INITIAL FALL IN SKELETAL-MUSCLE FORCE DEVELOPMENT DURING ISCHEMIA IS RELATED TO OXYGEN AVAILABILITY

We examined the hypothesis that the initial decline (first 1-2 min) in force development that occurs in working muscle when blood flow is halted is caused by O-2 availability and not another factor related to blood flow. This was tested by reducing O-2 delivery (muscle blood flow X arterial O-2 content) to working muscle by either stopping blood flow [ischemia (I)] or maintaining blood flow with low arterial O-2 content [hypoxemia (H)]. If initial decline in force development were similar between these two methods of reducing O-2 delivery, it would suggest O-2 availability as the common pathway. Isolated dog gastrocnemius muscle was stimulated at similar to 60-70% of maximal O-2, uptake (1 isometric tetanic contraction every 2 s) until steady-state conditions of muscle blood flow and developed force were attained (similar to 3 min). Two conditions were then sequentially imposed on the working muscle: I, induced by shutting off pump controlling arterial perfusion of the muscle and clamping venous outflow, and H, induced by perfusing the muscle with deoxygenated blood (collected before testing while animal breathed N-2) at steady-state blood flow level. Rates of the fall in force production in 17 matched conditions of H and I (similar to 40 s for each condition) were compared in 6 muscles tested. The blood perfusing the muscle during H had arterial Po-2 = 8 +/- 1 (SE) Torr, arterial Pco(2) = 37 +/- 1 Torr, and arterial pH = 7.39 +/- 0.03. The rate of decline in developed force was not significantly different (P = 0.46) between the 17 matched conditions of H (0.66 +/- 0.10 g force.g mass(-1).s(-1)) and I (0.79 +/- 0.15 g force.g mass(-1).s(-1)). These findings suggest that the initial fall in developed force in working skeletal muscle that occurs with ischemia is related to O-2 availability.