Exercise hyperemia in potassium-depleted dogs.

The experiments reported here are designed to evaluate the role of potassium (K+) in exercise hyperemia. Desoxycorticosterone acetate was implanted subcutaneously in six dogs, which were then placed on K+-deficient diets. Experiments were performed 3 or 4 wk later. Exercise vasodilation was much reduced in K+-depleted animals. However, when muscle stimulation caused very little vasodilation (i.e., in the most depleted animals) the muscle also produced little tension and extracted very little O2. O2 extraction was not limited by O2 availability. When the change in vascular resistance was plotted against O2 extraction, the data from K+-depleted dogs fell on a line constructed for control dogs. We conclude that the reduced exercise hyperemia of K+-depleted dogs is a result of reduced muscle O2 consumption rather than decreased K+ release. However, there was reduced vasodilation in response to brief tetanus and a loss of the triphasic initiation of exercise vasodilation with twitch work. This suggests that absence of K+ release does directly affect initiation of exercise vasodilation.

A model of potassium ion efflux during exercise of skeletal muscle.

Potassium (K+) is a vasoactive agent and is released from muscle cells during exercise. A simple diffusion model does not predict the time course of K+ efflux during exercise, which decreases as the exercise progresses. We constructed a mathematical model using the concept of an active Na+-K+ ion pump to account for the decreased efflux during and uptake after exercise. Passive fluxes are calculated by the Nernst equation. Active fluxes are constrained to balance these passive fluxes at rest. The pump activity increases as either extracellular K+ or intracellular Na+ concentration increases. To test the model, the venous K+ efflux profile was simulated for direct stimulation (4/s) of the anterior calf mus cles of dogs. The model simulated the K+ release during the stimulation period and [K+] undershoot after the stimulation. The active Na+-K+ ATPase transport concept used in the model was further tested by observing K+ efflux after administration of ouabain. Ouabain infusion decreased K+ uptake during exercise slightly and abolished [K+] undershoot after the stimulation. These experimental data were matched by the model only if a discontinuous effect of ouabain is assumed. This suggests that ouabain may more completely block the sensitivity of the pump to intracellular [Na+] than to extracellular [K+].