake.
o Characteristic of chemotherapy.
o Characteristic of starvation.
o In evolution, may have provided hunger moderation when food unavailable.
LECTURE 17: EATING DISORDERS AND EXERCISE & REPRODUCTIVE FUNCTION
 Eating disorders
o Psychological or psychiatric disorders
 Anorexia nervosa
 Bulemia nervosa
 Anorexia athletica
 Binge eating disorder
o Range in severity - clinical & subclinical conditions.
o Usually diagnosed with psychological investigations.
 Binge eating disorder

o Regular and compulsive over eating.
o Eat when not hungry.
o Eat even when full.
o Eat fast; not register taste or content.
o Eat in secret (may horde food)
o Not countered by vomiting/fasting/exercising.
o May be associated with depression and poor self-esteem – Feel powerless to
stop eating.

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 Anorexia nervosa
o Gender – Women >> men (M ~ 5-10%) – young.
o Genetic predisposition – Strong family links.
o Triggers – multiple theories – Abuse may contribute to severe cases.
o Age – late childhood-adolescence (most widely recognized).
o Anorexia more common in older people- previously unrecognised extent of
this problem.
o Expressed as behavioural disorders.
o Often co-exists with obsessive-compulsive disorder- over-represented in high
entry uni programs & elite sport (high achievers).
o Disordered self-image a component of the psychosis.
 Health risks of eating disorders

o Malnutrition
o Amenorrhoea (cessation of menstruation) & osteoporosis risk
o Acid damage to GI tract & teeth/oral cavity with bulimia
o Electrolyte imbalances (Na, K)
o Oedema
o Cardiac arrhythmias (cause of death in anorexia).
o Death – Anorexia nervosa most lethal psychiatric disorder in young women
(0.5-1% of population).
 Eating disorders and appetite

o Minnesota semi-starvation project
 Determine how to re-feed starving people.
 Conscientious objectors as subjects.
 Observed these people became obsessed with food- obsessions went
away with feeding.
o People with eating disorders are often obsessed with food.
o Thought if they re-fed them (forcibly) they would recover.
o War-people starved but not by choice- obsessed to get food.
o Eating disorder people appalled by food- obsessive about avoiding food.
 Eating disorders and exercise

o Excessive exercise is a not uncommon component of anorexia nervosa
(athletica) – Increases the rate of weight loss (BW 35-40 kg).
o Athletes with eating disorders not uncommon.
o Exercise as therapy for eating disorders
 Usually try to exclude aerobic activities.
 Recommend resistance training to try & maintain muscle mass.
 Exercise and reproductive function

o Energy imbalance causes energy deficit (drain).
o This affects reproductive function of both men & women.

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 Consequences for female reproductive function

o Altered menstrual cycles
 Delayed menarche possible – Oligomenorrhoea (35-90 days between
menstrual cycles).
 Amenorrhoea- no menstrual cycles for 3 consecutive months.
 Low body fat is indicator of energy balance issue.
 Thyroid hormone status big influence.
o Who is at risk of amenorrhoea?
 Females with high training volumes.
 Females with weight loss or a particular aesthetic as a goal.
o Female (athlete) triad – Energy drain, amenorrhoea, osteoporosis.
o Short term consequences;
 Recurrent or multiple stress fractures (↓ oestrogen).
 Low body mass & muscle mass
 Depression
o Long term;
 Increased risk of osteoporosis.
 Reduced risk of oestrogen dependent cancers.
 Uncertain (but usually not adverse) influence on long term fertility potential
- unless disordered eating is the major problem.
o Effects on bone;
 Cessation of menstruation associated with loss of oestrogen – Increase
calcium loss, decrease bone density.
 Severity of menstrual dysfunction depends on energy imbalance.
 Severity of bone disorder proportional to severity and duration of menstrual
dysfunction.
 Treatment of athletic amenorrhea

o Reduce training volume 10-20%
o Increase energy intake 5-10% – Attain small increase in body weight as indicator of
energy balance change.
o Calcium intake of ~ 1500mg daily.
o Also often put on contraceptive pill as source of oestrogen.
 Consequences for males

o Decreased testosterone levels to low normal range.
o Reduced fertility potential
 Lower sperm counts
 Reduced sperm motility
 Increased morphological abnormalities
o Effects on bone? Not yet clear
o Who is at risk?
 Males with high training volumes.
 Males with weight loss or energy restriction as a goal.
o Consequences similar to females
 No simple signal like loss of menstruation.

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 More likely to not be identified until severe.

o Exercise on reproductive function
 Increased intrascrotal temperature – Alters sperm viability – Common with
cycling.
 Testicular microtrauma – Common in contact sports.
 Obesity and reproductive health

o Obesity associated with decreased fertility in men and women.
o Obesity associated with erectile dysfunction in men.
o Weight loss associated with improved erectile function in men.
LECTURE 18: EXERCISE AND PREGANANCY
 Higher levels of physical fitness prior to pregnancy recommended

o Musculoskeletal fitness
o Aerobic fitness
o Body composition
 Considerations for exercise during pregnancy

o Maternal changes during pregnancy
 Weight gain (10-14 kg; most in 3rd trimester).
 Increased nutrition required ~ 1200kJ/day after 1st trimester.
 More carbohydrate needed
 Increased weight usually has little negative impact on joints.
o Lordosis and back pain occur in ~ 50% of women late in pregnancy.
 Balance problems & falling uncommon- Usually preclude activities
with high risk of falls.
o Increase in ligament laxity due to relaxin.
o Respiratory changes - increased VE – Can limit exercise in latter stages.
o CV changes - are progressive.
 Increase blood volume, HR, SV, CO
 Decrease in MAP ~ 5-10 mmHg mid-pregnancy; returns to normal in
latter stages of pregnancy.
 Supine or prolonged standing may decrease VR (vena cava
compression).
o Thermoregulation
 Increase in BMR
 Increased need for hydration monitoring
 Concern greater than evidence of problems.
o Risks to foetus
 Concern greater than evidence except with contraindications.
o Urinary incontinence– Affects 32-64% of women.

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 Exercise during pregnancy

o Caution recommended but based mostly on theoretical rather than evidence-
based risk.
o There are some high risk situations where exercise is contraindicated.
o Medical considerations;
 Heart Problems.
 Asthma or Chronic Lung Problems.
 High Blood Pressure.
 Extreme weight problems (Under or Over).
 Muscle or Joint Problems.
 History of premature labor.
 History of several miscarriages.
 Multiple Pregnancy
 History of Incompetent Cervix
 Persistent Bleeding
 Placental Problems (Previa, etc.)
o Warning signs to stop exercise;
 Headache
 Dizziness
 Heart palpitations
 Chest pain
 Swelling of the face, hands or feet
 Calf pain or swelling
 Vaginal bleeding
 Contractions
 Deep back or pubic pain
 Cramping in the lower abdomen
 Walking difficulties
 An unusual change in baby's movements
 Amniotic fluid leakage
o If no regular exercise prior to pregnancy;
 Check with Dr Prior to commencing program.
 Generally recommend lower to moderate intensity aerobic exercise – 30
min daily at 3-5 METS (moderate intensity walk).
o If no pre-pregnancy exercise;
 Don’t try to obtain substantial fitness gains.
 Don’t use exercise for large weight loss (unless medically recommended &
supervised).
 Use exercise to stabilise weight & maintain fitness.
o If exercised prior to pregnancy;
 Generally OK to continue training.
 Usual aim is to maintain fitness not improve.
 Many female athletes maintain high level of training until late in pregnancy.
 Aerobic exercise recommendations

o Large muscle group dynamic activity – E.g. walk, jog/run, dance, swim, cycle,
row.

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o 30 min/day low-mod intensity.

o 20-60 min 3-5 x/week if higher intensity.
o RPE of 11-13 often recommended – Heart rate NOT reliable for monitoring.
o Recommend that program is NOT progressive i.e. maintain intensity.
o Exclude higher intensity activities in latter stages of pregnancy.
 Reisistance training recommendations

o Limited data for evaluation – Generally no evidence of adverse effects.
o 1 set of 12 reps for variety of muscle groups.
o Avoid sustained isometric & heavy resistance activities.
o Core exercises important for addressing abdominal separation (diastasis
rectus) but long list of conventional exercises to avoid too.
 Flexibility training
o Limit activities to normal range of motion.
o Activities associated with lying supine usually excluded.
 Exercise exclusions
o Scuba diving (foetus affected).
o Altitude - depends on level.
o Supine exercise - decreased VR.
o Skiing - falls risk.
o Contact sports
 Benefits of exercise
o Increased fitness to cope with load.
o Limit weight & fat gain.
o Improve digestion
o Decrease constipation
o Decrease back pain
o Increase mental health
o Easier labour & decreased complications.
o Fewer pregnancy complications.
o Faster recovery after delivery.
o Decreased risk of caesarian delivery.
o May decrease blood pressure in those at risk of gestational hypertension-
effects variable.
 Foetal benefits of exercise

o Decreased risk of excess birth weight.
o Decrease in fat cell growth.
o Increased tolerance of stress.

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o Increased neurological development.

o Assumes adequate but not excessive maternal nutrition.
 Special pregnancy populations

o Diabetes – Type I and Type II- Exercise may aid blood glucose regulation.
o Obesity (BMI > 33 during pregnancy)
 Exercise may reduce risk of gestational diabetes.
 Obesity increases risk of pregnancy complications
o Chronic hypertension – Little data available.
o Small evidence reduces risk of pre-eclampsia (rapid change BP).
 Post-pregnancy exercise
o Return to exercise slowly after delivery.
o Influenced by delivery complications;
 Usually OK 6-8 weeks postpartum.
 Consider abdominal separation
o Exercise does not compromise breast milk quality or quantity if nutrition
appropriate.
 Recommend breast feeding prior to exercise
 Less breast discomfort during exercise.
 Less lactic acid in milk.
o Benefits;
 Maintain or regain fitness.
 Maintain or lose body weight.
 Decrease risk of post-partum depression.
 Stress relief
 Pregnancy & the pelvic floor

o Pelvic support structures
 Bony pelvis- Protect/support GIT & genitourinary structures.
 Peritoneum- Holds viscera
 Pelvic diaphragm (muscles & connective tissues)- stretches across pelvic
floor.
o Muscular floor of pelvis – Sling-like support for;
 Uterus - pregnancy
 Vagina - delivery
 Bladder - urination
 Rectum – defecation
o Openings for urethra, rectum, vagina- Introduce weakness into structure.
o Ligaments hold structures in place;
 Uterosacral - hold uterus forward.
 Broad - uterus, fallopian tubes & ovaries.
 Round & cardinal - cervix

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o Pelvic floor structures operate against;

 Gravity
 Increased abdominal pressures e.g. cough, sneeze, defecate, and laugh.
o Pregnancy/childbirth
 Overstretches pelvic floor- May or may not cause immediate problems.
 Worsens with aging (50-60 yrs.) as lose elasticity & muscle tone in tissues.
o Range of conditions associated with damage to pelvic floor;
 Cystocele - bladder herniates into vagina
 Alters bladder emptying
 Increases risk of cystitis
 Stress incontinence (squat, lift, cough, sneeze etc.)
 Rectocele
 Herniate rectum into vagina.
 Difficulty defecating
 Enterocele- Herniate small bowel between uterosacral ligaments.
 Produces low back pain
 Uterine prolapse- Stretched cardinal ligaments.
 Causes; Childbirth, pelvic tumours, neurological disorders where pelvic
muscles denervated.
o Role of pelvic floor exercises;

 Recondition pelvic floor muscles after pregnancy.
 Recommended for all men and women as they age.
 May improve quality of sex life.
 Tighten the ring of muscles around your front and back passages, drawing the
muscle up inside.
 Hold this position for as many seconds as you can.
 Try this exercise up to ten repeats, three times a day.
 Identify the correct muscles to exercise by imagining you are trying to stop yourself
passing wind (farting) or stopping the flow of your urine stream.
LECTURE 19: RESPIRATORY FUNCTION & EXERCISE
 Are skeletal muscles.

 Different muscles used for inspiration & expiration.
 Inspiration always requires muscle activation.
 Expiration passive at rest (except in disease) but active during physical activity.
 These muscles can suffer weakness & fatigue.
 Neural regulation
o Neural control centre: Respiratory centres in pons & medulla. Site of
integration for control of breathing.
o Interconnected with CV and somatic nerves.
o Somatic motor outputs – respiratory muscles (skeletal muscles).
o Motor outputs - autonomic nerves;
 parasympathetic (airway smooth muscle, drive ↓→ dilated airways )
 Sympathetic (blood vessels, ↑ drive → vasoconstriction).

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o Sensory inputs
 Chemoreceptors
 Central & peripheral
 Major inputs at rest
 Respond to pH, pCO2, pO2 (in that order)
Chemoreceptors (major inputs at rest).
Proprioceptors (important during exercise).
Thermoreceptors (stimulated by heat).
Lung stretch receptors (least influence - may protect against over
inflation).
o Other inputs – higher motor commands (Motor cortex).
o Control of breathing
 Automatic breathing is NOT under autonomic neural regulation.
 Most breathing controlled from brainstem.
 Voluntary breathing controlled from cortex- overrides brainstem.
o Hormonal influences
 Adrenaline – exercise hormone
 Important bronchodilator
 Acts on Beta-2 receptors
 Asthma reliever drugs act on these receptors (e.g. Ventolin)
 Lung volumes & capacities

o 4 volumes – TV, IRV, ERV, RV
o 4 capacities – IC, FRC, VC, TLC
o Capacities are combinations of volumes;
 IC – TV + IRV
 FRC – RV + ERV
 VC – IRV + TV + ERV
 TLC - IRV + TV + ERV + RV
 Ventilation at rest
o VE ~ 6 L/min
o VE = Tidal volume (TV) X frequency of breathing
(f) [ie respiratory rate]
o TV ~ 500 ml / breath
o f ~ 12 breaths / min
 Response to exercise
o Increases in VE involve:
 Increases in TV (up to FRC)
 Increases in breathing rate (up to ~ 70 /min)
o VE increases in anticipation of physical activity.
o VE increases in proportion to workload.

