Exercise Physiology

Immediate Physiological Changes during Exercise

• Sympathetic Nervous System Activation: Initially, exercise induces a sympathetic nervous
response and a decrease in vagal tone, leading to an increase in heart rate (HR) and stroke
volume (SV), which collectively elevate cardiac output (CO), from resting values of
approximately 5 L/min to 15-20 L/min .

• Hemodynamic Adjustments: In the early phases of exercise, CO is maintained through

increases in both SV and HR. As exercise continues, SV plateaus, and HR continues to rise
to sustain CO.

• Vasoregulation: There is a vasoconstriction in arterioles in non-active tissues and

vasodilation in active muscles, directing blood flow to where it is most needed. This is
facilitated by the local release of metabolites like adenosine, potassium ions, ATP, CO2, and
lactate, causing a rise in systolic blood pressure (due to ↑CO), but a moderated increase
in mean arterial pressure due to reduced systemic vascular resistance (SVR), which slightly
decrease DBP.
Long-term Physiological Changes in Atheletes -
Adaptation
• Athletes typically have a higher resting stroke volume than sedentary
individuals, due to either increased muscle mass in strength athletes or
greater end-diastolic volume in endurance athletes. Their maximal heart
rate is similar to non-athletes, so their elevated cardiac output mainly
arises from this higher stroke volume. Additionally, athletes have lower
systemic vascular resistance, a result of increased capillary density that
enhances blood flow and reduces afterload, thereby boosting cardiac
output further.
 Endurance Athletes
• Highly trained endurance athletes, such as marathon runners,
exhibit large increase in cardiac output.
• Maximum heart rate does not significantly increase in highly
trained athletes; therefore, the increased maximum cardiac
output is primarily due to increased stroke volume (cardiac
output = stroke volume x heart rate).
• To meet the metabolic demands of frequent and intense
endurance training (eg, long-distance swimming, marathon
running) the body gradually increases both red blood cell
mass and plasma volume to increase oxygen carrying
capacity. In addition, skeletal muscles develop increased
arteriolar and capillary density, which improves oxygen uptake
and also causes overall reduced systemic vascular resistance
(SVR).
• These changes contribute to increased venous return (ie,
preload), which places increased volume load on the left
ventricle. In response, the left ventricle undergoes eccentric
hypertrophy to increase left ventricular cavity size and
improve diastolic filling capacity. This increase in EDV is the
primary driver of the increase in SV in endurance training.
• Because end-diastolic volume and stroke volume are both
proportionally increased, left ventricular ejection fraction is
mostly unchanged.
Strength Athlethes
• Highly trained strength athletes, such as powerlifters or
sprinters, may not exhibit as large an increase in cardiac
output as endurance athletes.
• The cardiovascular adaptations of strength athletes are
characterized more by changes in muscular strength. For
instance, there might be only a modest increase in red blood
cell mass and plasma volume.
• Strength training can lead to specific muscular adaptations
such as an increase in the size and number of mitochondria in
muscle cells, but unlike endurance training, it does not
significantly increase arteriolar and capillary density within the
muscle. While there is increased blood flow to the active
muscles, this does not typically result in a reduced systemic
vascular resistance (SVR) to the same extent as seen in
endurance training.
• In terms of ventricular changes, strength training
predominantly causes concentric hypertrophy of the left
ventricle, which increases the thickness of the ventricular
walls to enhance the heart's ability to generate force during the
powerful, acute phases of lifting. The left ventricular cavity size
does not increase significantly; hence, the stroke volume at
rest may not increase substantially (but it DOES), so the end-
diastolic volume may not be the primary driver of changes in
stroke volume for strength athletes.
Parameter Endurance Training Strength/Resistance Training
Cardiac Output (CO) Significantly increases Moderate increase

Maximal Heart Rate (HR) Does not significantly increase Does not significantly increase

Moderate increase due to increased contractility and muscle

Stroke Volume (SV) Increases due to increased end-diastolic volume
mass

Systolic increases; mean arterial pressure increases

Blood Pressure (BP) Milder increases
moderately

Systemic Vascular Resistance (SVR) Overall decrease due to increased capillary density Milder decrease

Ventricular Adaptation Eccentric hypertrophy, increased cavity size Concentric hypertrophy, increased wall thickness
Cavity enlargement to support increased CO Increased strength, minimal change in cavity size