EFFECT OF HIGH-INTENSITY TRAINING AND ACUTE EXERCISE ON Ca2+-SEQUESTERING FUNCTION OF SARCOPLASMIC RETICULUM : ROLE OF OXIDATIVE MODIFICATION
- VernacularTitle:高強度トレーニングおよび一過性の運動が筋小胞体の Ca2+取り込み機能に及ぼす影響 —酸化的修飾との関連—
- Author:
SATOSHI MATSUNAGA
;
TAKAAKI MISHIMA
;
TAKASHI YAMADA
;
MASANOBU WADA
- Publication Type:Journal Article
- Keywords:
muscle fatigue;
reactive oxygen species;
Ca2+-uptake;
adaptation
- From:Japanese Journal of Physical Fitness and Sports Medicine
2008;57(3):327-338
- CountryJapan
- Language:Japanese
-
Abstract:
To investigate the influences of high-intensity training and/or a single bout of exercise on in vitro Ca2+-sequestering function of the sarcoplasmic reticulum (SR), the rats were subjected to 8 weeks of an interval running program (final training : 2.5-min running×4 sets per day, 50 m/min at 10% incline). Following training, both trained and untrained rats were run at a 10% incline, 50 m/min for 2.5 min or to exhaustion. SR Ca2+-ATPase activity, SR Ca2+-uptake rate and carbonyl group contents comprised in SR Ca2+-ATPase activity were examined in the superficial portions of the gastrocnemius and vastus lateralis muscles. For rested muscles, a 12.7% elevation in the SR Ca2+-uptake rate was induced by training. Training led to improved running performance (avg time to exhaustion : untrained-191.1 vs trained-270.9 sec ; P<0.01). Regardless of training status, a single bout of exercise caused progressive reductions in SR Ca2+-ATPase activity and SR Ca2+-uptake rate. Increases in carbonyl content only occurred after exhaustive exercise (P<0.05). At both point of 2.5-min and exhaustion, no differences existed in SR Ca2+-sequestering capacity and carbonyl content between untrained and trained muscles. These findings confirm the previous findings that oxidative modifications may account, at least partly, for exercise-induced deterioration in SR Ca2+-sequestering function ; and raise the possibility that in the final phase of acute exercise, high-intensity training could delay the progression of protein oxidation of SR Ca2+-ATPase.