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o VE decreases immediately when cease activity (but takes time to return to

resting levels).
o Only small increases in VE during most isometric activity.
o Large increases in VE during large muscle dynamic activity.
o Maximum VE > 200 L/min during physical activity in larger males.
o This is hyperpnoea NOT hyperventilation (when VE is over what is required
for metabolic demand).
 Ventilation relative to Vo2

o Increases in VE are proportional to VO2 with mild/moderate physical activity.
o VE increases more than VO2 at higher exercise intensities.
o Point where VE increases more than VO2 is called ‘Ventilatory anaerobic
threshold’.
 Ventilatory anaerobic threshold

o Associated with:
 Onset of Blood Lactate Accumulation (OBLA).
 Rise in blood lactate & H+ levels increased recruitment of FT fibres (ie
harder work, more force, produce more lactic acid) - feed-forward.
 Acid base balance in high intensity exercise

o Respiratory adjustments important for acid-base balance in body
H+ + HCO3 ↔ H2CO3 ↔ H20 + CO2
o Involves enzyme carbonic anhydrase.
o Increase in VE aids expiration of increasing CO2 with exercise.
o Increased VE helps deal with acid produced by muscles during exercise.
o Breathing not only aids provision of oxygen but coping with acid produced by
muscles.
o Provides O2 and eliminates CO2 and H+
o H+ + CO3- ↔ H2CO3 ↔ H20 + CO2
o Any disease that limits breathing makes it difficult to sustain hard physical
work.
o People with respiratory diseases will usually fatigue more rapidly than
healthy people.
 Work of breathing
o Moderate intensity exercise – Increase TV more than frequency.
 Better for gas exchange.
 Costs less energy
o Higher intensity exercise – Most increase is in frequency.
 Higher energy cost & RPE for breathing.
o In normal person, breathing effortless up to mod intensity exercise.
o Increases in surfactant secretion (Type II alveolar cells) contribute to
decreased effort- May contribute to ‘Second Wind’ phenomenon.

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 Energy cost of breathing

o Energy cost of VE low at rest & mild-mod exercise.
o Energy cost of VE increases disproportionally with high intensity exercise;
 May reach 15% of VO2
 Requires greater blood flow to respiratory muscles.
 Respiratory limitations uncommon in healthy people

o Most young people have a substantial respiratory reserve.
o Even maximal exercise rarely requires us to use our maximal respiratory
capacity – Ventilation rarely limits endurance performance in young healthy
people.
o This excess capacity is gradually reduced with aging.
 Respiratory responses to endurance training in healthy people

o Little change in static lung volumes.
o Increase diffusing capacity of gases in lungs.
o Decrease VE at submaximal workloads
 Less work, less energy expended
o Increase VE during maximal exercise
 Increase aerobic performance
 Use more of MVV
 Increase both tidal volume & breathing rate
 Increase endurance of ventilatory muscles
 Adaptions to regular swimming & diving

o Increase size of static lung volumes
 Increased strength & endurance of inspiratory muscles
o Increased FVC
o Entrain breathing to locomotor pattern – More uniform breathing.
LECTURE 20: RESPIRAYORY FUNCTION & EXERCISE II
 Ageing & respiratory function

o Reduced elasticity and increased stiffening of respiratory structures.
o Decreased lung capacity (VC).
o Respiratory muscle atrophy and reduced respiratory muscle performance.
o Decreased breathing efficiency.
o Decrease TV; Increase RR (16-25 br/min).
o Decreased number and size of alveoli
o Decreased surface area for gas exchange.
o Decreased cilia – increased infection risk
o Blunted cough reflex
o Respiratory illness impacts on work (and energy cost) of breathing and
capacity to exercise or perform physical activity (decrease tidal volume).

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o Increase frequency of breathing.

o Dyspnea - difficulty breathing at rest or during exercise.
 Is mostly symptomatic of respiratory illness.
 Is symptomatic of most respiratory illness.
 Cycle of declining function

o Breathlessness, discomfort and effort associated with physical activity.
o Consequence - ↓ physical activity.
o Progressive deconditioning – Reduced respiratory muscle performance –
Reduced peripheral (eg locomotor) muscle performance.
o Muscle atrophy, reduced aerobic enzyme capacity, etc.
o Aerobic muscle fibres more aerobic.
o Further discomfort associated with physical activity – Reduced quality of life.
 Aggravating factors
o Poor nutrition – Common in aging.
o Medications – Long-term corticosteroid (anti-inflammatory) use.
 General exercise recommendations

o Endurance exercise – Interval training a particularly effective strategy.
o Requires higher intensity respiratory stress.
o Strength (resistance) exercise.
o Once was contraindicated.
 Benefits of exercise
o Decrease dyspnea (reduce breathlessness).
o Increased efficiency of breathing
 ↑ tidal volume
 ↓ respiratory rate
 ↓ ventilation during submaximal activities
o Reverse muscle dysfunction
 ↓ weakness and fatigue
 Both strength and endurance training can help.
o Improve exercise (physical) performance and tolerance – 6-min walk test.
o Increase energy expenditure – ↑ fat loss to address obesity, especially
abdominal obesity, & sleep apnea.
o Increase quality of life.
o Some benefits with low intensity activity.
o Benefits increase with intensity – Interval training increases intensity.
o Benefits vary with program duration
 See effects with 4 weeks training
 Longer programs, better effects
o Individualised programs better than generic programs.

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 Respiratory muscle training

o Benefits unclear in healthy people.
o Improvements in inspiratory and expiratory measures in older people- Trials
promising in patient populations.
o Don’t need to use exercise alone- can combine with; pharmacological,
oxygen, surgery, nutrition.
 Respiratory abnormalities
o Obstructive disorders- Normal airflow impeded.
 Obstruction of airways → impaired airway flows.
 Destruction of lung parenchyma – ventilation/perfusion mismatch →
compromised gas exchange.
 E.g. COPD, CF, asthma
 Indices of air flow; FIF – Forced Inspiratory Flow, PEF – Peak Expiratory Flow,
FEF - Forced Expiratory Flow, FVC – Forced Vital Capacity (FEV1:FVC should =
>80% normal).
o Restrictive disorders – Reduced lung volumes.
o Consequences of CV dysfunction.
o Infection related disorders.
 Asthma
o Characterised by wheeze, breathlessness, tight chest & night cough.
o Range of triggers induce response – Exercise can be a trigger.
o Incidence increased over last 50 years – Role of obesity- increases probability
and severity of asthma.
o Hygiene hypothesis- increasingly sterile environments causing attacks.
o Still contributes to death as well as disability.
o Also EIA (exercise-induced asthma), EIB (exercise-induced
bronchoconstriction).
o Variety of triggers; allergens, RTIs, dry air, change in airway osmolality, cold
air, exercise (EIA & EIB), hyperventilation, drugs (eg aspirin), airborne
chemicals (e.g. cooking gas; cig smoke), food preservatives, gastroesophageal
reflux, hormonal disturbances, emotional upsets (neural/hormonal).
o Wide variations in capacity to exercise.
o Exercise tolerance varies with current status – exacerbations may require
reducing or abstaining from exercise.
o Exercise testing;
 TM or cycle for maximal exercise test.
 Protocol of 8-12 min duration.
 Assess exercise-induced bronchospasm
 Pre-exercise spirometry assessment
 Post-exercise spirometry assessments every 5 min for 30 min.
 Decrease in FEV1 of 15% post-exercise is diagnostic.

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 Eucapnic ventilatory hyperpnea (EVH) may be an effective surrogate

challenge to exercise (breath hard & fast as if you were exercising).
 Benefits;
 Increased aerobic fitness
 Decreased frequency & intensity of asthma symptoms.
 Decreased visits to emergency depts
 Decreased anxiety with physical activity.
 No evidence that regular exercise can prevent the development of
asthma.
 Limited evidence that regular exercise can limit many of the
symptoms of asthma (Fewer attacks, less anxiety, less dyspnea).
 Moderate evidence that regular exercise can increase quality of life.
 Strong evidence that regular exercise can increase physical fitness
(VO2max) and PWC in asthmatics.
 Training recommendations
 Aerobic conditioning
o Mode: swim, cycle, run, games
o Choice is age & personal preferences dependent.
o Frequency: 3-5xWk
o 5xWk if lower intensity- 3xWk if higher intensity.
o Intensity: Mod to High - 60-90% HRmax
o If unfit, commence with low-moderate intensity.
o Interval training an excellent approach
o Duration of sessions: 20 min minimum to 60 mins
 Resistance training – 70% 1RM; 2-3 times a week
 Considerations;
 Environment and trigger exposure
 Warm air better than cold air
 Moist air better than dry air
 Avoid known triggers e.g. Foods, allergens, pollution, dry
windy conditions, etc.
 Medications;
 Pre-exercise B2-agonist or leukotriene antagonist medication 20 min
prior to exercise.
 NB 20% Caucasians have adverse B2agonist polymorphism- Ventolin
makes respiratory system worse/no effect in these people.
 Regular use of preventative medications (15-20mins before exercise.
 Contraindications
 During acute exacerbation of condition.
 During respiratory infection.
 Why recommend swimming?
 Humidified air
 Reasonable air temperature
 Reduced allergen exposure
 Structure to breathing pattern – Entrain breathing to swim stroke.

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 Wide availability to structured programs for children.

 Interval training typical.
 Cystic fibrosis
o Genetic (autosomal recessive) disorder.
o Mutation of chloride channel.
o Relatively common in Caucasians – Rare in other populations.
o Most common cause of chronic lung disease in kids
 Prognosis ~ 50% survive to age 20yrs
 Prognosis improves with aerobic fitness
 Priority candidates for lung transplants
o Pancreatic effects more variable
 Mainly exocrine pancreas affected
 ~ 10% are diabetic
o Considerations for exercise
 Age of client (~70% kids/adolescents)
 Severity of disease
 Nutritional/GI status
 Climate – Warm & humid preferred but increases concerns for salt/fluid loss
& replacement.
 Altitude problematic.
o Aerobic training;
 Mode: Involve major muscle groups
 Frequency: 3-5 x wk
 Intensity: 70-85% measured peak HR if tolerated
 Duration: 20-60 min (~age & fitness)
 Progression: gradual
o Interval training
 Provides variety & higher intensity
 Improves anaerobic capacity, muscle strength & endurance
 Common in swimming
 Appropriate for team sport conditioning
 Frequency – Not more than 3 x week if high intensity.
 Duration – 20-30 min per session.
o Resistance training
 Emphasis on repetitions rather than load.
 Avoid Valsalva maneuvers (may cause pneumothorax).
 Improves anaerobic capacity, muscle strength & endurance.
 Frequency - 3-5 x week
 Intensity - 60% of 1RM; 10-15 repetitions; 2-3 sets.
 Duration - 20-30 min per session.
 Progression - slow; increase reps before loads.
o Flexibility training
 Frequency - 2-7 x week
 Intensity - 10-30s per stretch
 Duration ~ 10 min per session
 Progression - slow

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 Often a benefit of dance training in kids

o Body composition
 Underweight a challenge
 Regular exercise- may increase muscle mass but needs adequate nutritional
support (If nutrition inadequate can result in further muscle tissue loss).
o Thermoregulation
 Sweat responses – Lose more salt than normal.
 Lower thirst response to fluid loss.
 Recommendations;
 Structured fluid intake
 Sports beverages improve palatability.
 Add salt to food
LECTURE 21: THE RESPIRATORY SYSTEM & EXERCISE III
 Obstructive disorders
o COPD
 Progressive disorder
 Most prevalent in older men
 Major risk factor is smoking – Greater risk from smoking for women.
 Not symptomatic until late in disease.
 Dramatic decrease in exercise tolerance typical.
 Major cause of death & morbidity.
 Combination of emphysema & chronic bronchitis.
 “Pink puffer”
 More emphysema
 Hyperventilate to compensate
 Costs energy - weight loss
 Eat/chew & breathe may be difficult.
 A-P chest depth increased - barrel chest
 “Blue bloater”
 More bronchitis
 Worse V/Q mismatch
 Often hypoxemic (abnormal blood gases
o Chronic bronchitis
 Inflammation of large & small airways
 Bronchiolar wall thickening (fibrosis)
 Hypertrophy of submucosal glands
 Hypersecretion of mucous
 Blockage of small airways
 Pulmonary oedema (damage alveoli)
 V/Q mismatch (cyanosis) develops
 Viral & bacterial infections common
 Key symptoms - Cough & mucous production.

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o Emphysema
 Abnormal permanent enlargement of alveoli but often poor blood supply
(perfusion).
 Loss of alveoli
 Lose surface area for gas exchange
 Results in V/Q mismatch (tissue hypoxia leads to digital clubbing)
 Loss of elastic lung fibres
 Lose lung recoil (passive expiration reduced)
 Increased compliance – Lose radial traction of airways → Dynamic airway
narrowing → airway collapse (atelectasis).
 Impairs expiration & expiratory flow rates.
 Consequences: Lung hyperinflation
 Increased RV, FRC, TLC
 Increased physiological dead space
 Increased anterior-posterior chest depth
 Reduced FEV1 & FVC, & FEV1/FVC ratio
 Extreme dyspnoea
 Predisposing factors;
 Smoking/pollution/repeated infections (Inflammatory responses release
proteases e.g. elastase).
 Genetic alpha1-trypsin deficiency.
o Alpha1-trypsin is an anti-protease - protects lungs from excess
protease damage.
o Deficiency - get extensive tissue damage.
 Exercise & COPD

o Patients with COPD have:
 Ventilatory impairment
 Skeletal muscle dysfunction
o Both contribute to decreased exercise tolerance.
o Exercise goals;
 Improve ventilatory capacity.
 Relieve dyspnea during ADLs.
 Decrease energy cost of breathing.
 Increase general physiologic function.
 Increased functional capacity.
 Increased QoL.
o Skeletal muscle changes
 Decreased whole body muscle mass.
 Decreased muscle strength (e.g. quads) - decreased muscle CSA.
 Atrophy of Type I & II muscle fibres.
 May be due to;
 Lack of regular physical activity.
 Limited nutrition intake (Protein malnutrition, calorie malnutrition).
 Chronic steroid use (possibly).

