EFFECTS OF REDUCED O-2 DELIVERY WITH ANEMIA, HYPOXIA, OR ISCHEMIA ON PEAK VO2 AND FORCE IN SKELETAL-MUSCLE

This investigation was designed to describe alterations in O2 uptake (VO2) and tension development in a contracting in situ gastrocnemious-plantaris muscle preparation during three conditions of reduced 0, delivery [arterial O2 concentration X blood flow (Q)]. The three conditions, hypoxemia (H), ischemia (I), and anemia (A), were matched for O2 delivery. A normoxic normal flow condition was also utilized for comparison. H was produced by respiring the animals with 9% 02 in N2; I was produced by lowering Q, and A was produced by hemodilution with 6% dextran. The stimulation pattern for the isometric tetanic contractions used was 1 train/s, and each train was 200 ms, 70 Hz, and 6 V. The muscle was maximally contracted during each of the experimental conditions, and the conditions were administered in random order. In each bout the contractions continued for 5 min with 30 min of rest between bouts. Samples of arterial and muscle venous blood were obtained during the last 30 s of each bout. VO2 during I (125 ml.kg-1.min-1) was less than during N (145 ml.kg-1.min-1; P < 0.05) and greater than during H or A (104 and 101 ml.kg-1.min-1, respectively; P < 0.05). Venous PO2 (PV(O2)) was significantly lower during H (17.1 Torr) compared with the other conditions; no differences existed between N, I, and A (26.8,26.0, and 28.1 Torr, respectively). Tension development was reduced by the reduction of O2 delivery during I, H, and A compared with N. Tension developed among the reduced O2 delivery groups was not significantly different. These results are consistent with the notion that factors other than the rate of O2 delivery to muscle are important determinants of VO2. The variation in Q and Pv(O2) among the various conditions of reduced O2 delivery also suggested that the mechanisms controlling muscle VO2 differ among the three conditions.