During exercise, skeletal muscle blood flow increases up to 15-fold. Which local metabolic factor most potently causes functional hyperemia (exercise hyperemia) in skeletal muscle?

• A Combination of increased CO2, H+, K+, adenosine, lactate, and decreased PO2 causing arteriolar dilation — no single factor dominates, but adenosine and K+ are the earliest rapid mediators ✓
• B Increased local PO2 causing direct O2-mediated arteriolar dilation
• C Sympathetic cholinergic vasodilator fibers to skeletal muscle arterioles are the primary mediator
• D Release of atrial natriuretic peptide from exercising muscle fibers causing vasodilation

Explanation

Functional (exercise) hyperemia in skeletal muscle is multifactorial: locally released metabolites from active muscle act synergistically to dilate arterioles. Key vasodilator metabolites include: adenosine (from ATP hydrolysis), interstitial K+ (released during action potentials — rapid onset), CO2 (from aerobic metabolism), H+ (lactic acid), decreased O2 tension, and possibly prostacyclin and NO from endothelium. No single metabolite is solely responsible; redundancy ensures robust hyperemia. Sympathetic cholinergic vasodilator fibers exist in some species (anticipatory vasodilation) but are NOT the primary mechanism in ongoing exercise hyperemia in humans. ANP is a cardiac peptide, not a muscle product.

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

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