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Cardiovacular Adaptations To Training
Cardiovacular Adaptations To Training
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CARDIOVASCULAR
ADAPTATIONS TO PHYSICAL
TRAINING
Annu. Rev. Physiol. 1983.45:169-189. Downloaded from arjournals.annualreviews.org
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C Gunnar Blomqvist
Bengt Saltin
Students
After After Olympic
Control bedrest training athletes
Maximaloxygenuptake, liters/rain 3.30 2.43 3.91 b5.38
Maximalvoluntary ventilation, liters/min 191 201 197 219
Transfer coefficient for 02, (ml/min)/(mmHg) 96 83 86 95
Annu. Rev. Physiol. 1983.45:169-189. Downloaded from arjournals.annualreviews.org
CARDIOVASCULAR
ADAPTATIONSTO TRAINING 171
172 BLOMQVIST
& SALTIN
MYOCARDIALADAPTATIONS
The increased stroke volumethat is a salient effect of training in normal
subjects can be achieved simply by increasing cardiac dimensions or by
improving the performance characteristics of the heart. Pumpperformance
maybe increased by (a) enhancingthe intrinsic contractile properties of the
myocardiumand the responses to inotropic stimulation and (b) extramyo-
eardial adaptations that have secondary effects on performance--e.g, by
increasing ventrieular filling or decreasing myocardialwork.
Comprehensiveanalysis of myocardial function includes simultaneous
consideration of force, velocity, and fiber length (64). The velocity axis can
often be disregarded without serious loss of information in the analysis of
the performanceof the intact heart. The ventricular pressure-volume rela-
tionship (34, 86, 106, 115) provides a useful frameworkfor analysis and
link between muscle mechanicsand ventricular function. It is also helpful
when considering peripheral or extracardiac factors. The pressure-volume
relation defines contractile state as the maximalpressure (or tension) that
can be developed at any given volume(or fiber length). Maximalventricular
pressure is normally a linear function of volume.Implicit in the concept is
that the amountof shortening or stroke volumethat can be achieved from
any given diastolic volumeor fiber length can be increased only by reducing
afterload or by enhancing contractile state. Similarly, an increase in the
amount of shortening at a given afterload requires either an increased
end-diastolic volumeor an increased contractile state. The linear relation-
ship betweenpeak systolic pressure and end-systolic volumeclosely approx-
imates the rdation between maximal tension and volume. End-systolic
volumeis independent of preload. This modelmakes it feasible to evaluate
intra- and intedndividual physiological differences in ventdeular contractile
performance even if the experimental conditions make it impossible to
control preload and afterload. However, the slope and intercept of the
systolic pressure-volumerelationship are affected both by the basal or in-
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Cardiac Dimensions
There is a large body of older, mainly Germanand Scandinavian data on
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176 BLOMQVIST
& SALTIN
Contractile Performance
Avariety of preparations have beenused to evaluate training effects on
myocardialfunction. Isolated papillary muscles and isolated perfused
hearts have been employedto analyze the effect on intrinsic myocardial
conttractile propertiesmi.e, the performanceof denervatedheart muscle
under rigidly controlled conditions. Nutter & Fuller (70) reviewedsix
studies of the effect of training on the mechanicalperformance of isolated
left ventricular papillary muscles.Passiveor diastolic myocardiallength-
tension relationships did not change.Isometricor isotonic contractile per-
formancewas increased in two series, decreased in two, and showedno
changein two.
Severalinvestigators haveexamined the effects of training on the perfor-
manceof the isolated perfusedheart. Scheuerandassociates (5, 7, 94, 95)
havemadea systematicstudy of the responseto different formsof training
--i.e. running and swimming in maleand femalerats. Theyconcluded(94)
that both activities produceskeletal .muscleadaptations (e.g. increased
cytochromeoxidaseactivity) in both maleand femalerats and an increased
heart-weight/body-weight ratio. Absoluteincreases in heart weightrelative
to weight-matched control rats occur only in femaleswimmers.Theyfound
evidence for improvedcontractile performance(measurementsnormalized
with respect to heart weightandobtainedat severallevels of left ventrieular
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filling pressure) in male and female swimmersand male runners but not in
female runners. These findings correlated closely with increased calcium
binding in isolated sarcoplasmie reticulum and increased aetomyosin
ATPase(95). However, Fuller & Nutter (29), who studied the effects
running in male rats and essentially replicated the methodsused by Scheuer
and collaborators, were for reasons that are not apparent unable to demon-
strate any training effects on contractile performance.Studies of the intact
in situ heart of anesthetized rats (19) and in the awakechronically instru-
menteddog (11) have also failed to demonstrate any significant changes
Annu. Rev. Physiol. 1983.45:169-189. Downloaded from arjournals.annualreviews.org
growth normally continues throughout adult life. Furthermore, the rat has
myocardialmembranecharacteristics that differ significantly from those of
other mammals(78). Other animal models also present problems in terms
of ~Lpplicability of findings to humans. The dog has a very high native
aerobic capacity, often well abovethe levels recorded in olympicathletes.
The heart-weight/body-weight ratio is also about twice as high as in hu-
marts--i.e. 8 g/kg body weight vs 4-5 in humans(96). The horse (101)
pig (93) mayprovide modelsin which baseline characteristics and responses
to training more closely resemble those in humans.
