ジチオトレイトールが高強度運動後の骨格筋筋小胞体のCa^<2+>-ATPase活性に及ぼす影響

体力科学 : Japanese Journal of Physical Fitness and Sports Medicine Volume 50 Issue 3 Page 325-331 published_at 2001-06-01
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Title ( jpn )
ジチオトレイトールが高強度運動後の骨格筋筋小胞体のCa^<2+>-ATPase活性に及ぼす影響
Title ( eng )
EFFECT OF DITHIOTHREITOL ON Ca^<2+>-ATPase ACTIVITY OF SARCOPLASMIC RETICULUM IN RAT SKELETAL MUSCLE AFTER HIGH-INTENSITY EXERCISE
Creator
Tsuchimochi Hirotsugu
Inashima Shuichiro
Source Title
体力科学 : Japanese Journal of Physical Fitness and Sports Medicine
Volume 50
Issue 3
Start Page 325
End Page 331
Abstract
Although the precise mechanisms underlying the dysfunction of sarcoplasmic reticulum(SR) that occurs during skeletal muscle fatigue remain obscure, it has been hypothesized that it may be attributable to oxidation of critical sulfhydryl groups residing in SR Ca^<2+>-ATPase protein by endogenously produced reactive oxygen species. In order to test this hypothesis, SR Ca^<2+>-ATPase activities in the absence or presence of the disulfide reducing agent, dithiothreitol(DTT), were examined in muscle homogenates of the soleus muscles(SOL) and the superficial portions of the vastus lateralis muscles(VS) from the rat subjected to exhaustive running at 50 m/min on a 10% grade. Immediately after exercise, the catalytic activity of SR Ca^<2+>-ATPase was significantly depressed in VS, but not in SOL. The loss of SR Ca^<2+>-ATPase activity observed in VS was fully recovered after treatment with DTT(1 mM). These recovery effects of a potent disulfide reducing agent suggest that important proteins of SR Ca^<2+>-ATPase may be oxidized during high-intensity exercise and that the onset of muscular fatigue may be delayed by the improved function of the cellular antioxidant
Keywords
sarcoplasmic reticulum
muscular fatigue
oxidation
sulfhydryl
reducing agent
NDC
Medical sciences [ 490 ]
Language
jpn
Resource Type journal article
Publisher
日本体力医学会
Date of Issued 2001-06-01
Rights
日本体力医学会
本文データは学協会の許諾に基づきCiNiiから複製したものである
Publish Type Version of Record
Access Rights open access
Source Identifier
[ISSN] 0039-906X
[NCID] AN00137986
[NAID] 110001918779