The possible role of acetate in exercise hyperemia in dog skeletal muscle.

The possible role of acetate in the genesis of exercise hyperemia was studied in five series of dogs. Intraarterial infusion of an isomotic solution of sodium acetate at 0.76 ml/min in the dog forelimb decreased the resistance to flow through skeletal muscle by 48%, primarily by decreasing resistance to flow through small vessels. Skin lymph flow and lymph protein concentration were unaffected. The hindlimb of the conscious dog took up acetate at rest (A-V difference, + 58.3 +/- 19.6 nmoles/ml) and put out acetate during treadmill exercise (A-V difference, -105.6 +/- 20.12 nmoles/ml); femoral venous blood acetate concentration increased by 145 nmoles/ml (control 195 nmoles/ml). In the gracilis muscle of the anesthetized dog, simulated exercise at 0.5, 1.0 or 2.0 Hz increased acetate tissue content (72, 248 and 442 nmoles/g, respectively), output (18,899, and 1,830 nmoles/100 g/min, respectively) and venous concentration (82, 49 and 39 nmoles/ml, respectively) and changes in tissue acetate content correlated with changes in vascular resistance r = 0.75, P less than 0.001. Intraarterial infusion of an isosmotic solution of sodium acetate in the quiescent gracilis muscle perfused at constant flow produced a significant (6%) decrease in resistance when arterial blood acetate was increased by a calculated 96 nmoles/ml. These studies suggest that acetate might be included among those metabolites that contribute to exercise hyperemia.U