| Project/Area Number |
06680122
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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 | Toho University school of Medicne |
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Principal Investigator |
MURO Masuo Toho University, School of Medicne, Associate Professor, 医学部, 助教授 (80112887)
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| Co-Investigator(Kenkyū-buntansha) |
OKA Kazuyuki Toho University, School of Medicne, Lecturer, 医学部, 講師 (10120247)
OSHIMA Hiroshi Toho University, School of Medicne, Lecture, 医学部, 講師 (30104152)
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| Project Period (FY) |
1994 – 1996
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| Project Status |
Completed (Fiscal Year 1996)
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| Budget Amount *help |
¥2,200,000 (Direct Cost: ¥2,200,000)
Fiscal Year 1996: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1995: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 1994: ¥1,100,000 (Direct Cost: ¥1,100,000)
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| Keywords | damage / muscle lesion / repair period / DNA / motor unit / fatigue / eccentric contraction / computer simulation / 疲労 / 筋線維破壊 / アポトーシス / 筋繊維破壊 |
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| Research Abstract |
This study was carried out to determine the process of segmental lesion and repair in skeletal muscle fibers by using artificial injury model of mammalian limb muscles. Segmental necrosis was caused progressing after injury with insertion of a fine needle in muscle. Demarcating membrane isolate the survival cytoplasm from the damaged cytoplasm, and phagocytosis is observed in the damaged cytoplasm. In this model, the fragmentation of nuclear DNA was verified by the TUNEL (Terminal deoxynucleotidyl transferase (TdT) -mediated dUTP-biotin Nick-End labeling) method. Nucrea DNA in the damaged cytoplasm was fragmented before the onset of phagocytosis. The nuclear DNA in the areas distant from the injured region was intact. On the other hand, rat's exercise-induced muscle damage was caused much the same muscle lesions of the artificial injury model. These lesions were noted localization in a muscle, and focal disruptions and localized in the A-band dissolution of the A-band or segmental necr
… More
osis (clotting of muscle fibers). The complete repair period of muscle lesion was necessary for more than 20 days in rats.
The triceps suare eccentric contractions in human were performed by selective recruitment of fast-twitch MUs, accompanied by derecruitment of slow-twitch MUs. However, eccentric contractions were caused strongly fatigue by selective activation of fast-twitch MUs. During dosal flexions, the strongest fatiguing of triceps suare came about randomly vibratory eccentric contractions. Consequently, the prolonged eccentric contractions produced increases in CK and G6PDH and the development of muscle soreness that all common indicators of muscle damage. It suggest that blood CK and G6PDH were increased to damage the development of muscle fatigue by selective activation of fast-twitch MUs during prolonged eccentric contractions. Furthermore, the effects of the three basic types of motoneuron pool were invesigated by the use of computer simulations. The properties of the simulated MUs and their synaptic inputs were based as closely as possible on the experimental data from human and other primates. It is indicated that regulation of target force performe grossly by central command of motor cortex but make a mior adjustment by motoneuron pool of spinal cord. It indicated that in the muscle fatigue, regulation of target force cause mistake of maching in central command to activation of MUs and from peripheral afferents. These results suggest that fast-twitch fibers were damaged selectively by strong fatigue during eccentric comtractions. Less
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