During maximal aerobic exercise, cardiac output can increase 4–5-fold. The mechanism accounting for the majority of the increase in cardiac output during exercise is:

• A Increased heart rate (chronotropy) due to sympathetic stimulation and vagal withdrawal accounts for most of the increase, with stroke volume contribution primarily from reduced end-systolic volume (inotropy) rather than increased end-diastolic volume ✓
• B Frank-Starling mechanism, with increased venous return stretching the ventricle to generate greater stroke volume
• C Reduced afterload from peripheral vasodilation is the dominant mechanism, with heart rate unchanged
• D Parasympathetic activation of SA node accelerates firing via acetylcholine-mediated positive chronotropy

Explanation

During dynamic exercise, cardiac output rises primarily due to a 3-fold increase in heart rate (sympathetically mediated chronotropy + vagal withdrawal). Stroke volume increases modestly (~25–30%), predominantly from enhanced ventricular contractility (sympathetic inotropy via β1 receptors) which reduces end-systolic volume (ESV). End-diastolic volume (EDV) does not markedly increase (Frank-Starling plays a secondary role) because the shortening diastolic filling time at high HRs tends to limit EDV. In trained athletes, larger stroke volume improvements via cardiac hypertrophy (larger chamber volume) allow higher cardiac outputs at lower heart rates.

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

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