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o Recommendations;
 Aerobic conditioning
 Mode: Lower extremity muscle mass preferred (e.g. walking, stationary
cycling (initially).
 Frequency: 3-5 times per week.
 Intensity: 3-6 on dyspnea rating scale (~50-85% VO2peak) as tolerated.
Heart rate not reliable indicator.
 Can use interval training, especially initially.
 Duration: 20-30 min desirable minimum.
 UL strength training
 Should involve accessory inspiratory muscles.
 Should form part of whole body resistance training program.
 Free weights or weight machines OK though free weights give more
flexibility.
 70% 1RM.
 Ventilation may rely on accessory muscles for inspiration (Scalenes,
sternocleidomastoids, serratus anterior).
 Upper body aerobic exercise (e.g. arm ergometry) may compromise VE use
of these muscles.
 Dyspnoea is common performing ADLs with upper extremities.
 Whole body strength training

 Mode: variety of upper and lower body exercises.
 Frequency: 2-3 times per week.
 Intensity: 8-15 reps per set (~70% 1RM)- Progressive.
 Volume: 1-2 sets if 15 reps; 2-3 sets if < 10 reps; 1 set if many exercises.
o Initial benefits in ~ 4 weeks.

o Strongly recommend program is ongoing for at least 3 months.
o Once appropriate function achieved may move to maintenance program.
o Adaptations may be dependent on adequate nutrition.
 COPD obesity paradox

o People who are in the BMI overweight category with COPD do better than
those with lower BMI.
o May reflect better muscle mass.
o Prevention of sarcopenia should be a higher priority than weight loss in
overweight COPD (and aging generally).
 Restrictive lung disorders

o Reduced compliance a key feature.
o Tissues involved – Lungs, pleura OR chest wall.
o Major etiologies
 Maturation (RDS, aging)
 Pulmonary (asbestosis, pneumonia, ARDS)
 Cardiovascular (Pulmonary oedema or embolism)

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 N-M (SCI, ALS, polio, Guillain-Barre, MG, etc)

 M-Skel (kyphoscoliosis, ankylosing spondylitis)
o May occur acutely with;
 Pregnancy
 Obesity
 Pneumonia
 Trauma
 Radiation, drug treatment
 Consequences of restrictive disorders

o Dyspnoea on exertion
 Often first symptom.
 Increased work with higher levels of VE
o Abnormal gas exchange – Possible hypoxemia.
 Exercise and restrictive lung disease

o Exercise may be an important diagnostic tool.
o Exercise training may be performed in RLD rehabilitation.
o Capacity to exercise affected by;
 ↓ Lung volumes
 ↓ Inspiratory & expiratory capacities
 ↓ Maximal TV
 ↓ Maximal VE
 ↑ Work of breathing

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 Aging & respiratory adaptions to exercise

o ↓ lung compliance
 ↓ Lung elastic tissue, lung stiffer
 ↑ Stiffness of chest wall
o Loss of alveoli – ↑ RV, ↓ IRV, ERV.
o Lung compliance is maintained better with regular (especially endurance)
exercise.

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LECTURE 22: ACUTE CV RESPONSE TO EXERCISE
 CV responses to exercise
o Aim: Increase O2 delivery to skeletal muscle.
o Increase blood flow to skeletal muscle
 Increase cardiac output (↑ HR, ↑ SV, ensure venous return).
 CO= HR x SV
 CO= venous return
 Increase arterial pressure (P1-P2)
 Decrease TPR – Alter distribution of blood flow.
 Increase O2 extraction from blood.
 Heart rate response to exercise

o Heart rate has linear relationship with progressive exercise. Slope affected by
fitness.
o HR increases more doing same work during exercise with small muscle
groups compared to large muscle groups. Higher with arms than with legs.
o HR increases more during dynamic exercise than isometric exercise (more
work performed during dynamic exercise).
o Neural control of HR;
 Parasympathetic
 Sympathetic
 Influence of circulating adrenaline (released by sympathetic drive).
 Input from motor cortex
 Feedback from metaboreceptors in muscle (more
metabolites produced- more blood flow needed?).
 Modulation by baroreceptors
 Decrease in PSNS increases HR to ~ 100 b/min (PNS
withdrawal used initially during low intensity
exercise).
 Increase in SNS increases HR above ~ 100 b/min to
max.
 Adrenaline may contribute to rise in HR during more
intense exercise.
 Input from motor cortex to CV centres in medulla primarily sets HR.
 Heart rate after transplant- No neural innervation of heart (at least initially).
Heart paced (pace maker).
 Very modest and delayed increase to progressive exercise after heart
transplants (due to effect of adrenaline).

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 Stroke volume response to exercise

o SV = EDV-ESV (end diastolic - end systolic).
o Increases in SV smaller with isometric than dynamic exercise (less work).
o Increases in SV smaller with smaller muscle mass- higher HR required to
maintain CO.
o Increases in SV smaller if no leg muscle contractions due to decreased VR.
o Heart contracts more forcefully (↑ SV, lower EDV, increased venous return→
changes length tension relationship allowing greater force generation &
contractility → greater SV).
o Neural control of SV;
 Not under parasympathetic drive
 Sympathetic drive
 Influence of adrenaline
 Input from motor cortex
 Feedback from
metaboreceptors in muscle
 Modulation by baroreceptors
 Venous return during exercise

o 3 main mechanisms enhance VR during
exercise;
 Neural venoconstriction (minor).
 Skeletal muscle pump (major).
 Respiratory pump
o NB valves in veins important for ensuring direction of flow.

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 Increasing blood flow to muscle- increasing

arterial pressure.
o Flow = pressure difference between
arteries & veins divided by resistance.
o Immediate ↑ in SP.
o Then steady ↑ as Q ↑
o Little ↑ in DP (even slight fall) until near
maximal exercise in health peoples.
o DP indication of TPR and SP indication of
CO.
o Slow rise in BP both SP and DP.
o Increases proportional to workload and duration of contraction.
o Large rises with high intensity contractions even of short duration (e.g.
resistance exercises - isometric component).
o SP and DP rise progressively during sustained isometric exercise.
 Increasing blood flow to muscle- reducing TPR

o Redistributes blood flow- withdrawal of sympathetic drive results in
vasodilation.
o Large increase to skeletal muscle.
o Large decrease to splanchnic & renal.
o Small increase to brain.
o Increase to heart but same %total BF.
o Increase to skin during moderate exercise but may decrease during intense
exercise.
o Note: much less blood in venous system- at rest most blood in veins (64%).
o Proportional to exercise intensity.
o Mediated by changes in vascular resistance in different regional circulations.

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o Vasoconstriction is SNS mediated.

o Vasodilation in muscle vessels is both SNS (arterioles) and locally (capillaries)
mediated.
 Neural control of HR & SV

o Outputs (SNS and PSNS).
 Change HR and SV
 Vasoconstrict or
vasodilate.
o Inputs
 Motor cortex
 Muscle metaboreceptors
 Baroreceptors (arterial
and C-P).
 Increasing oxygen extraction from

blood
o Extract more O2 from blood
distributed to exercising muscle.
o Improves with training. Improved extraction means less changes needed to CO.
o Venous O2 content decreases from ~ 15 ml/100ml at rest to as low as 2ml/100ml
during maximal exercise.
o a-vO2 difference increases from ~ 5ml O2/100ml to 18 ml O2/100ml.

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 Summary
o The harder the exercise (greater the intensity), especially dynamic exercise,
the greater the demands on the CV system.
o Duration of exercise – for exercise longer than 30+ min (especially in heat),
get CV drift; harder to maintain SV so HR gradually increases.
o The higher the level of physical fitness, the less the demands of any absolute
level of exercise on CV function.
o The type of exercise and the posture in which it is performed also affect the
responses.
LECTURE 23: CV RESPONSE TO EXERCISE II
 Exercise & CVD risk factors

o Exercise exerts is effects on many CV conditions via its effects on known CV
risk factors.
o Risk factors for CVD include;
 Smoking
 Diet
 Lipids
 Obesity
 Diabetes
o All influence subclinical disease – Arterial endothelial dysfunction,
inflammation, and atherosclerosis. Can lead to clinical CVD.

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 Arteriosclerosis
o Term for degeneration of arterial wall.
o Usually associated with narrowing of lumen of vessel.
o Some ‘hardening’ i.e. stiffening of the arteries.
o Occurs at varying rates with aging.
o Influences blood pressure.
 Atherosclerosis
o Type of arteriosclerosis.
o Thickening of the intima of blood vessels.
o ‘Athero’ (paste) & ‘sclerosis’ (hardening).
o Progressive disorder associated with vessel wall injury → accumulation of
lipids → fibrosis & calcification.
o Atheroma development;
 Injury to epithelial lining of arteries.
 Inflammatory response initiated.
 Macrophages distended with lipid (mainly cholesterol) to form
foam cells.
 Covered by fibrous connective tissue & smooth muscle cells.
 Lesions (plaques) continue to increase in size & number- may
occlude vessels.
 Weaken vessel walls – Aneurysms.
 Increases risk of clots.
 Risk & extent of atherosclerotic response varies.
 Basic stages= injury → inflammation → plaque formation → lesion
complications.
o Possibly begins in childhood – Fatty streaks observed.
o Rate of progression in adulthood variable – Fibrous plaque development
and complexity & extent of lesions varies.
o Consequences;
 Hypertension
 Arteriosclerotic aneurysms
 Coronary artery disease
 Stroke
 Peripheral artery disease
o Peripheral artery disease (PAD) is the major peripheral vascular disease
(PVD). Most common symptom is painful cramping in the hips, thighs, or
calves during PA.
o Risk factors for atherosclerosis;
 Hypertension- risk factors & consequence
 Smoking
 Diet
 Lipids
 Obesity
 Diabetes

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 Risk factors for CV disease
o Hypertension
 Increases risk of stroke, MI, CHF, RF- increase turbulent blood flow; increase
clot formation.
 Increases adverse Left Ventricular Hypertrophy- decreases heart efficiency.
 Risk of hypertension increases with age.
 Risk greater in females after menopause.
 Genetics influence BP.
 Sodium intake only increases BP in some people (but more as age).
 Pharmacological treatment may utilise;
 Beta-blockers (Adrenergic inhibitors ↓ heart contractility & HR).
 Alpha-blockers (Adrenergic inhibitors causing vasodilation).
 Calcium-channel blockers (induce vasodilation).
 Diuretics (↑ renal excretion ↓ plasma volume).
 Ace-inhibitors (inhibits kidneys production of angiotensin which acts to
vasconstrict & retain water).
 Exercise & hypertension;
 Exercise may contribute to lower blood pressure.
 Exercise capacity may be compromised by anti-hypertensive medications
(especially beta-blockers).
o Smoking
 Increases vessel wall injury.
 Increase risk of CAD 2-4 times.
 Increase risk of sudden death with CAD.
 Quitting smoking ↓ risk of COPD, CAD, PAD & amputation, oral & throat
cancer, lung cancer.
 Less likely to smoke if exercising.
 More likely to quit smoking if starting exercise program.
 Exercise may partly offset weight gain commonly associated with quitting
smoking.
o High blood lipids

 Blood lipids - cholesterol, TGs, & lipoproteins (LDLs, HDLs).
 High cholesterol, TGs, & LDLs – Increase risk of atherosclerosis (plaques).
 Simple lipids e.g. triglycerides.
 Compound lipids e.g. phospholipids.
 Derived lipids e.g. cholesterol (essential to body function but detrimental in
excess).
 Lipids have low solubility in water (blood).
 Most lipids transported in blood bound to proteins as lipoproteins.
 Protein portion called apoprotein – 4 major types: A, B, C and E.
 Lipoprotein structure;
 Protein – Apoprotein
 Outer layer – Phospholipid
 Core – Cholesterol or Triglycerides

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 Types of lipoproteins
o 5 types of lipoproteins circulate in the blood;
 Chylomicrons (formed in SI wall & enter blood via lymphatic system).
 Transport TGs to skeletal muscle & adipose tissue.
 Remnant chylomicrons to liver.
 VLDLs & HDLs formed in liver.
 IDLs, LDLs formed when TGs delivered to muscle & adipose tissue.
o LDLs (ApoB) & HDLs (ApoA) have different apoproteins.
o Chylomicrons are lowest density, HDLs highest density.
o LDLs contain large quantities of cholesterol- ‘bad’ lipoprotein or cholesterol.
o HDLs remove cholesterol from tissues & transport to liver- ‘good’ lipoprotein or
cholesterol.
o 2 sources of cholesterol;
 Obtained from diet
 Produced in liver- feedback regulation (dysfunctional with genetically high
cholesterol).
o Risk of CAD increases with;
 Increased cholesterol
 Increased LDLs
 Decreased HDLs
o Risk reduced with;
 Increased HDLs
 Statin medications
o Influences on blood lipids;
 Genetics (large impact) - account for
very high cholesterol levels.
 Diet (high saturated fat, cholesterol,
calories increase blood cholesterol &
LDLs).
 Metabolic diseases – Diabetes, Thyroid disorders, anabolic steroids
(hypothyroidism increases cholesterol).
 Smoking (decreases HDLs).
 Physical activity levels – Regular exercise increases HDLs.
 Alcohol consumption – modest intake increases HDLs.
 Unsaturated fat (moderate quantities) – Increase HDLs and decrease LDLs.
 Omega-3 fatty acids- lower TGs and increase HDLs.
 Lipid lowering drugs (statins).

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LECTURE 24: THE CV SYSTEM & EXERCISE III
 Adaptions to endurance training

o Cardiac (heart muscle) hypertrophy
 Increased left ventricular (LV) mass
 Increased LV end diastolic diameter (Bigger left ventricle chamber).
 Response to high levels of ventricular filling (Volume overload).
 Contributes to increase SV.
o Coronary blood vessels
 Increase size of coronary vascular bed
 Possible increase in collateral circulation
 Increased capacity to dilate coronary arteries during exercise- increases
blood flow to cardiac muscle.
o Rate pressure product (RPP)
 Myocardial VO2 lower at rest
 Myocardial VO2 lower during submaximal exercise.
 Reflects lower heart rate- less work for the heart.
o Changes in blood & blood volume
 Increased blood volume
 Initially an increase in plasma volume only (10days)- Hct & Hb values low -
Sports Anaemia.
 Increase in RBC slower (3-4wks)- Increase O2 carrying capacity.
 Slightly lower hematocrit may persist – Blood less viscous; less resistance
to flow.
 Normal blood ~55% plasma, 45% erythrocytes, <1% buffy coat (WBC,
lymphocytes, platelets).
 Normal haematocrit ~45%.
o Changes in skeletal muscle blood flow
 Decrease blood flow to muscle during submaximal exercise.
 Increase blood flow to muscle during maximal exercise.
 Due to increased CO and better ability to direct blood to working muscles.
o Blood pressure
 No change in BP at rest in normotensives.
 Lower exercise blood pressure at same absolute submaximal workloads
after training.
 May increase SBP at maximal exercise after training (higher absolute
workload).
 May lower resting blood pressure in hypertensives (unpredictable). Typically
↓ 5-10mHg but not in everyone.
o Total peripheral resistance
 Unchanged at rest
 Unchanged during submaximal exercise
 Lower during maximal exercise.
 Due to increased capillarisation of trained skeletal muscle.

