EFFECT OF HIGH-INTENSITY TRAINING AND ACUTE EXERCISE ON Ca^<2+>-SEQUESTERING FUNCTION OF SARCOPLASMIC RETICULUM : ROLE OF OXIDATIVE MODIFICATION

To investigate the influences of high-intensity training and/or a single bout of exercise on in vitro Ca^<2+>-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, 50m/min at 10% incline). Following training, both trained and untrained rats were run at a 10% incline, 50 m/min for 2.5min or to exhaustion. SR Ca^<2+>-ATPase activity, SR Ca^<2+>-uptake rate and carbonyl group contents comprised in SR Ca^<2+>-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 Ca^<2+>-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 Ca^<2+>-ATPase activity and SR Ca^<2+>-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 Ca^<2+>-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 Ca^<2+>-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 Ca^<2+>-ATPase