Rapid force recovery in contracting skeletal muscle after brief ischemia is dependent on O-2 availability

We tested the hypothesis that contracting skeletal muscle can rapidly resto re force development during reperfusion after brief total ischemia and that this rapid recovery depends on O-2 availability and not an alternate facto r related to blood flow. Isolated canine gastrocnemius muscle (n = 5) was s timulated to contract tetanically (isometric contraction elicited by 8 V, 0 .2-ms duration, 200-ms trains, at 50-Hz stimulation) every 2 s until steady -state conditions of muscle blood flow (controlled by pump perfusion) and d eveloped force were attained (3 min). While maintaining the same stimulatio n pattern, muscle blood flow was then reduced to zero (complete ischemia) f or 2 min. Normal blood flow was then restored to the contracting muscle; ho wever, two distinct conditions of oxygenation (at the same blood flow) were sequentially imposed: deoxygenated blood (30 s), blood with normal arteria l O-2 content (30 s), a return to deoxygenated blood (30 s), and finally a return to normal arterial O-2 content (90 s). During the ischemic period, f orce development fell to 39 +/- 6 (SE)% of normal (from 460 +/- 40 to 170 /- 20 N/100 g). When muscle blood flow was restored to normal by perfusion with deoxygenated blood, developed force continued to decline to 140 +/- 20 N/100 g. Muscle force rapidly recovered to 310 +/- 30 N/100 g (P < 0.05) d uring the 30 s in which the contracting muscle was perfused with oxygenated blood and then fell again to 180 +/- 30 N/100 g when perfused with blood w ith low Po,. These findings demonstrate that contracting skeletal muscle ha s the capacity for rapid recovery of force development during reperfusion a fter a short period of complete ischemia and that this recovery depends on O-2 availability and not an alternate factor related to blood flow restorat ion.