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Given the potential of reactive oxygen species to damage intracellular proteins during subsequent bouts of muscle contractions, it was suggested that, when this production exceeds the antioxidant capacity, the preexisting antioxidant pathways may be complemented by the synthesis of the defense mechanism represented by heat shock proteins (HSPs), stress proteins with the function of repair and maintaining protein folding. To test this hypothesis, we analyzed reactive carbonyl derivatives in plasma and the expression of HSP72 and activities of enzymes from the oxidative and antioxidant defense systems in the soleus muscle of sedentary rats and rats trained by two protocols: continuous and intermittent. We analyzed all three groups at rest and 2 h after acute exercise. After 8 wk of training, the animals from both groups clearly demonstrated higher resistance to exercise. Both trained groups showed significantly higher citrate synthase, catalase, and glutathione reductase activities than the control group (P < 0.01). After acute exercise, catalase and glutathione reductase activities significantly decreased (P < 0.01) and plasma reactive carbonyl derivatives significantly increased (P < 0.05) in the sedentary group, suggesting an oxidative-stress condition as responsible for exhaustion in this group. Finally, after acute exercise, the induction of HSP72 expression occurred only in the sedentary group, suggesting that HSP72 acts as a complementary protective mechanism in exercise-induced oxidative stress.

The decline in performance in the NFOR group could be related to the decrease in muscle oxidative capacity. We observed a trend in the Gm/Ga and leukocytosis that is similar to what has been sometimes observed in overtrained humans. This controlled training-overtraining animal model may be useful for seeking causative mechanisms of performance decline.

Exercise training is known to induce an increase in free radical production potentially leading to enhanced muscle injury. Vitamins C and E are well known antioxidants that may prevent muscle cell damage. The purpose of this study was to determine the effects of these supplemental antioxidant vitamins on markers of oxidative stress, muscle damage and performance of elite soccer players. Ten male young soccer players were divided into two groups. Supplementation group (n=5) received vitamins C and E supplementation daily during the pre-competitive season (S group), while the placebo group (PL group, n=5) received a pill containing maltodextrin. Both groups performed the same training load during the three-month pre-season training period. Erythrocyte antioxidant enzymes glutathione reductase, catalase and plasma carbonyl derivatives did not show any significant variation among the experimental groups. Similarly, fitness level markers did not differ among the experimental groups. However, S group demonstrated lower lipid peroxidation and muscle damage levels (p<0.05) compared to PL group at the final phase of pre-competitive season. In conclusion, our data demonstrated that vitamin C and E supplementation in soccer players may reduce lipid peroxidation and muscle damage during high intensity efforts, but did not enhance performance.

This study showed the blood appearance kinetics of muscle injury markers and some metabolites. It is suggested that the increase in these enzymes came primarily from muscle damage, rather than liver damage, and that white blood cells are selectively mobilised independently of haemoconcentration. The early appearance of muscle injury markers in this kind of exercise was also shown.

The evaluation of performance through the application of adequate physical tests during a sportive season may be a useful tool to evaluate training adaptations and determine training intensities. For runners, treadmill incremental VO(2)max tests with gas exchange analysis have been widely used to determine maximal and submaximal parameters such as the ventilatory threshold (VT) and respiratory compensation point (RCP) running speed. However, these tests often differ in methodological characteristics (e.g., stage duration, grade, and speed increment size), and few studies have examined the reproducibility of their protocol. Therefore, the aim of this study was to verify the reproducibility and determine the running speeds related to maximal and submaximal parameters of a specific incremental maximum effort treadmill protocol for amateur runners. Eleven amateur male runners underwent 4 repetitions of the protocol (25-second stages, each increasing by 0.3 km·h in running speed while the treadmill grade remained fixed at 1%) after 3 minutes of warm-up at 8-8.5 km·h. We found no significant differences in any of the analyzed parameters, including VT, RCP, and VO(2)max during the 4 repetitions (p > 0.05). Further, the results related to running speed showed high within-subject reproducibility (coefficient of variation < 5.2%). The typical error (TE) values for running speed related to VT (TE = 0.62 km·h), RCP (TE = 0.35 km·h), and VO(2)max (TE = 0.43 km·h) indicated high sensitivity and reproducibility of this protocol. We conclude that this VO(2)max protocol facilitates a clear determination of the running speeds related to VT, RCP, and VO(2)max and has the potential to enable the evaluation of small training effects on maximal and submaximal parameters.

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