ADENOSINE INFUSION DOES NOT IMPROVE MAXIMAL O-2 UPTAKE IN ISOLATED WORKING DOG MUSCLE

We asked whether maximally working muscle could increase O-2 extractio n at fixed O-2 delivery [i.e., improve maximal O-2 uptake (VO2max)] wh en vascular resistance was decreased with adenosine (A) infusion. We p ostulated that a reduction in vascular resistance at the same blood fl ow (Q) might result in more uniform vascular perfusion and also possib ly increase red blood cell transit time, thereby potentially improving the ability of the tissue to extract O-2. Pump-perfused isolated dog gastrocnemius muscle (n = 6) was stimulated maximally at each of two l evels of Q: 110 +/- 3 and 54 +/- 4 (SE) ml.100 g(-1).min(-1) [normal c ontrol (C) and ischemia (I), respectively], both before and after givi ng 10(-2) M of A solution in each case. Arterial and venous blood samp les were taken to measure blood gases, and the Fick principle was used to calculate O-2 uptake. Resistance decreased significantly after A t reatment in both groups (1.2 +/- 0.1 vs. 0.9 +/- 0.1 and 1.3 +/- 0.1 v s. 1.1 +/- 0.1 mmHg.ml(-1).100 g.min for C vs. C + A and I vs. I + A, respectively; P < 0.01). O-2 delivery was lower with I but did not cha nge at either perfusion rate when A was infused. VO2max also decreased significantly with I but was no different when A was added (13.8 +/- 0.7 vs. 13.8 +/- 0.9 and 8.4 +/- 0.5 vs. 8.2 +/- 0.6 ml.100 g(-1).min( -1) for C vs. C + A and I vs. I + A, respectively). These results show that the decrease in resistance with A did not lead to changes in VO2 max. In addition, any changes in Q distribution with A infusion had li ttle effect on the ability of muscle to extract O-2 during O-2-limited conditions.