学術雑誌論文 Intracellular oxygen tension limits muscle contraction-induced change in muscle oxygen consumption under hypoxic conditions during Hb-free perfusion

Takakura, Hisashi  ,  Ojino, Minoru  ,  Jue, Thomas  ,  Yamada, Tatsuya  ,  Furuichi, Yasuro  ,  Hashimoto, Takeshi  ,  Iwase, Satoshi  ,  Masuda, Kazumi

5 ( 2 )  , p.e13112 , 2017-01-01 , American Physiological Society / Wiley Open Access
ISSN:2051-817x
内容記述
Under acute hypoxic conditions, the muscle oxygen uptake (m (Formula presented.) O2) 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 presented.) O2 under hypoxic conditions at the peripheral tissue level. Therefore, this study set out to test the hypothesis that the restriction in m (Formula presented.) O2 is regulated by the net decrease in intracellular oxygen tension equilibrated with myoglobin oxygen saturation (∆PmbO2) 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 O2 gas: 95.0%O2, 71.3%O2, and 47.5%O2. 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 (SmbO2), and the PmbO2 was then calculated based on the SmbO2 and the O2 dissociation curve of the Mb. The SmbO2 and PmbO2 at rest decreased with the decrease in O2 supply, and the muscle contraction caused a further decrease in SmbO2 and PmbO2 under all O2 conditions. The net increase in m (Formula presented.) O2 from the muscle contraction (∆m (Formula presented.) O2) gradually decreased as the ∆PmbO2 decreased during muscle contraction. The results of this study suggest that ΔPmbO2 is a key determinant of the Δm (Formula presented.) O2. © 2017 The Authors. Physiological Reports published by Wiley Periodicals, Inc. on behalf of The Physiological Society and the American Physiological Society.
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