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EXTRAMYOCARDIAL ADAPTATIONS
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Peripheral VascularAdaptations
Annu. Rev. Physiol. 1983.45:169-189. Downloaded from arjournals.annualreviews.org
load during exercise after training. Changesin physical activity and maxi-
mal oxygen uptake are paralleled by small but statistically significant
changes in total blood volume (88), usually without major changes
hemoglobinconcentration or hematocrit. Well-trained athletes have higher
cardiac outputs and pulmonary arterial wedge pressures during maximal
supine exercise than sedentary normal subjects (6, 24).
Measurements during maximal exercise following volume overload in
sedentary and highly trained subjects provide further insights into the role
of ventricular filling as a potential primary limiting factor. Robinsonet al
(82) studied exercise performancein a group of essentially normalsubjects
(maximaloxygenuptake 3.2 liters/min) before and after autotransfusion
1 .O-1.2 liters wholeblood. This was sufficient to cause an increase in central
venous pressure of 7 mmHg but there was no significant change in stroke
volume or cardiac output during maximal work. Fortney et al (28) exam-
ined a group with slightly higher maximaloxygen uptake (3.5 liters/min)
and found a small but significant increase in maximalstroke volumeafter
blood volumeexpansion. Spriet et al (100) reported a large increase
maximalstroke volume(+31%) and cardiac output after reinfusion of 800
ml whole blood in highly trained athletes. Kanstrup & Ekblom(47) also
examineda group of subjects with high maximaloxygenuptake (4.4 liters/-
min), stroke volume, and cardiac output. Plasma volumeexpansion averag-
ing 700 ml produced a 20%increase in stroke volume and a 13%increase
in maximalcardiac output. The combineddata from these four studies seem
to indicate a difference between sedentary and well-trained subjects with
respect to the cardiovascular response to an acute blood volumeincrease.
Analysis of the pooled individual data demonstrate that there is a strong
linear relationship between maximal stroke volume at the control study
(SVo, ml) and the magnitudeof the increase (ASV,ml) after volumeloading
(ASV= 0.51 SVo- 48, 2 =0.49). It is tempting to speculate tha t end urance
training alters the apparent ventricular compliancecharacteristics by modi-
fying right/left ventricular-pericardial interactions. The result is an increase
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tracardiae pressures were not measuredin their study but other investiga-
tors have found progressively increasing left ventricular filling pressure with
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mass is activated and the systemic oxygen demandexceeds the supply (14,
15, 50, 91). Maximaloxygen uptake during one-leg work is normally about
75% of the absolute or two-leg maximum.Plasma norepinephrine levels
during maximal work are proportional to the active muscle mass (9).
Training of only one leg (20, 30, 91) or of both legs separatdy (50)
produces a large increase in one-leg maximaloxygenuptake (20%or more),
a muchsmaller increase in two-leg maximum (10%or less), and no change
during maximalexercise of the untrained leg. Changesin submaximalheart
rates are reciprocal to the changes in maximal oxygen uptake. Maximal
oxygenuptake during exercise with the trained leg also represents a larger
portion of the two-leg maximum, 85-90%after training. There is a signifi-
cant post-training increase in leg blood flow and conductanceduring maxi-
mal work with the trained leg but little or no change during two-leg
maximalexercise. Analogous results have been reported from experiments
in which either the lower or upper limbs have been trained and both pairs
tested separately. The most prominent training effects are always evident
whenexercise is performed with the trained limb(s) (13-16). The combined
data from these experiments support the concept that training causes an
important increase in the maximalvascular conductance of working skele-
tal muscle. This increase is limited to the trained limb or limbs--i.e, me-
diated primarily by local rather than systemic mechanisms.
Older studies based on 133Xeclearance rates have generated conflicting
data on the effects of training on maximalflow rates in skeletal muscle(14).
However, the 133Xemethod severely underestimates flow (1).
The extent to which the increase in the capacity to vasodilate can be
translated into an increased maximaloxygen uptake is clearly modified by
an opposing vasoconstrictor drive. The strength of this drive is determined
by the relation between systemic oxygen demandand transport capacity.
Thus changes in systemic oxygen transport capacity and the systemic im-
pact of the local vascular adaptations are interdependent. Local adaptations
with increased vascular conductanceare prerequisites for effective utiliza-
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blockade
abolishedthctrainingeffectina scales
ofyoung healthy
subjects.
Liangctal (58)concludedthatthemajorcardiovascular
trainingeffects
can
be,elicitedsimplyby fl-adrenergic
cardiacstimulationbychronicdobuta-
mineinfusionin dogs.However, themethodusedby Sablect al (85)
determine
theintensity of training
(equalization
ofheartrates, expressed
as percentof maximal heartratemeasured duringt-blockadeandplacebo
trc~Ltmcnt)
islikely tohaveproduceda lower
relativeintensity
inthecxpcd-
mcntalgroupthanin thccontrol group.Theresults reportedby Lianget
al(158)includeda largedecrease
incardiac output
during submaximal
levels
Annu. Rev. Physiol. 1983.45:169-189. Downloaded from arjournals.annualreviews.org
ofexercise.Thisfindingrepresents
a significant
deviation fromthehcmody-
namiceffectsusuallyobservedaftertraininginnormal subjects.
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CONCLUSIONS
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