IS THE MUSCLE METABOREFLEX IMPORTANT IN CONTROL OF BLOOD-FLOW TO ISCHEMIC ACTIVE SKELETAL-MUSCLE IN DOGS

Ischemia of active skeletal muscle induces a reflex increase in sympathetic activity, heart rate, cardiac output, and arterial pressure, termed the muscle metaboreflex. Whether this presser response contributes importantly in the regulation of blood flow to the ischemic active skeletal muscle is not well understood. If the presser response is achieved without substantial vasoconstriction in the ischemic muscle, this increase in arterial pressure would act to improve muscle blood flow. Dogs performed treadmill exercise at mild (3.2 km/h, 0% grade) and moderate (6.4 km/h, 10% grade) workloads. During each workload, resistance to blood flow in the hindlimbs (R(h)) was increased via graded partial inflation of a vascular occluder implanted on the terminal aorta. The closed-loop gain of the muscle metaboreflex (G(cl)) was calculated, based on the steady-state changes in terminal aortic blood flow (TAQ). If no presser response occurred, then TAQ should decrease in proportion to the increase in total R(h) (the sum of resistance due to partial vascular occlusion and hindlimb vascular resistance); i.e., no reflex restoration of hindlimb blood flow would occur. However, with a reflex increase in systemic arterial pressure, TAQ could rise above the level predicted on the basis of the increase in R(h). We observed that with the initial increase in R(h) during mild exercise, G(cl) was not significantly different from zero (P > 0.05). However, with a more substantial reduction in TAQ (43.8 +/- 8.6%), a presser response occurred and G(cl) increased significantly to 0.45 +/- 0.09; i.e., 45% of the reduction in hindlimb blood flow was restored by the large increase in arterial blood pressure. With the largest reduction in TAQ (53.4 +/- 8.3%), mean arterial pressure (MAP) increased from 109 +/- 4.7 mmHg during free flow exercise to 167 +/- 6.8 mmHg, and G(cl) averaged 0.50 +/- 0.05. During moderate exercise no threshold was detected and, with the initial reductions in TAQ, G(cl) was significantly different from zero (0.45 +/- 0.06). During moderate exercise, the largest reduction in TAQ (26 +/- 3%) increased MAP from 115.9 +/- 3.7 to 168.1 +/- 10.6 mmHg, and G(cl) averaged 0.53 +/- 0.05. During both mild and moderate exercise, once the reflex was fully activated Gd remained essentially constant and there was no significant difference in G(cl) between workloads. The major conclusion is that activation of the muscle metaboreflex restores similar to 50% of the flow deficit induced by partial vascular occlusion.