Ca(2+)-ATPase and Ca(2+)-pumping activities by the sarcoplasmic reticulum (SR) and the amounts of sulphydryl and carbonyl groups contained in the SR protein were examined in the superficial portion of the gastrocnemius and vastus lateralis muscles of the rat after high-intensity treadmill runs to exhaustion (average time to exhaustion: 363 s). Exercise at the estimated maximal O(2) uptake rate led to 16% and 34% reductions in SR Ca(2+)-ATPase activity ( P<0.01) and Ca(2+) uptake rate ( P<0.01), respectively. The carbonyl group content in SR Ca(2+)-ATPase, assessed by immunoblotting analysis, was increased by 127% after exercise ( P<0.05), while the sulphydryl group content in the purified SR fraction was unchanged. Consistent with the unchanged sulphydryl group content, treatment of homogenates with dithiothreitol, the disulphide reducing reagent, failed to restore the decreased catalytic activity of SR Ca(2+)-ATPase in exercised muscles. These findings show clearly that high-intensity, exhaustive exercise causes oxidation of SR Ca(2+)-ATPase protein and suggest that oxidation of amino acids, other than cysteine, in the SR Ca(2+)-ATPase may be responsible, at least in part, for exercise-induced inactivation of this enzyme.
The predictability of anaerobic threshold (AT) from maximal aerobic power, distance running performance, chronological age, and total running distance achieved on the treadmill (TRD) was investigated in a sample of 53 male distance runners, 17-23 years of age. The dependent variable was oxygen uptake (Vo2) at which AT was detected (i.e. Vo2 @ AT). A regression analysis of the data indicated Vo2 @ AT could be predicted from the following four measurements with a multiple R = 0.831 and a standard error of the estimate of 2.66 ml . min-1 . kg-1: Vo2max (67.9 +/- 5.7 ml . min-1 . kg-1), 1,500-m running performance (254.5 +/- 14.2 s), TRD (6.82 +/- 1.13 km), and age (19.4 +/- 2.2 years). When independent variables were limited to Vo2max (X1) and 1,500-m running performance (X2) for simpler assessment, a multiple R = 0.806 and a standard error of the estimate of 2.76 ml . min-1 . kg-1 were computed. A useful prediction equation with this predictive accuracy was considered to be Vo2 @ AT = 0.386X1 - 0.128X2 + 57.11. To determine if the prediction equation developed for the 53 male distance runners could be generalized to other samples, cross-validation of the equation was tested, using 21 different distance runners, 17-22 years of age. A high correlation (R = 0.927) was obtained between Vo2 AT predicted from the above equation and directly measured Vo2 @ AT. It is concluded that the generalized equation may be applicable to young distance runners for indirect assessment of Vo2 @ AT.
The present study examined the effects of acute high-intensity exercise on Ca(2+) uptake and release rates and Ca(2+)-adenosine triphosphatase (ATPase) activity of the sarcoplasmic reticulum (SR) from the costal diaphragm. The rats were run on a treadmill at an estimated requirement of 100% of maximal O2 consumption until fatigued (average time to exhaustion: 4.79 min). Muscle lactate and inorganic phosphate after exercise were increased by 65% (P < 0.05) and 35% (P < 0.05), respectively. With exercise, Ca(2+) uptake and release, which were detected in homogenates using the Ca(2+) fluorescent dye indo-1, were decreased by 24% (P < 0.05) and 22% (P < 0.05), respectively. The reduction in Ca(2+) uptake was paralleled by decreased activity of SR Ca(2+)-ATPase in both the absence and presence of Ca(2+) ionophore. These findings demonstrate that, in the diaphragm as well as in the locomotor muscles that have been explored in previous studies, the attenuations of the SR function is brought about by acute high-intensity exercise. These changes in the SR of the diaphragm may contribute, at least in part, to deteriorations in exercise tolerance and work productivity resulting from repetitive physical activities.
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