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o A-Vo2 difference
 Increased during submaximal & maximal exercise.
 Increased capillaries around muscle fibres – Increased blood & oxygen
delivery to fibres.
 Increased myoglobin stores in muscle – Increased diffusion of oxygen into
muscle.
o Summary of adaptions;
 Aerobic fitness (VO2max) increases.
 CV adaptations enhance O2 delivery.
 Local muscle adaptations enhance O2 use.
 Cardiac output response to endurance training

o Little change at rest (may increase a little).
o Decrease Q during same submaximal workload after training.
o Large increase Q at maximal exercise.
o Large Q characteristic of elite endurance athletes- around 30/40L per min.
 HR adaptions to endurance training

o Decrease resting HR – Bradycardia (<60bpm) common.
o Decrease submaximal exercise HR.
o No change (or slight decrease) in maximal exercise HR.
o Note: Low RHR is mostly genetic- often seen in children with low RHR.
 Stroke volume adaptions to endurance training

o Increase resting stroke volume (SV).
o Increase submaximal exercise SV.
o Increase maximal exercise SV.
o SV normally goes up to 40-50% of Vo2 max then plateaus in normal people.
o SV may not plateau in highly trained- up to 100mls per beat in highly trained.
 Performance increases include;

o Maximum working capacity (VO2max).
o Duration of submaximal work.
o Resistance to fatigue.
o Work efficiency
 CV response to resistance training

o Little CV change with low-intensity, low volume or short period of resistance
training.
o Changes occur with longer-term, high volume resistance training.
o Changes influenced by initial fitness level- not much change in already
efficient people.

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o Heart hypertrophy
 Increased left ventricular (LV) mass.
 Increased LV wall thickness.
 Increased septal wall thickness.
 Responses to high afterload pressures.
 No increase in internal chamber size.
 Increases only observed in some studies.
 Increases generally proportional to increases in lean body mass.
 Not particularly beneficial.
o Blood pressure
 Resting BP is average or below average in resistance-trained.
 Lower BP at same absolute & relative workloads after training.
 Lower resting BP in some hypertensives after training.
 Effects better with circuit training than conventional resistance training.
o Rate-pressure product (reflects myocardial VO2)
 Decreased at rest & during resistance exercise after training.
 May be due to lower peripheral resistance.
o Modest (4-9%) or no increase in aerobic fitness
 Little if any peripheral adaptations in active people.
 Some benefits in inactive people.
o Stroke volume;
 Resting SV may increase or not change with training.
 SV during resistance exercise is not known.
 Heart rate – Resting heart rate may decrease.
 Submaximal resistance exercise HR is lower.
 CV adaptations to circuit training

o Decrease resting HR.
o Decrease HR, Q & BP during submaximal exercise.
o Increase SV during submaximal exercise.
o Some cardiac hypertrophy.
o Improvements in VO2max.
 Role of exercise in dyslipidemia

o ↑ HDLs
o ↓ LDLs
o ↓ TG levels
o Mechanism – Possibly due to increased capacity of muscle to use fat.
o Mod-high intensity aerobic exercise most efficient.
o Including interval training – 30 min per session, 3-5 times a week.
o 12 week program to get effect (then maintain).
o More exercise, better the effect (volume more important than intensity).
o Two session per day particularly beneficial.
o Pathogenesis: Strong evidence lack of PA contributes to development of
dyslipidemia.

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markers of dyslipidemia.
o Quality of life: Moderate evidence PA level improves QoL in those with
dyslipidemia.
 Exercise for hypertension

o ↓ resting SBP (average decrease of ~ 7 mmHg).
o ↓ resting DBP (average decrease of ~ 6 mmHg).
o Can be used to treat mild hypertension without drugs.
o Type of exercise most beneficial:
 Mostly mod intensity aerobic exercise (Borg 12-13).
 Short periods of higher intensity (Borg 15-16) daily.
 Daily (effects partially acute and last ~24 hours).
 Studies exploring a variety of training regimes lacking.
o Multiple mechanisms of effect including:
 ↑ Left ventricular function
 ↓ Vascular stiffness
 ↓ Inflammation
 ↓ Endothelial dysfunction
 ↓ Sympathetic nervous system drive
o Pathogenesis: Strong evidence lack of PA contributes to development of
hypertension.
levels of hypertension.
o Physical fitness or strength: Strong evidence PA level influences BP.
o Quality of life: Strong evidence PA level influences QoL in those with
hypertension.
 Exercise for reducing obesity

o Direct effects on weight loss inconsistent.
o Decreases body fat mass (% body fat).
o Decreases abdominal fat mass.
o Counteracts loss of muscle mass associated with dieting for weight loss.
o Prevents weight gain, so assists weight loss maintenance.
o Large amounts of mod intensity aerobic exercise most effective (Borg 12-13).
o Combine with moderate amounts of strength training – At least 30 min daily.
o To lose weight using exercise, must create sustained energy deficit- this
usually requires 60 min PA daily in obese.
o Pathogenesis: Strong evidence lack of PA contributes to obesity.
obesity.
o Physical fitness or strength: Strong evidence PA level influences CV health in
obese.
o Quality of life: Strong evidence PA level improves QoL in obese.

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 Exercise can also be effective for;

o Reduce risk of Type 2 diabetes.
o Aid in quit smoking.
o Reduce stress

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LECTURE 25: DIEBETES & EXERCISE
 Diabetes means “excess urine”

o Diabetes insipidus- Excess dilute urine (lack ADH).
o Diabetes mellitus – Glucose in urine.
 Diabetes Mellitus
o Collection of disorders relating to insulin.
o Current classification system 1997
 Based on aetiology
 Previous system focused on pharmacological treatment.
 Includes diagnostic system based on stages of glucose intolerance.
 Over 300 million affected in 2010.
 500 million estimated by 2035.
 Most rapid increase in Asians and Indians.
o Disorder of CHO, fat & protein metabolism.
o May involve impairments of:
 Insulin synthesis in beta-cells of pancreas
 Release of insulin
 Ability of tissue respond to insulin
 Insulin & blood glucose

o Only hormone that lowers blood glucose levels is insulin.
o Glucose enters cells via glucose transporters (GLUTs).
o Brain (neurons) relies on GLUT-1 & GLUT-3 – NOT dependent on insulin.
o Skeletal muscle uses GLUT-4
 Has to move to cell membrane
 Insulin dependent at rest- transport of and amount of glucose going into cell
low at rest.
 NOT insulin dependent during exercise.
o Adipose tissue uses GLUT-4 – Glucose needed for glycerol to form TGs- will
have markedly raised circulating blood lipid levels.
 Insulin facilitates storage of TGs in adipose – Uptake of glucose & FFAs •
Inhibits lipolysis
o Liver independent of insulin for glucose transport – Insulin facilitates
phosphorylation of glucose in cells & glycogenesis.
o Insulin & proteins- increases amino acids into cells.
 Plasma glucose classifications

o Normoglycemic
o Pre-diabetic state: Impaired fasting glucose, Impaired glucose tolerance test
→ Diabetes.
o Oral glucose tolerance test: 75g glucose after 8-10hrs fasting. Readings taken
in fasting state and at 1 & 2 hours.
o Factors may effect result: previous carb intake, illness, smoking, activity
levels.

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o Intermediate states suggest high risk

of developing diabetes- preventative
action should be taken.
 Signs & symptoms

o Polydipsia- thirst
o Polyuria
o Nocturia
o Visual disturbance
o Fatigue
o Weight loss
o Infection
o Hunger
 Type 1 Diabetes Mellitus

o Result of progressive beta-cell destruction- Deficiency of insulin.
o Approx. 10% of all diabetics – More common in Caucasians.
o Type 1A - autoimmune (95% of Type 1) – Genetic predisposition plus trigger.
o Type 1B - idiopathic (unknown cause).
o More common in young people – 98% of diabetic children have Type 1.
o Effects of lack of insulin
 Elevated blood glucose levels (Hyperglycemia).
 Glucose in urine (glucosuria).
 Greater fluid loss in urine and thirst
 Catabolism of fats & proteins
 Weight loss
 Prone to keto-acidosis
 Treatment requires insulin
 “Honeymoon period” where may be able to stop progression.

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 Type 2 Diabetes mellitus

o Slow, progressive disease
o High, normal or low insulin levels
o Peripheral cells resistant to insulin
o Few GLUT 4 transporters?
o Results in hyperglycaemia – Initial response hyperinsulinemia (releasing more
insulin but ineffective).
o Over time, may get beta-cell dysfunction.
o May lead to other metabolic disorders – High plasma TGs, low HDLs, systemic
inflammation (high CRP).
o Risk factors;
 Age
 Obesity (diabesity)- abdominal obesity
 High energy diet
 Lack of physical activity
 Polycystic ovary syndrome
 More common in non-Caucasians
o Accounts for ~ 90% of diabetics
o Increases risk of metabolic syndrome.
o Diet & exercise shown to significantly reduce risk of developing Type 2, slows
progression.
o One study found diet & exercise twice as effective as metformin in
preventing development of diabetes in pre-diabetic population.
o Good effect if lose 5-10% of body weight.
o Oral hypoglycemic medications commonly used. Insulin also used (20-30%).
o Metabolic syndrome; cluster of risk factors found in 70-80% of people with
type 2. Increases risk 3 fold of heart disease and stroke, 2 old of major CV
events.
 Gestational diabetes
o Any impaired glucose tolerance first observed during pregnancy.
o Risk factors;
 Age (increases) & more pregnancies
 Overweight
 Low physical activity levels
 Hormonal environment of pregnancy
 Genetic predisposition
 Non-Caucasian
 Other origins of diabetes mellitus

o Genetic defects or syndromes (Down syndrome).
o Pancreatic diseases (CF, pancreatitis).
o Endocrine disorders (GH, cortisol, Thyr).
o Drug or chemically induced (thiazide diuretics; phenytoin (epilepsy))
o Infection (Congenital rubella, CMV).

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 Complications of diabetes
o Macrovascular disorders
 Begin early in disease progression.
 Atherosclerosis
 CAD (leading cause of death in diabetics)
 PVD (increases risk of amputation)
o Microvascular disorders
 Retinopathy (main cause of adult blindness)
 Nephropathy (renal disease)
 30-50% of diabetics
 Diabetics make up 50% of people with end-stage renal disease
requiring dialysis or kidney transplants
 Neuropathies
 Demyelination & degeneration of neurons.
 Starts peripherally, progresses centrally.
 Autonomic neuropathy- Prone to problems with thermoregulation &
blood pressure control during exercise.
 Peripheral neuropathy- pain, parathesias, anaesthesia. Loss of
sensation leads to tissue damage, ulcers, infections, amputations.
 Diabetes is main cause non-traumatic amputations.
 Impacts on need for non-weight bearing activities.
 Considerations for exercise

o 80% of Type 2 diabetics are overweight or obese.
o 60% of Type 2 diabetics have hypertension.
o Metabolic dysfunction is a component of the disease.
o High risk of cardiac dysrhythmias.
o Many have macro & microvascular problems.
o Neural changes
 Goals of exercise
o Use exercise more for maintaining muscle mass while modifying diet.
o Type 1
 General management & long-term health
 Prevent co-morbidities (CAD)
o Type 2
 Prevention of Type 2 if pre-diabetic
 Prevent co-morbidities (CAD)
 Aid glycemic control
 Decrease risk of atherosclerosis
 Improve or maintain functional capacity
 Weight loss
o Aerobic exercise;
 Many modes (most walk, swim, cycle).
 Usual emphasis is moderate intensity.
 Frequency: 3-7 d/wk; daily if on insulin.

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 Intensity: 50-80% of HRmax (RPE 11-14).

 Duration: 30-60 min continuous desirable.
 Minimum of 10 min bouts if intermittent
 Weight loss (even 5-10kg positive)
 Increase insulin sensitivity
 Improve blood glucose levels
 Increase physical working capacity (PWC)
 Improve lipid profiles (increase HDLs, lower TGs); slow atherosclerosis.
 May reduce blood pressure a little.
 Limited CV fitness effects.
o Resistance exercise;
 Low loads, high repetitions (10-15 reps).
 No Valsalva manoeuvres.
 Extra caution if high BP
 1-2 sets per activity
 At least 2 x week (not consecutive days).
 Increase muscle mass.
 Increase insulin sensitivity.
 Increase strength, muscle endurance & balance.
o Flexibility training;
 Stretch muscle groups being strengthened (STRETCH WHAT YOU
STRENGTHEN).
 Work towards normalising ROM.
 Yoga, Tai Chi activities if feasible.
 Timing & considerations of exercise

o Important if using exogenous insulin.
o Don’t exercise when insulin dose effects at peak- could have rapid hypo.
o If intramuscular insulin, don’t use muscle group for exercise for an hour.
o Don’t exercise at night (before sleep) as risk hypoglycaemia while asleep.
o Warm up- 5-10min, gradually increase CV demands, warming tissues
increases distensability.
o Cool down – Gradual decrease in CV demands, maintains venous return &
cerebral blood flow.
o Ensure adequate fluid intake – Prior to exercise, during exercise, after
exercise.
o Consider composition of fluids – CHO- not if trying to lose weight.
o Water & electrolytes important.
o Pre-exercise program screening.
o Proper footwear (skin protection)
o Don’t exercise in climate extremes.
o Avoid or modify exercise when metabolic control is poor.
o Wear a form of diabetes identification.
o Contraindicated; poor glycemic control & ketones in urine, proliferative
retinopathy, severe neuropathy, nephropathy, some CV conditions.

