During maximal aerobic exercise, cardiac output can increase from 5 L/min at rest to 20–25 L/min in trained athletes. The primary mechanism for this rise is increased heart rate; however, stroke volume also increases from ~70 mL to ~120 mL. The most important reason stroke volume increases during vigorous exercise despite reduced diastolic filling time is:

• A Increased myocardial contractility (positive inotropic effect) driven by catecholamines acting via beta-1 adrenoceptors, increasing ejection fraction and reducing end-systolic volume
• B Increased venous return via muscle pump and venoconstriction that enhances preload (Frank-Starling mechanism), increasing end-diastolic volume and stroke volume
• C Both increased contractility AND increased preload synergistically increase stroke volume; however, the dominant contribution shifts with exercise intensity — at moderate intensity preload dominates; at high intensity, contractility dominates ✓
• D Reduced afterload due to peripheral vasodilation in exercising skeletal muscle reduces impedance to ejection, allowing greater stroke volume with the same contractility

Explanation

The increase in stroke volume during exercise results from both preload and contractility mechanisms acting together. Muscle pump, respiratory pump, and venoconstriction augment venous return, increasing EDV (Frank-Starling). Simultaneously, sympathetic catecholamines acting on beta-1 receptors (increased cAMP → PKA → phospholamban phosphorylation → faster SR Ca²⁺ reuptake → enhanced Ca²⁺ transient) increase contractility (and lusitropy), reducing ESV. Both effects augment stroke volume. Peripheral vasodilation reduces afterload, further facilitating ejection. Research shows that preload augmentation is relatively more important at low-moderate intensities (supine exercise) while contractility gain is critical at high intensities and upright exercise.

Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.

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