| Project/Area Number |
13680030
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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 |
体育学
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| Research Institution | Hiroshima University |
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Principal Investigator |
WADA Masanobu Hiroshima University, Faculty of Integrated Arts and Sciences, Associate Professor, 総合科学部, 助教授 (80220961)
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| Co-Investigator(Kenkyū-buntansha) |
HASEGAWA Hiroshi Hiroshima University, Faculty of Integrated Arts and Sciences, Research Associate, 総合科学部, 助手 (70314713)
YASUDA Toshihiro Fukushima University, Faculty of Education, Associate Professor, 教育学部, 助教授 (50323184)
MATSUNAGA Satoshi Osaka City University, Institute for Health and Sports Sciences, Assistant Professor, 体育学研究室, 講師 (70221588)
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| Project Period (FY) |
2001 – 2003
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| Project Status |
Completed (Fiscal Year 2003)
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| Budget Amount *help |
¥3,300,000 (Direct Cost: ¥3,300,000)
Fiscal Year 2003: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 2002: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 2001: ¥1,900,000 (Direct Cost: ¥1,900,000)
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| Keywords | sarcoplasmic reticulum / fatigue / antioxidant / reactive oxygen species / calcium pump / oxidation / カルシウム / 筋収縮 / 運動 / 酸化 / Ca^<2+>取り込み速度 / Ca^<2+>放出速度 |
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| Research Abstract |
The purpose of the first experiment was to examine a cause of exercise-induced decreases in Ca^<2+>-sequestering capacity by sarcoplasmic reticulum (SR) using the superficial portions of the gastrocnemius and vastus lateralis muscles of the rat after treadmill running to exhaustion. Exercise led to 16% and 34% decreases in SR Ca^<2+>-ATPase activity and Ca^<2+> uptake rate, respectively. The carbonyl group content in SR Ca^<2+>-ATPase protein was increased by 127%. In the second experiment, the hypothesis was tested that N-acetylcysteine (NAC) that is one of antioxidants may influence diaphragmic fatigue by modulating SR Ca^<2+> handling capacity. In the absence or presence of NAG, rat diaphragm was electrically stimulated with titanic trains (350 msec) delivered at 0.5 train/sec for various durations. At 60 sec after the onset of stimulation and beyond, force developed by NAC-treated muscle was significantly greater that that of non-treated muscle. In muscles where force was reduced to 50-80% of the initial level, treatment of NAG inhibited reductions in SR function. These results suggest that oxidation of SR Ca^<2+> -ATPase protein may account for decreases in Ca^<2+> -sequestering capacity by the SR and that antioxidant-induced inhibition of a decline in SR function may be responsible, at least partly, for a delay of the rate of fatigue development in the middle phase of muscular fatigue.
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