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LECTURE 26: THE CARDIOVASCULAR RESPONSE TO EXERCISE IV
 Coronary artery disease

o Angina pectoris or myocardial infarction.
o Involves atherosclerosis
o Use exercise for primary prevention of MI re angina
o Use exercise for secondary prevention after MI.
o May be difficult (or impossible) to improve LV function after MI (especially if
severe MI)- Harder to increase SV, COmax, VO2max.
o Other improvements appear to occur regardless of this limitation.
o Exercise improves survival (↓ mortality ~20%).
 Improve lipid profiles
 ↓ Blood pressure
 ↓ Thrombocyte aggregation
 ↓ Endothelial dysfunction
 ↓ Sympathetic nervous system drive
o Strong evidence lack of PA contributes to development of CAD.
o Strong evidence regular PA decreases CAD.
o Strong evidence PA level influences fitness for those with CAD.
o Strong evidence PA level influences QoL for those with CAD.
 Goals of exercise to improve CV function

o ↑ Physical working capacity
o ↓ HR & RPP during submaximal PA
 ↑ Angina threshold
 ↓work of heart
o ↑ Anaerobic/VE threshold
o Protect against PA induced MI (>6METs)
o ↑ Vagal tone & SNA
 ↑ HRV (heart rate variability)
o ↓ Submaximal activity BP
o Promote vascular regeneration
 ↑ Endothelial progenitor cells
 ↑ Angiogenic cells
o ↓ Blood platetet adhesion
 ↓ fibrinogen; blood viscosity
 ↑ fibrinolysis
o ↓ Systemic inflammatory markers (CRP)
o ↑ Self efficacy & wellbeing
 Aerobic recommendations- Basics for post MI & most CV conditions

o Large muscle ergometry
o RPE 11-16/20
o 40-80% of VO2max or HRR
o 20-60 min /session

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o > 3d/wk
o Type of exercise most beneficial for patients with mild myocardial ischemia:
 Aerobic exercise
 10 min warm up (Borg 10-12)
 10 min at Borg 12-13
 5 min cool down at Borg 10
 Twice a week initially then 3 x wk for 4 wks then evaluate and modify
training.
 Interval training for most CV conditions

o Warm up @ 40-60% VO2max (RPE 10-11).
o 3 x work intervals of 4-5 min @ 60-80% VO2max and RPE 13-15.
o Relief intervals of 4-5min @ 40-60% VO2max and RPE 10-12.
o Cool down of 6-10 min, gradually decreasing intensity.
o 3-5 times a week.
 Circuit for most CV conditions

o For strength & muscle endurance.
o 30-40% of 1RM for upper body activity
o 50-60% of 1RM for lower body activity
o 8-10 exercises
o 12-15 reps per exercise
o Progress to 2-4 sets of each exercise
o 2-3d/wk
 Other exercise recommendations for CV conditions

o Ensure adequate warm up/cool down.
o Flexibility (stretching/ROM)
 Static – Hold 10-30s, 2-3d/wk (Best in cool down).
o Initially exercise under supervision of physiotherapist or AEP recommended
ie cardiac rehab program.
o Monitoring of BP and ECG informative for programming.
o Recommendations on how to continue to exercise should be provided on
discharge.
o Heartmoves- community program. Complies with NHF guidelines &
intensities- referral appropriate.
 Chronic heart failure

o CAD and hypertension main contributor.
o Impaired pumping capacity of heart- Decrease SV, CO, blood flow to
periphery.
o Impaired physical performance common – Skeletal muscle atrophy; strength
loss; muscle less aerobic.

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o Exercise improves function in CHF.

o Treatment with drugs extensive – Diuretics, ACE inhibitors, beta-blockers.
o VO2max 30-40% below healthy.
o Rise in SBP less than normal during exercise – Blood flow to muscle often less
than needed.
o Ventilation elevated during submax exercise but not limiting at maximal
exercise – Shortness of breath during exercise common.
o Benefits of exercise;
 ↑ muscle mass and strength
 ↑ general physical performance and tolerance of PA
 ↑ VO2max (15-25%)
 ↑ anaerobic threshold
 ↓ dyspnoea
o Aerobic training most beneficial
 Intervals: 30s on, 60 s rest to begin
 Gradually increase duration, intensity
 Up to 7 x week
 Distance walked per day good indicator of effectiveness (role for
pedometers).
o Strength training beneficial
 35-80% 1RM, variety of exercise
 2-3 x week
o Respiratory muscle training may also be beneficial
 30% max inspiratory pressure
 Daily to 3 x week
o Strong evidence lack of PA contributes to risk of heart failure.
o Strong evidence regular PA decreases heart failure.
o Strong evidence PA level influences in those with heart failure.
o Strong evidence PA level influences QoL in those with heart failure.
 Peripheral artery disease (PAD)

o Intermittent claudication – Pain in leg muscles associated with PA but
symptoms disappear with short rest.
o >10% of population > 65 y.
o If pain at rest, more severe blood supply insufficiency and may require
surgery.
o Goal of exercise usually to increase walking distance with less pain.
o Aerobic;
 Intermittent walking preferred i.e. walking-based interval training.
 3/4 on claudication scale followed by rest
 3-5 d/wk for at least 3 months (6 months better)
 Start with 15 min /session- progress by 5 min per week to 60 min /d.
 Evaluate with 6MWT distance.
o Resistance training is an option;
 8-10 exercises, 10-12 reps, 1-2 sets, 2 d/wk.

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o Benefits of exercise for PAD;

 Increase daily activity, walking distance and pain threshold.
 As effective as surgical and pharmacological interventions but much
cheaper.
o ↑ production of vascular endothelial growth factor (VEGF).
o ↑ endothelial function in the lower extremities.
o ↑ formation of vascular collaterals and blood flow.
o Change in gait pattern.
o Change in pain perception
o Strong evidence for value in preventing & managing PAD and improving QoL.
 Modifications for other CV conditions

o Revascularisation
 Aerobic- Intensity < ischemic (angina) threshold, 4-7 d/wk.
 Circuit- 40-50% of MVC (NO valsalva). Initiate with a single set of each
exercise to volitional exhaustion. 20-60 min for total session.
o Valvular disease
 Post-surgery aerobic – RHR + 20-30 b/min. 10-15 min warm up and cool
down.
 Post-surgery circuit – 30-40% of MVC (NO valsalva).
o Heart transplant
 11-14/20 RPE
 40-70% of VO2max or HRR
 Ideal to initiate with 2-3 sessions per day of 10-20 min each.
 Progress to 60 min per day.
 Metabolic syndrome
o Cluster of conditions which increase risk of CVD, T2DM, dementia, some
cancers.
 Hypertension, insulin resistance, dyslipidaemia (low HDL, high TGs),
abdominal obesity.
o Associated factors;
 Impaired fibrinolysis
 Increased inflammation
 Elevated levels of uric acid and fatty liver
o Strong association with lack of PA.
LECTURE 27: HORMONES & EXERCISE
 Hormones & exercise

o Stress hormones are exercise hormones.
o Hormones involved in fluid balance & reproduction also influenced by
exercise.
o Major ‘acute’ impacts of exercise hormones are metabolic- exercise is
catabolic.

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 Metabolic hormones
Anabolic processes;
o Glucose uptake: Occurs in most tissues. Insulin regulated (rest).
o Glycogenesis: Occurs in skeletal muscle & liver. Insulin regulated.
o Lipid uptake: Occurs in adipose tissue & skeletal muscle. Insulin regulated.
o Amino acid uptake: Occurs in all tissues. Regulated by insulin, GH, androgens,
oestrogens.
Catabolic processes
o Glycolysis: Glucose → pyruvate. Occurs in skeletal muscle. Regulated by adrenalin &
glucagon.
o Glycogenolysis: Glycogen → glucose. Occurs in skeletal muscle & liver. Regulated by
adrenalin & glucagon. T3 & T4 (permissive).
o Lipolysis: Occurs in adipose tissue. Regulated by adrenalin & cortisol, prolactin &
GH, T3 & T4 (permissive).
o Gluconeogenesis: Generation of glucose from non-CHO sources. Occurs in liver.
Regulated by cortisol & glucagon.
 Endocrine responses to exercise

o Main effects are to provide energy during exercise.
o Increase glyocogenolysis
o Increase glycolysis
o Increase lipolysis
o Increase gluconeogenesis
 Permissive Hormones
o Permissiveness is a biochemical phenomenon in which the presence of one
hormone is required in order for another hormone to exert its full effects on
a target cell. E.g. Thyroid hormone increases the number of receptors
available for epinephrine at the latter's target cell, thereby increasing
epinephrine's effect on that cell.

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o Thyroid hormones;
 Released from thyroid gland.
 Release stimulated by TSH from anterior pituitary (hormonal regulation).
 T3 more active than T4.
 Most bound; little free (unbound).
 Exercise increases free T4 by ~35% – Increased with higher exercise
intensity.
 Effects of T3 and T4;
 Increased ATP synthesis rate in mitochondria.
 Increased metabolic activity of most cells (↑ enzyme activity).
 Increased speed of neural reflexes.
o Growth Hormones;
 Also called somatotropin.
 Released from anterior pituitary – Mostly released during sleep.
 Hormonally regulated (GH-IH, GH-SH).
 Direct effects during exercise- ↑ lipolysis, ↑ gluconeogenesis.
 Indirect effects (post-exercise)- Tissue growth, ↑ amino acid uptake.
 Release of GH increases with exercise – Release proportional to exercise
intensity.
 In children; deficiency → pituitary dwarfism. Excess → gigantism.
 In adults; deficiency → acromegaly (abnormal growth of hands/feet/face,
excess → pituitary diabetes (can also be caused by taking excess GH).

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 Pancreatic Hormones
Insulin
o Secreted from beta cells of pancreas.
o Release humoral – Stimulated by increased blood glucose.
o Release is inhibited during exercise- by adrenaline.
o Elevated insulin during exercise not desirable.
o Insulin effects are ANABOLIC.
o Insulin important during recovery from exercise;
 ↑ glucose uptake into cells
 ↑ glycogenesis (glycogen formation) in liver & skeletal muscle.
 ↑ Uptake of FFAs and glycerol into adipose tissue (form TGs).
 ↑ Uptake of amino acids into tissue and protein synthesis.
o Not all cells dependent on insulin (i.e.: GLUT4).
o Brain, kidneys, GIT cells, & RBCs obtain glucose independent of insulin (GLUT1-3).
o Skeletal muscle is not dependent on insulin for glucose uptake during exercise
(alternate pathway).
Glucagon
o Secreted from alpha cells of pancreas.
o Release humoral – Stimulated by low blood glucose levels.
o Release increases during exercise – Stimulated by intensity & duration of exercise.
o ↑ Glycogenolysis in liver and skeletal muscle.
o ↑ Lipolysis (breakdown of TGs) in adipose tissue (increase FFAs in blood).
o ↑ Gluconeogenesis (from amino acids and glycerol) in liver.
o Glucagon effects are CATABOLIC.

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 Adrenal Hormones
Adrenalin & Noradrenalin

o Release increases at higher exercise intensities (> 50-60% of VO2max).
o Beneficial to exercise performance;
 ↑ mental alertness
 ↑ force of muscle contractions
 ↑ heart rate (a little)
 Alters blood flow to tissues - dilates skeletal muscle blood vessels but constricts
most other blood vessels.
 ↑ sweat production
o Adrenalin;
 ↑ glycogenolysis in liver & skeletal muscle
 ↑ lipolysis in adipose tissue
 Inhibits insulin release
Cortisol
o ACTH (adenocortotrophic hormone) and cortisol levels increase with higher intensity
and longer duration.
o Cortisol levels remain elevated for some time after exercise;
 Amino acid breakdown
 Insulin antagonist
 Triglyceride breakdown
 Immune suppression- anti-inflammatory.
 ↑ Lipolysis in adipose tissue.
 ↑ Protein catabolism – Increases amino acid availability to liver for
gluconeogenesis.
 Other Hormones
Prolactin
o Released from anterior pituitary- release hormonal.
o Initiates and supports milk production from mammary glands.
o Release increases during high intensity exercise – increases more in females
exercising without bra support.
o Increases lipolysis.
Gonadal Hormones
o Testosterone, Oestrogen, Progesterone, other androgens.
o Release of all increases with exercise.
o Effects unclear - May increase lipolysis.
LECTURE 28: NUTRITION & EXERCISE
 General dietary guidelines

o Wide variety of foods
o No energy deficits or surpluses

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o No nutrient deficits
o Low in saturated fats
o Low in simple sugars
o High in complex carbohydrates
o Small meals eaten frequently
o Avoid ‘fad’ diets
o Mediterranean diet- less red meat more fish.
 Nutrients
o Macronutrients
CHO
 Monosaccharides – Glucose, fructose & galactose.
 Disaccharides – Lactose, maltose, sucrose, trehalose.
 Polysaccharides – Starch, fibre (nonstarch structural polysaccharide), &
glycogen.
 Primary energy source for CNS and higher intensity physical activity.
 Metabolic primer for fat catabolism.
 Adequate CHO spares protein catabolism.
 Glycogen stores needed for most exercise training and much exercise
performance.
 15g per kg BW
 For 80 kg person; glycogen stores “Equivalent to a 30 km run” (1 hr 40 mins
exercise – running @ 18km/h).
 Most glycogen stored in muscle, some in liver, very small amount in plasma.
 Healthy diet contains ~40-50% CHO- recommend 50%.
 More active people may need 60% CHO.
 Highly active may need 70% CHO.
 Recommended CHO intake;
 Low intensity exercise 5-7g/kg BW/d
 High-intensity long duration 7-12g/kg BW/d
Proteins
 Complete protein sources contain all essential amino acids –easier to obtain
from animal sources.
 Plant sources often lack 1 essential amino acid – Need greater variety of
foods to get protein needs from plants.
 Role of amino acids;
 Major structural components of tissues.
 Major regulatory chemicals- used as signals.
 Provide creatine for creatine phosphate
 Typically 15-20% of daily energy intake.
 Not usually restricted in athletes – Sometimes low in vegetarian athletes.
 Normal 0.8-1.0 g/kgBW/d
 Athlete 1.2-1.4 g/kgBW/d
 Strength athletes 1.6-1.8 g/kgBW/d
 Females need ~ 15% < males
 Need higher intake if on a low kJ diet or on a low CHO diet.

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 Urea in sweat is directly proportional to how much protein is being broken

down.
 Exercise in a CHO depleted state causes a lot of protein to be used for
energy. Hence high CHO stores “spare proteins”.
Fat
 2 major groups- Saturated & Unsaturated.
 Also derived lipids – E.g. cholesterol.
 Main energy reserve
 Primary energy source during low-mod intensity activity.
 Component of cell membranes.
 Components of hormones & other cell regulators.
 Provides satiation (depresses hunger).
 Major vitamin carriers.
 Typically ~ 35-40% of daily energy intake.
 Recommendations;
 < 30% of energy intake from fats
 < 20% of energy intake from fats (Cancer Council)
 Not < 15% of energy intake from fats (JADA re sports performance).
 < 10% of energy intake from saturated fat.
 For Athletes – 20-35% recommended.
 Typically low fat diets involve low in meat & dairy products- may get low
intakes or deficiencies in: Fe, Mg, Ca, Zn, Folate, and Vitamin E.
 ~15% BM males & 25% BM females
 Large energy store - enough for a 1200K run. (120 hrs exercise).
 Most fat stored in adipose, some in muscle, small amount in plasma.
o Micronutrients – Vitamins & minerals

Vitamins
 13 vitamins
 Fat soluble: A, D, E, K
 Need some dietary fat for absorption
 Store well; toxic in large doses.
 Water soluble: 8 x B vits, C.
 Need regular intake; not store well; excess excreted.
 Contain metal ions
 Co-enzymes in many reactions.
Minerals
 22 elements, mostly metals
 Form components of enzymes, hormones, vitamins & tissue
structures.
 7 major minerals: – Ca, Mg, Na, K, P, S, Cl.
 Minor minerals called trace minerals – Fe, Fl, Zn, Cu, Se, I & Cr.

