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Takakura, Hisashi ; Masuda, Kazumi ; Hashimoto, Takeshi ; Iwase, Satoshi ; Jue, Thomas
概要:
金沢大学人間社会研究域人間科学系<br />Although the O2 gradient regulates O2 flux from the capillary into the myocyte to meet the energy
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demands of contracting muscle, intracellular O2 dynamics during muscle contraction remain unclear. Our hindlimb perfusion model allows the determination of intracellular myoglobin (Mb) saturation () and intracellular oxygen tension of myoglobin () in contracting muscle using near infrared spectroscopy (NIRS). The hindlimb of male Wistar rats was perfused from the abdominal aorta with a well-oxygenated haemoglobin-free Krebs-Henseleit buffer. The deoxygenated Mb (Δ[deoxy-Mb]) signal was monitored by NIRS. Based on the value of Δ[deoxy-Mb], and were calculated, and the time course was evaluated by an exponential function model. Both and started to decrease immediately after the onset of contraction. The steady-state values of and progressively decreased with relative work intensity or muscle oxygen consumption. At the maximal twitch rate, and were 49% and 2.4 mmHg, respectively. Moreover, the rate of release of O2 from Mb at the onset of contraction increased with muscle oxygen consumption. These results suggest that at the onset of muscle contraction, Mb supplies O2 during the steep decline in, which expands the O2 gradient to increase the O2 flux to meet the increased energy demands. © 2010 The Physiological Society.
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| 2.
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Furuichi, Yasuro ; Sugiura, Tomoko ; Kato, Yukio ; Takakura, Hisashi ; Hanai, Yoshiteru ; Hashimoto, Takeshi ; Masuda, Kazumi
概要:
Since carnitine plays an important role in fat oxidation, influx of carnitine could be crucial for muscle metabolism. OC
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TN2 (SLC22A5), a sodium-dependent solute carrier, is assumed to transport carnitine into skeletal muscle cells. Acute regulation of OCTN2 activity in rat hindlimb muscles was investigated in response to electrically induced contractile activity. The tissue uptake clearance (CL uptake) of l-[ 3H]carnitine during muscle contraction was examined in vivo using integration plot analysis. The CL uptake of [ 14C]iodoantipyrine (IAP) was also determined as an index of tissue blood flow. To test the hypothesis that increased carnitine uptake involves the translocation of OCTN2, contraction-induced alteration in the subcellular localization of OCTN2 was examined. The CL uptake of l-[ 3H]carnitine in the contracting muscles increased 1.4-1.7-fold as compared to that in the contralateral resting muscles (p<0.05). The CL uptake of [ 14C]IAP was much higher than that of l-[ 3H]carnitine, but no association between the increase in carnitine uptake and blood flow was obtained. Co-immunostaining of OCTN2 and dystrophin (a muscle plasma membrane marker) showed an increase in OCTN2 signal in the plasma membrane after muscle contraction. Western blotting showed that the level of sarcolemmal OCTN2 was greater in contracting muscles than in resting muscles (p<0.05). The present study showed that muscle contraction facilitated carnitine uptake in skeletal muscles, possibly via the contraction-induced translocation of its specific transporter OCTN2 to the plasma membrane. © 2012 Elsevier Inc
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| 3.
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Takakura, Hisashi ; Ojino, Minoru ; Jue, Thomas ; Yamada, Tatsuya ; Furuichi, Yasuro ; Hashimoto, Takeshi ; Iwase, Satoshi ; Masuda, Kazumi
概要:
Under acute hypoxic conditions, the muscle oxygen uptake (m (Formula presented.) O2) during exercise is reduced by the r
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estriction 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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Takakura, Hisashi ; Furuichi, Yasuro ; Yamada, Tatsuya ; Jue, Thomas ; Ojino, Minoru ; Hashimoto, Takeshi ; Iwase, Satoshi ; Hojo, Tatsuya ; Izawa, Tetsuya ; Masuda, Kazumi
概要:
At onset of muscle contraction, myoglobin (Mb) immediately releases its bound O2 to the mitochondria. Accordingly, intra
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cellular O2 tension (PmbO2) markedly declines in order to increase muscle O2 uptake (mVO2). However, whether the change in PmbO2 during muscle contraction modulates mVO2 and whether the O2 release rate from Mb increases in endurance-trained muscles remain unclear. The purpose of this study was, therefore, to determine the effect of endurance training on O2 saturation of Mb (SmbO2) and PmbO2 kinetics during muscle contraction. Male Wistar rats were subjected to a 4-week swimming training (Tr group; 6 days per week, 30 min x 4 sets per day) with a weight load of 2% body mass. After the training period, deoxygenated Mb kinetics during muscle contraction were measured using near-infrared spectroscopy under hemoglobin-free medium perfusion. In the Tr group, the mVO2peak significantly increased by 32%. Although the PmbO2 during muscle contraction did not affect the increased mVO2 in endurance-trained muscle, the O2 release rate from Mb increased because of the increased Mb concentration and faster decremental rate in SmbO2 at the maximal twitch tension. These results suggest that the Mb dynamics during muscle contraction are contributing factors to faster VO2 kinetics in endurance-trained muscle. © 2015, Nature Publishing Group. All rights reserved.
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