The aim of the present study was to clarify the effects of O
2 diffusion limitation resulting from hypoxic interventions on O
2 uptake (VO
2) in unloaded (that is, near-zero initial force) and loaded skeletal muscle in a high-frequency stimulation. We measured VO
2, muscle venous PO
2 (PV
O2) and initial force in gastrocnemiusplantaris 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 O
2-affinity erythrocytes (having a low value of PO
2 at 50% saturation of hemoglobin (P
50)) at 4 Hz twitch stimulation. Averaged unloaded VO
2 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 O
2 delivery (arterial O
2 concentration × flow) significantly decreased both unloaded and loaded VO
2 with a decrease in PV
O2 (p<0.05). The unloaded VO
2 was reduced to 8.5 ml·min
-1·100 g
-1. Low P
50-hypoxia decreased VO
2 at high and low initial force conditions with a decrease in PV
O2 (p<0.05) at the same O
2 delivery. If these decreases in VO
2 correspond with a decrease in VO
2 correspond with a decrease in VO
2 at zero initial force (unloaded VO
2), the unloaded VO
2 value is calculated to be 7.57 ml·min
-1·100 g
-1 from VO
2-initial force data. Despite the different conditions of O
2 delivery, the unloaded VO
2 decreased by both hypoxia showed similar values. Thus the decreased unloaded VO
2 does not seem to be derived from only the limited O
2 delivery. Some other factors such as the limitation of O
2 diffusion may contribute to the decreased VO
2.
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