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 Glycaemic index
o Index of effect of CHO ingestion on insulin secretion.
o High GI food;
 Increase insulin secretion
 Increase glucose uptake & use
 Increase lactate production
 Inhibit lipolysis
 Increase the rate of glycogen depletion
 Glucose released into blood more quickly higher the GI
 Alcohol
o No nutrient merit
o High kJ content
o Diuretic effect may contribute to dehydration
o May be some health benefits to small regular intake
o No demonstrated benefits to exercise performance - many adverse effects.
o Easily the most problematic drug in sport.
o May impair healing & recovery from exercise.
 Supplements
o Product labels often inaccurate - contents and claims.
o Some products are better described as drugs (e.g. current AFL/NRL peptides).

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o Quality research lacking.

o The US 1994 Dietary Supplement and Education Act allowed ergogenic claims
to be made without verification – has had big impact on claims of effects
worldwide.
o Athletes primarily take supplements to gain a performance benefit (ergogenic
aid).
o Carbohydrates;
 Evidence supports appropriate CHO intakes are beneficial.
 Main dietary supplement shown to be widely beneficial.
 High (unaccustomed) doses may cause gastric distress (diarrhroea).
o Pyruvate;
 Product of glucose metabolism.
 No ergogenic benefit established.
 Also marketed for weight loss and cholesterol lowering – unproven.
 High doses can cause gastric distress.
o Amino acids/Protein;
 Athlete’s rarely amino acid deficient.
 Most heavily marketed supplements.
 Impact if healthy diet questionable.
 Excess used or stored as energy (fat).
 May provide necessary energy sources for endurance athletes – Branched
chain AAs especially.
 NOTE – food is better.
 Alternatives; fruit smoothies (with milk), 20g skim milk power added to milk,
or liquid meal supplements (eg PowerBar Protein Plus powder).
o Creatine supplements;
 Some benefits established – usually where repeated repeat effort events
than single effort events.
 More effective in cycling; less in running and swimming.
 Possible benefit to 1RM strength performance and adaptations to resistance
training.
 Improves strength, fibre CSA.
 From food;
 Fish & meat high content sources- most other foods very low.
 From de novo synthesis in liver, pancreas & kidneys (3 amino acids needed
- glycine, arginine & methionine).
 Benefits difficult to establish in athletes who eat red meat.
 Side effects;
 Weight gain
 Increased muscle compartment pressure- may increase muscle
cramps.
 Long-term use may compromise kidney function.
o Vitamins
 Not needed if eat a balanced diet.
 May be needed on low kJ or low fat diets.
 Megavitamins more likely to be harmful than beneficial.

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o Minerals;
 Only needed if levels below normal.
 Usually only occurs with very low kJ or extreme vegetarian diets.
 Most common deficiencies are Fe & Ca.
o Iron;
 Males: 8mg/d; Females 18 mg/d
 Athletes need higher iron intakes:
 During growth
 Due to sweat loss
 If GI upsets result in GI bleeding
 Mechanical trauma due to repeated foot strike (running)
 Supplements may be required if vegetarian diets or low energy diets.
 Iron absorption from non-haem (non-meat) diets is lower than haem.
 Including Vit C with meals improves iron absorption.
 Excessive tea, coffee & bran decreases iron absorption.
 Dried fruit, corn, green leafy vegetables are good sources of non-haem iron.
 Supplements can cause gastric distress & increase iron loss.
o B-hydroxy-B-methylbutyrate (HMB)
 Metabolite of amino acid leucine.
 Promoted to increase LBM and strength.
 Proposed to prevent muscle breakdown (i.e. anti-catabolic).
 Effects modest at best; most effective on untrained people.
 Effects on sports performance lacking.
o Colostrum
 Fluid produced by mammary glands around time of birth- low in fat, high in
protein, antibodies.
 Contains growth factors
 Supplements contain bovine colostrum- contains IGF-1 (broken down in gut
but may stimulate own production of IGF-1).
 Evidence of performance benefits lacking.
 WADA recommends against use.
 Are supplements hazardous?

o Present a high risk to athletes.
o Difficult to establish safety (many ingredients)
o 2001 IOC study: 15% of supplements tested contained a banned substance
not on label (none were Australian products).
o Side effects;
 Creatine - Nausea, dizziness, headaches, cramps, diarrhoea.
 HMB (Beta-hydroxy beta-methylbutyrate) Effectiveness not established
(increase muscle claimed).
 Beta-alanine – lactic acid buffer→ Flushing and tingling.
 Protein powders - increase muscle claimed. Often high sugar content.
 Sodium bicarbonate – lactic acid buffer → Nausea, vomiting, diarrhoea
 Caffeine

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 Maughan’s rules of Dietary supplements for Athletes

o If it works, it’s probably not allowed.
o If it’s allowed, then it probably doesn’t work.
o There may be some exceptions.
 What ergogenic substances & practices are illegal?

o WADA code (Jan 1 2014) - The use of any drug should be limited to medically
justified indications.
o 2016 List of Prohibited Substances and Methods;
1. Prohibited at all times (In & Out of competition)

Substances
 S0. Non-approved substances (new in 2012)
 S1. Anabolic agents
 S2. Peptide hormones, growth factors and related substances
 S3. Beta-2-agonists
 S4. Hormone and metabolic modulators
 S5. Diuretics and other masking agents
Methods
 M1. Manipulation of blood and blood components
 M2. Chemical and physical manipulation
 M3. Gene doping
2. Prohibited In-competition - Substances and Methods.
3. Prohibited in particular sports

Substances
 P1. Alcohol - Air Sports (FAI), Archery (WA), Automobile (FIA), Powerboating (UIM).
 P2. Beta-blockers Archery, Automobile, Billiards, Darts, Golf, Shooting,
Skiing/Snowboarding.
LECTURE 29: EXERCISE & BONE
 Bone tissue matrix

o Organic components;
 Collagen (tensile strength)
 Proteoglycans (compressive strength)
 Matrix proteins (osteocalcin, osteonectin, osteopontin)- mineralisation.
 Cytokines and growth factors
o Inorganic (mineral) components
 Calcium hydroxyapatite (compressive strength)
 Osteocalcium phosphate

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 Bone cells
o Osteoprogenitor cells
 Undifferentiated mesenchymal stem cells.
 Become osteoblasts or cartilage or fibrous tissue
o Osteoblasts- Bone builders. Produce matrix & initiate calcification.
o Osteocytes
 Derived from osteoblasts
 Mature bone cells
 Perform metabolic roles and maintain bone
o Osteoclasts
 Bone removers – resorb bone for remodelling.
 Derived from macrophage line hematopoietic cells.
 Bone structure
o Corticol (compact) bone
 Dense, hard, outer layer
 Slow turn over
o Trabecular (spongy) bone
 Cancellous, less dense, more elastic, relatively weaker.
 Most prevalent in vertebrae & head of femur.
 High turnover
o Cortical/trabecular composition differs by bone type (long, short, flat, irregular,
sesamoid).
 Bone turnover
o Balance between activity of osteoblasts (deposition) and osteoclasts (reabsorption).
o Osteoclasts regulated by hormones (parathyroid hormone, calcitonin, vitamin
D/calcitriol).
 Bone turnover & age

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o Bone ‘growth spurts’

 Post-natal – 0-2 years old
 Pubertal ~ 11-18 years of age in females and ~ 13-21 years of age in males.
o Bone turnover is very high in infancy & childhood- starts to decline with
puberty.
o Bone growth during puberty is mechanically driven- Modulated by hormonal
(growth hormone, thyroid hormone, androgens and sex hormones) & dietary
factors (Ca2+ intake).
o Benefits of physical activity on bone greatest before menarche in girls (&
equivalent in boys).
o Effects of oestrogens on bone growth;
 Low levels increase GH & increase bone growth (Peak height velocity).
 Higher levels stimulate fusion of growth plates (epiphyses).
 Later maturation leads to greater height due to later fusion of epiphyses.
 Higher levels lead to reduced bone turnover.
 Earlier menarche may lead to increased bone density.
 Fracture risk
o Fracture risk increases during puberty in boys & girls.
o Proposed asynchrony between bone growth rate and bone mineral accrual
(mineral density lags by ~ 1 year).
o Fracture rate during puberty is highest of lifetime.
o ~ 50% of children sustain a fracture.
o ~ 50% of childhood fractures are of forearm.
o Low calcium intake increases risk.
o Bone turnover stabilises on maturity (adulthood) and is usually well-
maintained until menopause in females- Higher oestrogen levels promote
death of osteoclasts by apoptosis.
o As oestrogen levels decline in females & males, osteoclast activity increases
& progressive bone loss occurs (aging bone loss).
o Oestrogen therapy slows rate of bone loss.
o Peak bone mass ~30yrs age.
o Age-related reduction in bone mass called osteopenia.
o Males lose ~ 0.4% pa after age 30.
o Females lose ~ 0.8% pa after age 30.
o Lose 3-6% for 5 years after menopause. Then lose ~ 1% /yr.
o Bone mass in older age influenced by:
 Peak bone mass achieved
 Age of menopause
 Influences on peak bone mass

o Age of menarche or pubertal development
 Earlier development, higher peak bone mass.
 Later development increases lifetime fracture risk due to reduced bone
mass.

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o Maintenance of hormonal environment.

o Level of physical activity;
 More activity, higher bone mass.
 Weight-bearing activity has greater effect.
 Higher mechanical loading increases bone mass.
 Site-specificity of effects.
 Exercise & bone mass

o Site specificity of exercise.
o Exercise acts by local mechanical stimulation of bone
 Mechanical stress stimulates osteoblasts.
 Osteoblasts increase Ca uptake
o Bone accrual proportional to
 Magnitude of mechanical force
 Frequency of exposure
o Bone density proportional to strength & local muscle mass.
 Osteoporosis
o Most common skeletal disorder.
o Characterized by:
 Loss of bone mass (mineral density).
 Deterioration of bone architecture.
 Increased bone fragility (fracture risk)
o Primarily a consequence of aging & genetics.
o May be a consequence of endocrine dysfunction or malignancy.
o 2 in 3 women, and 1 in 3 men over the age of 60 will suffer an osteoporotic
fracture in their remaining lifetime.
o Currently over 2 million Australians affected.
o Genetics, age & gender account for ~ 60-80% of risk.
o Family history of disease or fractures.
o Caucasians (non-Mediterranean) & Asians risk higher.
o Risk increases with age.
o Females > males (but previously under recognized in males).
o Risk factors;
 Slight build or underweight
 Prolonged amennorhoea in females
 History of eating disorder
 Cigarette smoking
 Sedentary lifestyle & low muscle mass
 Prolonged bed-rest
 Medications (Corticosteroids & anticonvulsants).
 Calcium deficient diet
 Childhood, adolescence, adulthood.
 Vitamin D or sunlight deficiency.
 Muslim women in Melbourne.

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 Excess alcohol intake

 High (animal) protein intake
 Excessive sodium intake
 Possibly high caffeine intake
o Consequences;
 Loss of height & postural stoop
 Wedging & loss of vertebral integrity- leads to kyphosis (Dowager’s hump).
 May result in neck & back pain.
 Secondary thromboembolism after falls
 Common cause of death in older women- more deaths than breast cancer.
 Fracture risk
 Increased risk if fall- 56% lifetime fracture risk in females with osteoporosis.
28% lifetime fracture risk in Males with osteoporosis.
 Possible spontaneous fracture resulting in falls.
 Greatest risk in hips, vertebrae, wrists.
o Prevention;
 Physical activity
 Vigorous weight-bearing exercise in childhood & adolescence.
 Regular weight-bearing exercise in adulthood.
 Specific resistance exercise programs recommended.
 Ideally, all women would start resistance training when young & continue
through life.
 Maintain muscle leg strength to reduce risk of falls.
 Balance exercises to reduce falls risk.
 Moderate exercise improves bone health (~5% increase in mineral density)
for sedentary adults - limited effect if already active.
 Appropriate diet- Calcium, Vit D, energy, limit alcohol, salt, possibly caffeine.
 Don’t smoke
 Medications- Biphosphonates, SERMs, HRT.
o Management of osteoporosis;
 Maintain muscle leg strength to reduce risk of falls.
 Balance exercises to reduce falls risk.
 Deconditioning common at diagnosis - Low intensity program initially.
 Aerobic 40-70% HRmax, 30-60 min/session; 3-5 d/wk.
 Resistance 75% 1RM; 8-12 reps; 2 sets; 2-3 d/wk
 Flexibility- Static; 30s hold; 5-7 d/wk
 Nutrition- Calcium & Vit D supplements
 Medications- Biphosphonates, SERMs, HRT.
 Risk of falls
o Weak leg muscles (major factor).
o Poor tactile sensitivity.
o Limited vision
o Body sway (reduced balance).
o Use of 2 or more psychoactive drugs.
o Use of antihypertensive medication in women

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LECTURE 30: EXERCISE & THERMOREGULATION
 Body operates optimally at core temp 37°C.

 >40° C denaturing proteins, <27° C changes ionic fluxes → cardiac
arrest/arrhythmias.
 Tolerate cold better than heat.
 Radiation (heat gained or lost) - e.g. sun.
 Conduction (heat gained or lost) - e.g. cool tiles- needs contact.
 Convection (heat gained or lost) - e.g. cool breeze.
 Evaporation (heat loss only) - e.g. sweat.
 Heat transfer depends on temperature gradient.
 Rate depends on environmental conductor (faster loss/gain in water than in air).
 Sources of heat
o Intrinsic (body) - resting metabolism, physical activity, posture, time of last
meal.
o Extrinsic (environmental) - temp, humidity, medium.
 Core & peripheral (shell) temperature

o Vasoconstriction in periphery when cold, vice versa when hot.
 Thermoregulation
o Temp receptors centrally & peripherally- determine temp in core vs shell.
o Thermoregulation integrated in hypothalamus.
o Responses to thermal inputs;
 Physiological
 Behavioural
o Physiological response to cold;

 Decrease blood flow to skin & extremities- most heat lost from
hand/feet/head.
 Muscular activities (voluntary or shivering).
 Hormonal secretions (TH, noradrenaline- increase metabolism).
o Behavioural responses to cold;
 Clothing (adding layers- traps air. Air good insulator).
 Muscular activity (voluntary movement generates heat)
 Seeking shelter/warmer environment
 Consume warm food/drink
o Physiological response to cold;

 Increase blood flow to peripheries
 Sweat
 Increase breathing
 Hormonal secretions (↓ TH, ↑ ADH & aldosterone- to maintain fluid
balance & blood volume).

