高強度運動における筋疲労の要因 : 無機リン酸, グリコーゲンおよび活性酸素種の影響 <総説>

体育學研究 Volume 51 Issue 4 Page 399-408 published_at 2006-07-10
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Title ( jpn )
高強度運動における筋疲労の要因 : 無機リン酸, グリコーゲンおよび活性酸素種の影響 <総説>
Title ( eng )
Possible factors contributing to muscle fatigue during intense exercise : effects of inorganic phosphate, glycogen and reactive oxygen species
Creator
Sakamoto Makoto
Sugiyama Minako
Matsunaga Satoshi
Source Title
体育學研究
Volume 51
Issue 4
Start Page 399
End Page 408
Abstract
Skeletal muscles induced to contract repeatedly respond with a progressive loss in their ability to generate a target force or power. This decline in function, referred to as muscle fatigue, has a complex etiology that can involve various metabolic and ionic factors. Of these, intracellular acidosis due to lactic acid accumulation has been regarded as one of the important causes of muscle fatigue that occurs with intense exercise. Recent surveys, however, have demonstrated little direct effect of acidosis on muscle function at physiological temperatures, and in fact several putative mechanisms by which intracellular changes can attenuate contractile function have been proposed. The most likely mechanisms to explain muscle fatigue include elevated inorganic phosphate concentrations that result from phosphocreatine breakdown, compartmentalized depletion of endogenous muscle glycogen and/or modification by reactive oxygen species that are produced extensively in contracting muscle fibers. This brief review seeks to examine how these three alterations contribute to muscular fatigue processes.
Keywords
sarcoplasmic reticulum
Ca2+ release channel
oxidative stress
myofibril
excitation-contraction coupling
筋小胞体
Ca2+放出チャンネル
酸化ストレス
筋原線維
興奮収縮連関
Descriptions
Japan J. Phys. Educ. Hlth. Sport Sci. 51: 399-408, July, 2006
NDC
Sports and physical training [ 780 ]
Language
jpn
Resource Type journal article
Publisher
日本体育学会
Date of Issued 2006-07-10
Rights
Copyright (c) 2006 日本体育学会
この論文の著作権は(社)日本体育学会に帰属します
Publish Type Version of Record
Access Rights open access
Source Identifier
[ISSN] 0484-6710
[NCID] AN00409623