Intracellular oxygen tension limits muscle contraction‐induced change in muscle oxygen consumption under hypoxic conditions during Hb‐free perfusion

Under acute hypoxic conditions, the muscle oxygen uptake (m [Formula: see text] O(2)) during exercise is reduced by the restriction in oxygen‐supplied volume to the mitochondria within the peripheral tissue. This suggests the existence of a factor restricting the m [Formula: see text] O(2) under hypoxic conditions at the peripheral tissue level. Therefore, this study set out to test the hypothesis that the restriction in m [Formula: see text] O(2) is regulated by the net decrease in intracellular oxygen tension equilibrated with myoglobin oxygen saturation (∆P(mb)O(2)) during muscle contraction under hypoxic conditions. The hindlimb of male Wistar rats (8 weeks old, n = 5) was perfused with hemoglobin‐free Krebs–Henseleit buffer equilibrated with three different fractions of O(2) gas: 95.0%O(2), 71.3%O(2), and 47.5%O(2). The deoxygenated myoglobin (Mb) kinetics during muscle contraction were measured under each oxygen condition with a near‐infrared spectroscopy. The ∆[deoxy‐Mb] kinetics were converted to oxygen saturation of myoglobin (S(mb)O(2)), and the P(mb)O(2) was then calculated based on the S(mb)O(2) and the O(2) dissociation curve of the Mb. The S(mb)O(2) and P(mb)O(2) at rest decreased with the decrease in O(2) supply, and the muscle contraction caused a further decrease in S(mb)O(2) and P(mb)O(2) under all O(2) conditions. The net increase in m [Formula: see text] O(2) from the muscle contraction (∆m [Formula: see text] O(2)) gradually decreased as the ∆P(mb)O(2) decreased during muscle contraction. The results of this study suggest that ΔP(mb)O(2) is a key determinant of the Δm [Formula: see text] O(2).