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o Behavioural response to cold;

 Clothing
 Reduce/alter PA
 Change environment/medium
 Decrease food intake/intake cool drinks
 Role of the sympathetic nervous system

o Alterations in blood flow (vasoconstiction/dilation).
o Sweating mediated by SNS- increased with increased drive.
 Physical activity & cold

o Cold favours blood flow to skeletal muscle.
o For long duration activities, moderate cold enhances performance.
o Exercise in water limited by cold- much more rapid heat loss. Kids & elderly
populations particularly vulnerable.
 Physical activity & heat

o Competition for blood flow between skin & muscle.
o In long duration activities, muscles will win out over skin- causing progressive
increase in temperature.
o If humidity high- compromises evaporation but still lose fluid.
 Factors affecting temperature

o High temperatures tolerated better tolerated with low humidity.
o Heat stress index used to determine time & day of year best suitable for
endurance events.
o Heat load increases with intensity & duration of exercise.
o Hydration status/fluid loss fluid intake should exceed fluid loss by ~25%.
o Sweat is hypotonic to blood.
o Acclimatisation to heat improve heat tolerance- occurs in about a week.
 Lower body temp at same intensity in hot environment.
 ↑ ADH → maintained blood volume → improved blood flow
 ↓ sweat threshold
 ↑ sweat output, sweat less concentrated- lose less electrolytes.
o Higher aerobic fitness levels improve exercise tolerance in heat.
o Higher blood volume in trained individuals may contribute to increased skin
blood flow.
o Lower HR in trained individual’s ↓ workload.
o Clothing can be designed to increase or decrease heat loss.
o Padding & head gear → heat retention.
o Body fat insulates & decreases heat loss.
o Large surface area to mass increases heat loss (this is reduced in overweight-
have high volume & ↓ surface area).

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o Little difference in thermoregulatory capacities of men & women- women

sweat less. Females use circulatory changes more, have larger surface area to
mass.
o Children have slower & lower sweat rate- increases at puberty.
o Children lose heat faster in cold (surface to mass effect)- especially in water.
o More salt in childrens sweat.
o Eldery also at risk.
o SCI patients limited ability to redirect blood flow below injury level.
o Heat loss from head maintained.
o Less risk of hyperthermia due to PA, more risk of hypothermia.
o SCI has less functional muscle mass-thermogenic mechanism lost.
 Heat cramp
o Involuntary muscle spasms.
o Probably due to electrolyte imbalance.
o Body temp remains normal
 Heat exhaustion
o Most common with sudden exposure to heat in un-acclimatised.
o Vasodilation & inadequate blood volume.
o Low BP, dizziness, weak/rapid pulse, HA.
o Core temp elevated but not dangerously (not >40).
 Heat stroke
o Core temp >40
o Serious medical illness
o Absence of sweating- skin hot but dry.
o Heat loss mechanisms overwhelmed.
o Prone to infection & circulatory or septic shock.
o 1 in 3 will be permanently impaired.
o Common in elite athletes who push past increasing temperature.
 Measurement of body temp

o Oesophageal- gold standard
o Rectal 2nd
o Aural 3rd
LECTURE 31: FLUID BALANCE
 Distribution of body water

o ~ 60% (40-70%) of body mass.
o Composed of intracellular volume (ICV) & extracellular volume (ECV).
o Intracellular
 2/3 total body water

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 Muscle cells are ~ 70% water

 Fat cells are ~ 10% water
o Extracellular
 ~ 1/3 total body water
 Interstitial fluid (between cells)- 19%
 Plasma (4%)
 Lymph, ducts, glands, mucous secretions, tears, CSF.
o Slightly lower in females (55%) vs males (60%) - muscle: fat ratio.
o Slightly lower with age.
 Functions of body water

o Transport medium for most body nutrients, waste & gases.
o Moistens surfaces for nutrient transfer.
o Lubricates joints (water & proteins).
o Gives structure & form to most body structures- water is non-compressible.
o Provides cushioning for many body structures.
o Contributes to maintenance of body temperature (takes a lot of heat to
change the temperature of water).
 Fluid balance
o Dehydration- Process (not a state) of losing body water → hypo-hydrated
state.
o Rehydration- Process of regaining body water to a euhydrated state. Can lead
to hyper-hydrated state.
o Fluid balance is usually very accurate.
o Water input;
 Fluids ~ 50-60%
 Food ~ 30-40%
 Metabolism ~ 10-15% (by-product of aerobic metabolism).
o Water input higher from fruit & veg, lower from high fat foods.
o Water output;
 Urine ~ 50-60%
 Faeces ~ 5%
 Sweat ~ 5%
 Insensible loss
 Skin ~ 20-30% (not sweating, just dehydration of skin).
 Lungs ~ 10-15%
 Greater in dry climate; less in humid climate
 Diarrhoea & vomiting increase fluid loss.
 Exercise influences fluid loss.
o Influence of hot climate & intense exercise on fluid loss
 Decrease urine output 1250 to 500 ml (urine more concentrated)
 Increase skin loss 850 to 5000 ml
 Increase lung loss 350 to 700 ml

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 Body fluid effects

o In the body, water influences:
 Electrolyte balance: concentrations of sodium (+++), potassium, calcium,
magnesium, chloride.
 Blood volume
 Arterial blood pressure
 Cardiac output (blood flow).
 Regulation of body fluids & electrolytes

o Integration centre in Hypothalamus.
o Inputs to hypothalamus;
 Osmoreceptors (hypothalamus)- sensitive to osmolarity.
 Atrial baroreceptors (blood volume)
 Arterial baroreceptors (blood pressure)
 Thirst (hypothalamus) - drives behaviour to drink.
o Outputs via hormones;
Antidiuretic hormone (ADH) or vasopressin

 Secreted (in response to low blood volume) from cells in posterior pituitary.
 ↑ Water absorption in distal tubule in kidneys → ↑ MAP.
 Release of ADH stimulated by activation of hypothalamic neurons.
 Respond to osmoreceptor inputs – If fluid volume down, osmolarity up.
 Respond to baroreceptor inputs – If fluid volume down, BP down.
 Release also stimulated by angiotensin II.
 Also causes vasoconstriction.
Aldosterone
 Stimulated by low arterial pressure/blood volume and/or low renal blood
flow.
 Stimulates release of renin from kidneys.
 Renin converts angiotensinogen to angiotensin I.
 ACE converts angiotensin I to angiotensin II.
Angiotensin converting enzyme (ACE)

 Secreted by lungs
 Converts angiotensin I to angiotensin II – Angiotensin II has major effects on
sodium & fluid balance.
 ACE inhibitors are a major class of drugs used in the treatment of
hypertension.
 Changes kidney permeability to Na+ and water.
Angiotensin II
 Increase aldosterone release
 Increase ADH release
 Arteriolar vasoconstriction (increase BP)
 Increase thirst
 Increase Na+ reabsorption in kidneys.

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 Increase water reabsorption (passive to Na + ) in kidneys.

 Decrease Na+ loss in sweat – Increase EVC (plasma volume)
Atrial natriuretic peptide (ANP)

 Secreted from atrial cells– mostly from right atrium (stretched by ↑ blood
volume).
 Release stimulated primarily by atrial stretch (increased central blood
volume).
 Increase diuresis (fluid loss).
 Blocks release of ADH.
 Blocks release of aldosterone.
 Blocks Na+ reabsorption in kidneys.
 Reduces sympathetic cardiac & vasoconstrictor drive & arteriolar
vasoconstriction directly.
 Decreases arterial BP.
 Mechanism of fluid loss when exposed to cold.
 Effects of exercise on fluid & electrolyte balance

o Increase sweating
o Increase in osmotic pressure in cells due to metabolites (H20 will try to go
into cells).
o Increase in hydrostatic pressure due to increased BP (raised blood pressure
forces H2O out into tissues).
o Effects:
 Water moves from plasma into interstitial & intracellular spaces (ie decrease
plasma volume).
 Water lost from body.
 Some electrolytes lost from body.
o Impact & risk:
 Decrease blood volume
 Compromise cardiac output & blood pressure.
o Increased blood osmolality stimulates osmoreceptors in hypothalamus and
intiates water retention processes (above).
o Repeated days of exercise;
 Increased secretions of fluid balance hormones.
 Increased plasma volume- dependent on adequate fluid intake.
 Possible haemodilution (decrease HCT).
 Possible pseudoanemia
 Preventing dehydration with exercise

o Ensure at least euhydration pre-exercise (~24hrs prior).
o Weigh before & after exercise – Consume fluid to volume lost plus 25%.
o Ensure urine colour returns to pale yellow.
o Hydrate during exercise if:
 Long duration
 High ambient temperature/humidity

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o Consume an appropriate sports drink if rate of rehydration is important

 Hypotonic (relative to blood)
 Low sugar concentration
 Cool
o Be conscious of salt intake- don’t exclude completely.
 Sodium balance & hyponatremia

o ‘Water intoxication’ - Serum Na < 136 meq/L (150 normal).
o Due to excess water relative to sodium - prolonged sweating & excess plain
water intake.
o Mild symptoms - Headache, confusion, nausea, cramps.
o Severe symptoms - Seizures, coma, pulmonary oedema, death.
o Ultra-endurance events ~ 9% of collapsed athletes.
o Rarely in events < 4 hours (usually in events > 6 hours).
o Associated with prolonged exercise, heat & prolonged sweating & sodium
loss.
o Who is most vulnerable?
 Less accustomed to prolonged exercise.
 Poorer physical condition
 Unacclimatized to heat & especially humidity.
 Consume a low salt diet
 Take diuretic medications
 Sweat profusely
 Consume large quantities of plain water.
o Prevention;
 No more than 1 L plain water per hour during or after exercise.
 Add some sodium & glucose to drinks.
 Sprinkle salt on food in days prior to exposure.
 Renal Disease
o Patient groups- haemodialysis, peritoneal dialysis, transplant.
o Very low levels of physical capability typical.
o Muscle mass predicts life expectancy.
o Very low aerobic capacities (VO2max)
 Activity limited by leg fatigue
 Rarely reach age-predicted HRmax
 Stress tests rarely useful as interpretations difficult (electrolyte
abnormalities distort ECG).
o Fitness tests use low level activities:
 ADLS (activities of daily living score)
 Stair climbing
 6 min walk test

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 Timing exercise in dialysis

o Pre dialysis- fluid load problems (e.g. breathlessness).
o Post dialysis- fatigue, hypotension
o During dialysis- possible during first 1-1.5 hours of dialysis.
 E.g. cycling; resistance training trial (St George Hosp)
o Nondialysis days: Exercise usually better tolerated.
o Training recommendations;
 Similar for dialysis & transplant patients.
 CV (endurance) activities
 Low intensity aerobic activities (walk, swim, and cycle).
 As many days as possible.
 RPE 12-15 (HR is poor indicator).
 Begin with intermittent (interval) activity.
 Progress to continuous activity.
 Aim for 30 min continuous - longer if overweight/obese.
 Strength training
 Aim to increase or maintain muscle mass.
 3 sets of 12-15 reps.
 Major muscle groups.
 3 x week or more
 Start with 1 set of 12 reps with low load.
 Motivation often difficult.
 Maintaining muscle mass is important.
 Prednisone (corticosteroid) part of anti-rejection regime- catabolic
effects impair maintenance or growth of muscle mass.
LECTURE 32: THE GIT & EXERCISE
 Pre-competition nutrition
o Main consideration usually glycogen stores
 Normal stores for exercise < 1 hr
 High CHO intake for exercise > 1 hr
o Disadvantages of high CHO intake
 Increase H20 storage (adds weight)
 May cause diarrhoea
o Adequate CHO
 Fasting depletes glycogen stores (e.g. when first waking up).
 Adequate CHO diet for at least 3 days pre competition recommended.
o Adequate fluid (hydration)
 Should start exercise optimally hydrated
 Requires appropriate fluid intake ~ 24 hrs
 Last Fluid intake: 0.5 L ~ 15 min pre-exercise
o Considerations;
 Timing ~ 3-4 hours prior to exercise.
 Digestibility & absorption rate of food.

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 Low in lipid & protein, higher in CHO (~ 3-5 g /kg BW).

 GI: Low to moderate (But avoid fructose as often causes GI upsets).
 Liquid meals useful
 Don’t try something new!
 Nutrition during exercise

o Maintain blood glucose
o Delay glycogen depletion
o May need CHO intake – If exercise > 1 hr
o Not needed for low intensity activity unless > 4 hr.
o May need for sprint finish.
o GI not an issue during exercise (insulin release suppressed by adrenaline).
o Initial spike in plasma glucose due to increased availability from liver, needs to be
topped up eventually by feeding.
o Influences on intake;
 Palatability – Influences amount consumed (flavouring, concentration, and temp).
 Previous GI symptom experiences – Often reduces amount consumed.
o Considerations for solutions consumed during exercise;
 Fluid content (hydration) – Influences blood volume/flow and thermoregulation.
 CHO content (energy) – Slow rate of muscle glycogen depletion.
 Electrolyte composition – Restore electrolyte composition of body fluids.
 Absorption of carbohydrates
o Mostly occurs in first 20% of small intestine.
o Only monosaccharides (eg glucose) are absorbed.
o Processes
Co-transport
 Requires carrier protein & coupling to another substance e.g. Glucose & galactose
coupled to Na+ transport.
Facilitated diffusion
 Diffuse into epithelial cells
 Diffuse into interstitial fluid
 Absorbed into blood
 Absorption of water
o Small intestine – some.
o Large intestine – most.
o Occurs by diffusion- follows osmotic gradients.
o As solutes absorbed, solute concentrations fall.
o Most water moves with sodium.
 Absorption of ions
o Sodium – Most abundant ion in chyme.
o Diffuses or co-transported into epithelial cells. Often co-transported with
glucose.
o Actively transported into interstitial fluid.

