Received August 29, 2007
Revised October 8, 2007
Accepted after revision December 18, 2007
Alterations in in vitro function and protein oxidation of rat sarcoplasmic reticulum Ca2+-ATPase during recovery from high-intensity exercise
Satoshi Matsunaga 1*,
Takaaki Mishima 2,
Takashi Yamada 3,
Shuichiro Inashima 4,
Masanobu Wada 5
1 Osaka City University
2 Hachinohe Junior College
3 Karolinska Institutet
4 Nagoya University
5 Hiroshima University
* To whom correspondence should be addressed. E-mail: matunaga{at}sports.osaka-cu.ac.jp.
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Abstract |
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The hypothesis tested in this study was that the extent to which sarcoplasmic reticulum (SR) Ca2+-ATPase is oxidized would correlate with a decline in its activity. For this purpose, changes in the SR Ca2+-sequestering ability and the contents of carbonyl and sulfhydryl groups during recovery after exercise were examined in the superficial portions of vastus lateralis muscles from the rats subjected to 5-min run at intensity corresponding to maximal oxygen uptake (50 m min-1, 10% grade). A single bout of exercise elicited a 22.4% reduction (P < 0.05) in SR Ca2+-ATPase activity. The decreased activity progressively reverted to normal levels during recovery after exercise, reaching normal levels after 60 min of recovery. This change was paralleled by depressed SR Ca2+-uptake rate and the proportional alteration between these two variables resulted in no change in the ratio of Ca2+-uptake rate to Ca2+-ATPase activity. The contents of SR Ca2+-ATPase protein and sulfhydryl groups in microsomes were unchanged after exercise and during recovery periods. On the other hand, the content of carbonyl groups contained in SR Ca2+-ATPase displayed a behavior opposite to that of SR Ca2+-ATPase activity. An approximately 80% augmentation (P < 0.05) in the carbonyl content occurred immediately after exercise. The elevated carbonyl content decreased toward normal levels during 60 min of recovery periods. These results are strongly suggestive that oxidation of SR Ca2+-ATPase would be responsible, at least in part, for a decay in the SR Ca2+-pumping function mediated through high-intensity exercise and implicate that oxidized proteins may be repaired during recovery after exercise.
Key Words:
Exercise, Oxidation, Sarcoplasmic reticulum
