The relationship between body fat growth and physical fitness and motor ability development in school age children is not well understood. We determined the similarities and differences in body fat growth and physical fitness and motor ability development curves by applying cross correlation functions, and attempted to show the structure of growth and development between these attributes. The subjects were 647 boys aged 7 to 15 years. The measurements were height, weight, body mass index and body fat percentage as physical characters; and 20-m sprint, Pro Agility test, side steps, standing long jump, vertical jump, and rebound jump (RJ) index as physical fitness and motor ability. The wavelet interpolation method was applied to growth and distance values for physique, body fat and physical fitness and motor ability, and growth and development curves were derived. Cross correlation functions were then applied to the respective pairs of the compared velocity curves. There were large changes in the behavior of the growth velocity curve around the take off age for height, and so the relationship between body fat percentage and physical fitness and motor ability was investigated using the respective cross correlation functions around the take off age. Before the take off age, positive correlations were seen between body fat percentage and physical fitness and physical fitness and motor ability except for the RJ index. After the take off age, in contrast, there were negative correlations between body fat percentage and physical fitness and motor ability except for the RJ index. These results show the new finding that after the take off age in boys, there are contrary similarity between body fat and speed, agility, and instantaneous force.

The purpose of this study was to investigate changes in sarcoplasmic reticulum (SR) Ca²⁺-sequestering capacity in rat fast-twitch plantaris (PL) and slow-twitch soleus (SOL) muscles during recovery after high-intensity exercise. The rats were subjected to treadmill runs to exhaustion at the intensity (10% incline at 50 m/min) estimated to require 100% of maximal O₂ consumption. The muscles were excised immediately after exercise, and 15, 30 and 60 min after exercise. Acute high-intensity exercise evoked a 27 % and 38 % depression (P<0.05) in SR Ca²⁺-uptake rate in the PL and SOL, respectively. In the PL, uptake rate remained lower (P<0.05) at 30 min of recovery but recovered 60 min after exercise. These alterations were paralleled by those of SR Ca²⁺-ATPase activity. On the other hand, SR Ca²⁺-uptake rate in the SOL recovered 15 min after exercise. Unlike the PL, discordant time-course changes between SR Ca²⁺-ATPase activity and uptake occurred in the SOL during recovery. SR Ca²⁺-ATPase activities were unaltered with exercise and elevated (P<0.05) by 25, 30 and 30% at 15, 30 and 60 min of recovery, respectively. These results demonstrate that SR Ca²⁺-sequestering ability is restored faster in slow-twitch than in fast-twitch muscle during recovery periods following a single bout of high-intensity exercise and suggest that the rapid restoration of SR Ca²⁺-sequestering ability in slow-twitch muscle could contribute to inhibition of disturbances in contractile and structural properties that are known to occur with raised myoplasmic Ca²⁺ concentrations.

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.

We tested the hypothesis that a force reduction in soleus muscles from hyperthyroid rats would be associated with oxidative modification of myofibrillar proteins. Daily injection of thyroid hormone [3, 5, 3’-triiodo-_L-thyronine (T₃)] for 21 days depressed isometric forces in whole soleus muscle across a range of stimulus frequencies (1, 10, 20, 40, 75 and 100 Hz) (P<0.05). In fiber bundles, hyperthyroidism also led to pronounced reductions (P<0.05) in both K⁺- and 4-chloro-m-cresol-induced contracture forces. The degrees of the reductions were similar between these two contractures. These reductions in force production were accompanied by a remarkable increment (103% ; P<0.05) in carbonyl groups comprised in myofibrillar proteins. In additional experiments, we have also tested the efficacy of carvedilol, a non-selective β₁-β₂-blocker that possesses anti-oxidative properties. Treatment with carvedilol prevented T₃-induced oxidation of myofibrillar proteins. However, carvedilol did not improve the hyperthyroid-induced reductions in force production. These data suggest that oxidative modification of myofibrillar proteins may not account for the reductions in force production of hyperthyroid rat soleus muscle.

The purpose of this study was to examine the effects of eccentric contractions (Ecc) on cation (i.e., K⁺, Na⁺ and Ca²⁺) regulation in skeletal muscle. The left anterior crural muscles of male Wistar rats were subjected in vivo to either Ecc or isometric contrations (Iso) for 200 cycles. The extensor digitorum longus and tibialis anterior muscles were removed immediately after and 2, 4 and 6 days following contractions and used for measures of force output and biochemical analyses, respectively. Ecc led to a 75% decrease in maximal tetanic force. Decreased force output did not revert to pre-exercise levels during 6 days of recovery. Sarcoplasmic reticulum (SR) Ca²⁺-ATPase activity was reduced by 52 and 60% 4 and 6 days after Ecc, respectively. The reduction in catalytic activity after 6 days was accompanied by a 63% decrease in SR Ca²⁺-ATPase protein and an approximately 3.5-fold increase in calpain activity. Na⁺-K⁺-ATPase acticity was decreased by 23% immediately after Ecc and restored during 2 days of recovery. These alterations were specific for Ecc and not observed for Iso. These results suggest that disturbances in cation regulation may account, at least partly, for Ecc-induced decreases in force and power which can take a number of days to recover and that the decrease in SR Ca²⁺-ATPase activity would result from the degradation of the enzyme.