The effect of 10 wk endurance swim training on 3-O-methylglucose (3-MG) uptake (at 40 mM 3-MG) in skeletal muscle was studied in the perfused rat hindquarter. Training resulted in an increase of approximately 33% for maximum insulin-stimulated 3-MG transport in fast-twitch red fibers and an increase of approximately 33% for contraction-stimulated transport in slow-twitch red fibers compared with nonexercised sedentary muscle. A fully additive effect of insulin and contractions was observed both in trained and untrained muscle. Compared with transport in control rats subjected to an almost exhaustive single exercise session the day before experiment both maximum insulin- and contraction-stimulated transport rates were increased in all muscle types in trained rats. Accordingly, the increased glucose transport capacity in trained muscle was not due to a residual effect of the last training session. Half-times for reversal of contraction-induced glucose transport were similar in trained and untrained muscles. The concentrations of mRNA for GLUT-1 (the erythrocyte-brain-Hep G2 glucose transporter) and GLUT-4 (the adipocyte-muscle glucose transporter) were increased approximately twofold by training in fast-twitch red muscle fibers. In parallel to this, Western blot demonstrated a approximately 47% increase in GLUT-1 protein and a approximately 31% increase in GLUT-4 protein. This indicates that the increases in maximum velocity for 3-MG transport in trained muscle is due to an increased number of glucose transporters.

We examined the effect of listening to two different types of music (with slow and fast rhythm), prior to supramaximal cycle exercise, on performance, heart rate, the concentration of lactate and ammonia in blood, and the concentration of catecholamines in plasma. Six male students participated in this study. After listening to slow rhythm or fast rhythm music for 20 min, the subjects performed supramaximal exercise for 45 s using a cycle ergometer. Listening to slow and fast rhythm music prior to supramaximal exercise did not significantly affect the mean power output. The plasma norepinephrine concentration immediately before the end of listening to slow rhythm music was significantly lower than before listening (p < 0.05). The plasma epinephrine concentration immediately before the end of listening to fast rhythm music was significantly higher than before listening (p < 0.05). The type of music had no effect on blood lactate and ammonia levels or on plasma catecholamine levels following exercise. In conclusion, listening to slow rhythm music decreases the plasma norepinephrine level, and listening to fast rhythm music increases the plasma epinephrine level. The type of music has no impact on power output during exercise.

No abstract

The purpose of this study was to examine whether vitamin E supplementation in humans would attenuate an increase of serum enzymes as an indirect marker of muscle damage following a sudden large increase in the running distance in a 6-day running training or not. A randomized and placebo-controlled study was carried out on fourteen male runners who were supplied vitamin E (alpha-tocopherol 1200 IU x day(-1); E) or placebo (P) 4 weeks prior to (T1) and during 6 successive days of running training (48.3 +/- 5.7 km x day(-1), means +/- SD). Resting venous blood samples were obtained before maximal treadmill running, at T1, the day immediately before (T2), the next day (T3), and three weeks (T4) after the running training. Serum levels of alpha-tocopherol, lipid peroxidation products (thiobarbituric acid; TBA), creatine kinase (CK), lactate dehydrogenase (LDH), and LDH isozyme 1-5 were quantitatively analyzed. No significant difference was found in maximal oxygen uptake (VO2max) and maximal heart rates following the exhaustive exercise between the P and E group during the experiments. Vitamin E supplementation significantly increased serum alpha-tocopherol (p<0.001) and decreased TBA levels (p < 0.001) compared with pre-supplementation levels. Although serum CK and LDH activities increased significantly at T3 in either group, significantly lower CK (p < 0.05) and LDH (p < 0.001) levels were observed in the E group compared with the P group. The ratio of LDH1 to LDH2 (LDH1/LDH2) decreased significantly at T3 in either group compared with the T1 levels, since there was no significant difference in the LDH1/LDH2 between the P and E group throughout the experiments. These results indicate that vitamin E supplementation can reduce the leakage of CK and LDH following 6 successive days of endurance running. The protective effect of vitamin E against free radicals probably inhibits free-radical-induced muscle damage caused by a sudden large increase in the running distance.

The effects of exercise on the generation of active oxygen species and radical-scavenging capacity were studied in physically active and sedentary young and old rats. Exercise increased the hydroxyl radical content in all tissues of physically active young rats, except in the plasma. In old rats, the basal level of the radical increased significantly in plasma, heart, and skeletal muscles, but decreased in liver; and physical activity decreased it to that of young rats in most cases. With exercise, the content of reduced glutathione increased in plasma, heart, and skeletal muscles of young rats, whereas that of oxidized glutathione markedly decreased in liver and increased in brain and white gastrocnemius muscle. The total glutathione levels in these tissues changed in a similar way, indicating that glutathione was released from the pool in the liver. In rats allowed to run voluntarily for 5 weeks, the effects were more pronounced than in the sedentary rats. The ratio of reduced to total glutathione, which indicates the capacity to reduce glutathione, increased in plasma, heart, and soleus muscle of sedentary young rats after exercise, and increased further in those undergoing physical activity. In old rats, the reduced glutathione level increased in plasma, heart, liver, and brain, even though the total decreased. These results suggest that physical activity enhances the endogenous ability to defend against oxidative stress. In old rats, even though glutathione synthesis is decreased, the regenerating capacity seems to be increased in order to compensate for the increased oxidative stress.