Contribution of potassium to exercise-induced vasodilation in humans.

It has been postulated that skeletal muscle release of potassium contributes to exercise-induced vasodilation of skeletal muscle arterioles. To determine whether potassium produces muscle arteriolar vasodilation in humans, we measured plethysmographic forearm blood flow and brachial venous potassium concentrations during brachial arterial infusion of potassium (0.6, 3, 6, 15, and 30 mueq.min-1.100 ml forearm volume-1) in nine normal subjects. Infusion of potassium decreased forearm vascular resistance, with an increase in brachial venous potassium of 1 meq/l decreasing forearm vascular tone by 25-30%. We then measured plasma potassium concentrations during forearm and upright bicycle exercise in 15 normal subjects. Forearm exercise at 0.6 W decreased forearm vascular resistance by 83%, whereas brachial venous potassium increased by only 0.5 +/- 0.2 meq/l (both P < 0.05). Maximal bicycle exercise increased systemic potassium concentrations by 1.2 +/- 0.2 meq/l. These findings indicate that potassium produces muscle arteriolar vasodilation in humans and therefore supports the hypothesis that potassium release from exercising muscle contributes to exercise-induced vasodilation. The relatively small change in venous potassium noted during forearm exercise despite marked forearm vasodilation suggests that local potassium release is only a small contributor to exercise-induced vasodilation. However, potassium release during maximal exercise may have significant vasodilatory effects on arterioles both in exercising and nonexercising tissues.