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 ha lted is caused by O-2 availability and not another factor related to b lood flow. This was tested by reducing O-2 delivery (muscle blood flow X arterial O-2 content) to working muscle by either stopping blood fl ow [ischemia (I)] or maintaining blood flow with low arterial O-2 cont ent [hypoxemia (H)]. If initial decline in force development were simi lar between these two methods of reducing O-2 delivery, it would sugge st O-2 availability as the common pathway. Isolated dog gastrocnemius muscle was stimulated at similar to 60-70% of maximal O-2, uptake (1 i sometric tetanic contraction every 2 s) until steady-state conditions of muscle blood flow and developed force were attained (similar to 3 m in). Two conditions were then sequentially imposed on the working musc le: I, induced by shutting off pump controlling arterial perfusion of the muscle and clamping venous outflow, and H, induced by perfusing th e muscle with deoxygenated blood (collected before testing while anima l 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 perf using the muscle during H had arterial Po-2 = 8 +/- 1 (SE) Torr, arter ial Pco(2) = 37 +/- 1 Torr, and arterial pH = 7.39 +/- 0.03. The rate of decline in developed force was not significantly different (P = 0.4 6) between the 17 matched conditions of H (0.66 +/- 0.10 g force.g mas s(-1).s(-1)) and I (0.79 +/- 0.15 g force.g mass(-1).s(-1)). These fin dings suggest that the initial fall in developed force in working skel etal muscle that occurs with ischemia is related to O-2 availability.