| Project/Area Number |
16500419
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Sports science
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| Research Institution | Osaka City University |
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Principal Investigator |
MATSUNAGA Satoshi Osaka City University, Research Center for Urban Health and Sports, Lecturer, 都市健康・スポーツ研究センター, 講師 (70221588)
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| Co-Investigator(Kenkyū-buntansha) |
WATANABE Hitoshi Osaka City University, Research Center for urban Health and sports, Professor, 都市健康・スポーツ研究センター, 教授 (50167160)
WADA Masanobu Hiroshima University, Graduate School of Integrated Arts and Sciences, Professor, 大学院・総合科学研究科, 教授 (80220961)
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| Project Period (FY) |
2004 – 2006
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| Project Status |
Completed (Fiscal Year 2006)
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| Budget Amount *help |
¥3,800,000 (Direct Cost: ¥3,800,000)
Fiscal Year 2006: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 2005: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 2004: ¥2,800,000 (Direct Cost: ¥2,800,000)
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| Keywords | acute exercise / high-intensity training / sarcoplasmic reticulum / protein oxidation / Ca^<2+>-ATPase / タンパク酸化 |
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| Research Abstract |
The cytosolic free Ca^<2+> concentration ([Ca^<2+>]_f) plays a central role in muscle contraction and relaxation. In skeletal muscle, the regulation of [Ca^<2+>]f is accomplished primarily by the kinetics of Ca^<2+> release and uptake by the sarcoplasmic reticulum (SR). Although the fatigue process involves multiple factors and mechanisms, recent evidence implies that functional impairment of the SR is a major contributor to muscle fatigue. We previously observed that a loss of SR function may be attributed, at least partly, to protein oxidation by reactive oxygen species, generation of which is elevated during muscle contraction. However, no published data presently exists that examines whether high-intensity training could protect against deteriorating SR Ca^<2+>2+-ATPase activity and oxidation of Ca^<2+>-ATPase with acute exercise. The purpose of this study was to investigate the influence of high-intensity training and/or a single bout exercise on SR function and oxidation of Ca^<2+>-ATPase.
Our in vitro measures on the superficial region of the vastus lateralis revealed that 8 weeks of running training elicited an increase in SR Ca^<2+>-uptake rate without concomitant changes in SR Ca^<2+>-ATPase activity and Ca^<2+>-release rate. These results implicate training-induced decreases in Ca^<2+> efflux from the SR lumen. Despite the extension of the run time to exhaustion, no differences existed in exhaustive exercise-induced reductions in SR Ca^<2+>-uptake ability and increases in carbonyls contained in Ca^<2+>-ATPase between trained and untrained muscles. These findings suggest that high-intensity training might protect Ca^<2+>-ATPase enzyme against oxidative modification that occurs during vigorous muscle contraction.
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