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o Influences on rate of absorption

 Concentration in chyme
 Aldosterone secretion
 Influences on gastric emptying rate

o Gastric volume
 Higher emptying rate with higher stomach volume.
 Pre load stomach by consuming 400-600 ml 15-20 min pre-exercise.
 Consume 150-250 ml every 15 min during exercise
 Provides ~ 1 L per hour of fluid to intestines.
o Fluid temperature
 Colder fluids may empty slightly faster than room temp fluids.
 Temperature may have more impact on intake – Colder than 15°C slows
ingestion rate in many people.
o Carbonation
 Slows rate of gastric emptying.
 Therefore delays absorption of water and CHO
 Enhances absorption of alcohol because absorbed from stomach.
o Osmolality
 Concentration of particles in solution.
 High osmolality (hypertonic solutions) slows gastric emptying.
 Influenced by: concentration & form of CHO.
 Glucose polymers decrease osmolality relative to CHO content e.g.
maltodextrin.
 Electrolytes
o Intensity of exercise
 Little effect with intensities up to ~ 75% max.
 Gastric emptying slows at higher intensities.
o Hydration level (lower lowers)
 Influences on absorption rate

o Osmolality
 Hypotonic to isotonic solutions absorbed well – Composition of solution may
influence.
 No clear evidence that hypertonic solutions slow absorption – May
contribute to GI upset.
o CHO content
 Low to moderate concentrations absorbed faster.
 Glucose absorbed faster than fructose.
 Water absorbed faster with low levels of glucose than without glucose.
 Water absorbed faster with glucose than fructose.
o Sodium content
 Low to moderate sodium concentrations increase absorption of water and
glucose.
 Other effects of sodium content;

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 Maintain plasma sodium concentration

 Decrease urinary output
 Sustain desire to drink
 Considerations for composition of sports drink

o 5-8 % CHO provides energy & fluid.
o Use lower CHO if hydration main factor (hot, humid, shorter duration ex).
o Use higher (8%) CHO if energy provision more important (long duration,
cooler).
o Consider energy content if exercising to lose weight!
o Higher CHO (20-25%) may be needed for replenishing glycogen stores post
exercise.
 GIT symptoms
o Upper GIT symptoms- Nausea, vomiting, belching, heartburn, chest pain.
o Lower GIT symptoms- Bloating, GI cramps, side-ache, farting, urge to
defecate/defecation, diarrhoea.
o Reported more with endurance activities.
o Influences on upper GIT symptoms
 More common in cycling
 Increased by diet high in fibre, fat & protein
 Increased by hypertonic drinks
 Increased by dehydration
 Influenced by intensity of exercise
 Increase intensity, increase symptoms.
o Influences on lower GIT symptoms
 More common with running
 Influenced by intensity of exercise
 Symptoms may be due to decreased gut transit times & reduced GIT blood
flow.
 All symptoms more likely if have mild symptoms at rest.
 Exercise may be a ‘stress test’ for your gut.
 Nutrition during recovery

o Replace fluid losses (first priority).
 Aim to consume 125% of lost fluid within 4-6 h of exercise.
o Replace electrolytes
 Sodium/electrolytes most important if large fluid loss.
o Restore glycogen stores
 Immediately post exercise consume a CHO rich snack or meal (1-1.2g /kg
BW) within 1 h of finishing ideal.
 High GI may be advantageous.
 Most important when need to train within 8 h.
 CHO intake most effective nutrient to prevent immune compromise
associated with training.

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o After RT – protein
 Immediately post exercise (within 1 h of finishing e.g. RT) consume 15-25 g
of high quality protein.
 Unclear if casein vs whey makes a difference.
 Adding CHO to this protein intake enhances adaptation.
 Goals of nutrition during exercise

o Prevent dehydration
o Assist energy provision with CHO intake
 Does the gut adapt to training?

o Gut itself is NOT an athletic organ – Does not adapt to exercise training.
o Less reduction in blood flow during submaximal exercise with training – This
reduces some GI symptoms.
LECTURE 33: EXERCISE & MENTAL HEALTH
 20% of AUS will experience

 14% in children & adolescents
 27% in 18-24 yr olds
 6% in > 65 yr olds
 Anxiety- 10%
 Depression- 20% (major 6%)
 Psychotic disorder- 3%
 Eating disorder- 2%
 Depression
o 25% of AUS women.
o 16% of AUS men
o 3rd leading cause of disability.
o Most days lost from work.
o Severity varies from mild to severe.
o Some feel unhappy/sad; some can’t feel anything.
o Guilt, reproach, inadequate.
o Uneasy, restless, anxious.
o Appetite change common – reduced or markedly increased.
o Sleep disturbance- fatigue a common symptom.
o Symptoms; Five or more of following, including either symptom 1 or 2, for
same 2-week period; and this is a change from previous functioning
1. Depressed mood, nearly every day, most of the day.
2. Marked diminished interest in almost all activities.
3. Significant weight loss (not dieting), weight gain or change in appetite.
4. Insomnia or hypersomnia (excess sleep).
5. Psychomotor agitation or retardation.

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6. Fatigue or loss of energy.

7. Feeling worthless or inappropriate guilt.
8. Impaired ability to concentrate or indecisiveness.
9. Recurrent thoughts of death, recurrent suicidal ideation.
 Can exercise treat depression?

o Major study – Blumenthal et al 1999
 N=156, severe depression, 50 years age plus.
 3 groups: aerobic exercise, antidepressant medication, combination.
 4 months treatment.
 Fastest onset of benefits with medication.
 After 4 months, no difference between groups re symptoms.
 After 6 months break, symptoms and relapse rate least in exercise-alone
group- Continuing to exercise contributed to this (possible natural bias).
o Dunn et al 2005
 N=80, Mild –moderate depression, age 20-45 years.
 4 groups with different exercise regimes.
 Better response if higher energy expenditure and 5 x week.
 Flexibility exercises not effective.
o Motivation is the real challenge.
o Recommendations;
 Individualised
 Supervised initially & physician monitored.
 Aerobic (run, swim, cycle) and strength training.
 Daily if possible
 RPE 12-13 initially (10-20 min) progress to 15-16 for 30 min.
 Need to improve fitness (measure of effective program)
 Use to supplement medication at present.
 Best if exercise is regular- best if daily or almost daily.
 Needs to be ongoing
 Better results if intensity higher
 More evidence needed for other outcomes.
 Healthy body healthy mind study

o Young people at highest risk of depression & suicide.
o Aim: To investigate the feasibility and preliminary efficacy of a 12-week
exercise training program with brief motivational interviewing (MI) as a
treatment for MDD in youth.
o Number of participants with depression and severity of depressive symptoms
decreased after 12-week exercise program.
o One of 12 still met criteria for MDD.
o 60 % reduction in depression symptoms – Average score of severe MDD to
mild-minimal.
o Benefits strongly associated with attendance at training – daily dose may be
more important than intensity.

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 Exercise & anxiety

o Best results with aerobic exercise.
o Best if regular.
o Better results if initial fitness low.
o Better if initial anxiety high.
o Mechanisms?
 Socially positive
 Mentally distracting (especially higher intensity exercise).
 Improved fitness reduces fatigue and improves sense of well-being.
 Hormones (adrenaline).
 Endorphins, serotonin, dopamine.
 BDNF – brain derived neurotrophic factor.
 Elevation in body temperature may reduce anxiety.
 Exercise & psychiatric disorders

o High rates of inactivity and high fat diets.
o High rates of smoking
o High rates of CV disease and diabetes
o May benefit from lifestyle interventions including exercise.
o Daily activity, even walking, a primary goal.
 Cognitive impairment
o E.g. Down’s syndrome
 Typically low aerobic fitness levels
 (low VO2max - < 25 ml/kg/min; low HRmax).
o Low strength; low bone density.
o Can respond to training- fitness & health benefits (CV, neuromuscular &
metabolic).
 Cognitive decline
o More PA, less cognitive decline with aging; less Alzheimer’s.
o Exercise > 3 x wk – 32% lower risk of dementia.
o Age > 85 yrs exercise 4 h/wk (88% decrease in risk of cognitive impairment).
 Cognitive & ADHD

o Elevates dopamine & noradrenaline
 Effects like Ritalin (stimulants).
o Small amounts of exercise before school may improve concentration.
o Must be enjoyable to engage.
o Activities requiring focus (karate, ballet) may be particularly beneficial.
o Exercise recess at school beneficial.

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 Exercise & learning

o Increases cellular components in brain responsible for learning, decision-
making and memory.
o Changes cellular environment (hormones, BDNF, etc) to enhance pathways.
o Stimulates neurogenesis.
 Exercise & sleeping

o Sleep and body temperature
 Body temp is higher in daytime; lower at night.
 A drop in body temp may signal sleep.
 Vigorous exercise raises body temp, but when temp then falls may help
sleep.
o Time in outdoor light may help sleep so exercise in sunlight may help.
o Vigorous aerobic exercise 3-5 hours before bedtime best – 20 min or longer.
o Vigorous exercise immediately before bedtime not helpful.
o Resistance training and low intensity not shown to be beneficial.
LECTURE 34: IMMUNE FUNCTION & EXERCISE
 Body systems
o Innate immune system (non-specific)
 Barriers
 Skin
 Mucous membranes
 Phagocytes
o Acquired (specific) immune system
o Immune system consists of cells, cell derivatives & modulators (cells are
leukocytes (WBCs)).
o Roles are to defend against:
 Microbes (pathogens)
 Foreign macromolecules
 Abnormal cells (cancer cells)
 Clean up dead or injured cells
 Immune dysfunction
o Fail to recognise & respond to microbes/abnormal cells.
o React inappropriately to good tissue (autoimmune disease).
 Leukocytes
o 1% of total blood volume.
o Originate in bone marrow.
o Serve roles in inflammation & immunity.
o Mobile units of the defence system.
o Mostly operate on a ‘seek & destroy’ strategy.

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o Myeloid derived
 PMN granulocytes (neutrophils, eosinophils, basophils)
 Monocytes
o Lymphoid derived (lymphocytes)
 White Blood cells in blood

o Many WBCs produced.
o Only a small number in blood at any time
 ~ 2/3 granulocytes
 Most of other 1/3 are lymphocytes
o Numbers do vary with defence needs of body e.g. infection (increase).
 Lymphocytes
o Bone-derived B cells – Produce antibodies & immunoglobulins.
o Thymus-derived T cells – Provide cell-mediated immunity.
o Natural killer (NK) cells – Provide general surveillance.
o In circulation;
 ~ 80% T cells
 ~ 10-15% B cells
 ~ 5-10% NK cells
 Role of lymphoid tissues

o Produce, process or store lymphocytes.
o Includes:
 Bone marrow
 Lymph nodes & spleen
 Thymus
 Tonsils, adenoids, appendix
 GALT (gut-associated LT)
 MALT (mucous membrane associated LT).
 Plasma B cells & immunoglobulins

o 5 classes of Ig – M, G, E, A, D. Each plays different
roles.
o IgA important in mucous membranes (GALT &
MALT).
o IgA found in GIT, respiratory tract, genito-urinary
tracts, milk & tears.
 Stressors affecting the immune system

o Illness
o Exercise
o Psychological distress
o Lack of sleep
o Lack of food

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 Exercise & immunity
o Upper respiratory symptoms account for 50% of medical consultations at AIS.

o GI upsets account for most other consultations for illness at AIS.
o Immune function stimulated by moderate intensity exercise.
o Immune function compromised by high intensity exercise.
o Acute exercise alters risk of URS & possibly URTI.
o Moderate exercise reduces risk, intense or prolonged exercise increases risk
(J-shaped relationship to activity level).
o Moderate exercise increases IgA secretion & NK cell activity (protects against
infection).
o Intense or prolonged exercise decreases IgA secretion.
o “Open window” hypothesis- suggests individuals are more vulnerable to
infection for a period of time following strenuous exercise.
 Post-exercise immuno-suppression (Reduced IgA).
 Reduce exposure to infection post-exercise e.g. don’t share drink bottles.
o Repeated days of intense or prolonged exercise decrease IgA further (does
not recover after previous exercise) & increase risk of URS.
o Are adverse effects of exercise on immune function or illness risk preventable
with nutrition? – CHO best effect so far.
o Aerobic training;
 Enhances NK cell activity
 May reduce cancer risk
 Reduces age related T-cell decline
o Resistance training;
 Few studies
 No benefits demonstrated
 Acute exercise may increase NK cells – May be intensity & volume related.

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 Exercise & acute illness

o If symptoms above neck – OK to train.
o If symptoms below neck (aches, chills) - best not to train (only if essential).
o If fever – Don’t exercise.
 Exercise & cancer risk

o Regular exercise reduces risk of;
 Colon cancer by 40-50% (decreases intestinal transit time).
 Breast cancer by 30%
 Lung cancer by 40%
 Prostate & endometrial cancer rates slightly lower in those who exercise.
o Risk decrease may be due to relationship between obesity & cancer.
o Pathogenesis – NO evidence (i.e. exercise training doesn’t cause cancer).
o Symptoms– MODERATE evidence (exercise training reduces some of the
symptoms in people with cancer).
o Physical fitness and strength - MODERATE evidence (exercise training can
improve fitness and strength in cancer patients).
o Quality of life - MODERATE evidence (exercise training can improve quality of
life in cancer patients).
o Recommendations to reduce cancer risk (options);
 Light exercise, 60+ mins, daily.
 Moderate exercise, 30 mins, daily.
 Vigorous exercise, 30 mins, 3 x weekly.
o Proposed mechanisms of benefit;
 Increased NK cell activity
 Increased phagocytic activity
 Increased antioxidant capacity
 Reduced levels of some tumour growth factors.
 Exercise for cancer survivors

o Loss of muscle mass & strength.
o Loss of endurance (fatigue).
o Constipation (may be related to pain medication).
o Possible lymphoedema
o Anxiety & depression
o Recommendations;
 Regular moderate intensity activity (walking, cycling & swimming effective).
 Symptom (fatigue) limited
 Daily if tolerated
 Intervals or multiple small bouts per day.
 Resistance training for muscle loss.
o Positive effects of regular aerobic exercise on selfesteem, anxiety &
depression inbreast cancer survivors.
o Dragon-boat racers often breast cancer survivors.

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o Prostate cancer often treated with androgen deprivation therapy → loss of

muscle mass. Exercise provides means of maintaining muscle (resistance
training particularly important).
o Evidence supports role of regular exercise in prevention of recurrence of
breast cancer and colorectal cancer.

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Clinical Exercise Physiology (University of Newcastle (Australia))

Studocu is not sponsored or endorsed by any college or university

HUBS2503 CLINICAL EXERCISE PHYSIOLOGY NOTES

LECTURE 1: INTRODUCTION TO EXERCISE PHYSIOLOGY

Overweight & Obesity

The Inflammation theory of disease

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o Also called isometric.

LECTURE 2: PRE-EXERCISE SCREENING

Purpose of pre-exercise screening

Types of pre-exercise screening

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ESSA Screening tool

Signs & symptoms of cardiopulmonary disease

Other serious conditions

Stages 2 and 3 – Risk factor assessment

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 Blood pressure (risk if on antihypertensive meds, SBP 140 or DBP 90).

Functional movement screening

LECTURE 3: STRESS TESTING

What does a GXT involve?

What does the test measure?

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Arm ergometer protocols

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Effort/symptom rating scales

What is a normal GXT response?

Reasons for stopping a GXT

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Analysis of ECG traces

Whats new in stress testing?

LECTURE 4: EXERCISE TRAINING

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The 4 principles of exercise training

Factors influencing training responses

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Aims of exercise training

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 Other training programs

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LECTURE 5: TYPES OF PHYSICAL FITNESS, FITNESS TESTING, AND PA GUIDELINES

Types of physical fitness

Health-related physical fitness

Sport specific physical fitness

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Physical fitness testing

Fitness testing in children

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 Stork stand for balance.

Fitness tests for the general population

Fitness tests for the sporting population

Fitness tests for the older or clinical populations

Safety of fitness testing