Unloaded skeletal muscle O2 uptake decreases with decreased venous PO2 at high-frequency stimulation.

The aim of the present study was to clarify the effects of O2 diffusion limitation resulting from hypoxic interventions on O2 uptake (V.O2) in unloaded (that is, near-zero initial force) and loaded skeletal muscle in a high-frequency stimulation. We measured V.O2, muscle venous PO2 (PvO2) and initial force in gastrocnemius-plantaris muscle in situ of anesthetized dogs: (1) during hypoxic hypoxia at 1 Hz tetanic stimulation, and (2) during hypoxia induced by the perfusion with high O2-affinity erythrocytes (having a low value of PO2 at 50% saturation of hemoglobin (P50)) at 4 Hz twitch stimulation. Averaged unloaded V.O2 during normoxia was 10.2 ml.min-1.100 g-1 at averaged blood flow of 74 ml.min-1.100 g-1 (n = 6). Hypoxic hypoxia of a decreased O2 delivery (arterial O2 concentration x flow) significantly decreased both unloaded and loaded V.O2 with a decrease in PvO2 (p<0.05). The unloaded V.O2 was reduced to 8.5 ml.min-1.100 g-1. Low P50-hypoxia decreased V.O2 at high and low initial force conditions with a decrease in PvO2 (p<0.05) at the same O2 delivery. If these decreases in V.O2 correspond with a decrease in V.O2 at zero initial force (unloaded V.O2), the unloaded V.O2 value is calculated to be 7.57 ml.min-1.100 g-1 from V. O2-initial force data. Despite the different conditions of O2 delivery, the unloaded V.O2 decreased by both hypoxia showed similar values. Thus the decreased unloaded V.O2 does not seem to be derived from only the limited O2 delivery. Some other factors such as the limitation of O2 diffusion may contribute to the decreased V.O2.