Effects of ischemia on VO2, tension, and vascular resistance in contracting canine skeletal muscle

This study examined the changes in O2 consumption (VO2), vascular resistance, and tension development during skeletal muscle contractions at reduced flow. We tested the hypothesis that when VO2 is limited by O2 supply, the skeletal muscle vasculature is not maximally dilated because of the fall in contractile force that accompanies the decrease in O2 supply. During 30 min of ischemic contractions, tension fell by 45 +/- 4% and VO2 fell 54 +/- 1% from preischemic levels. The O2 cost per unit tension did not change compared with nonischemic muscles. After the initial flow reduction, flow fell an additional 16 +/- 3% over 30 min. Adenosine infusion after 30 min of ischemic contractions increased flow by 42 +/- 3% but increased VO2 by only 9.8 +/- 2.3% and had no effect on tension development. When perfusion pressure was returned to normal after 30 min of ischemic contractions, twitch tension did not begin to recover within 20 min but tetanic tension showed a small improvement. VO2, although increased, remained well below the preischemic level. These results suggest that because of the reduced tension during ischemic contractions, the O2 supply-to-consumption ratio is nearly normal, which could explain the presence of the vasodilator reserve. The defect in tension development is long lived, producing a "stunned" muscle in which excess O2 supply does not restore function or VO2 to normal.