Normal adaptations to exercise despite protection against oxidative stress

Important paper which provides strong evidence against the hypothesis that antioxidants, such as vitamins C and E, block the physiological adaptations to exercise. These adaptations include greater insulin sensitivity and greater numbers of mitochondria. Normal adaptations to exercise despite protection against oxidative stress

Abstract

It has been reported that supplementation with the antioxidant vitamins C and E prevents the adaptive increases in mitochondrial biogenesis and GLUT4 expression induced by endurance exercise. We reevaluated the effects of these antioxidants on the adaptive responses of rat skeletal muscle to swimming in a short-term study consisting of 9 days of vitamins C and E with exercise during the last 3 days and a longer-term study consisting of 8 wk of antioxidant vitamins with exercise during the last 3 wk. The rats in the antioxidant groups were given 750 mg·kg body wt−1·day−1 vitamin C and 150 mg·kg body wt−1·day−1 vitamin E. In rats euthanized immediately after exercise, plasma TBARs were elevated in the control rats but not in the antioxidant-supplemented rats, providing evidence for an antioxidant effect. In rats euthanized 18 h after exercise there were large increases in insulin responsiveness of glucose transport in epitrochlearis muscles mediated by an approximately twofold increase in GLUT4 expression in both the short- and long-term treatment groups. The protein levels of a number of mitochondrial marker enzymes were also increased about twofold. Superoxide dismutases (SOD) 1 and 2 were increased about twofold in triceps muscle after 3 days of exercise, but only SOD2 was increased after 3 wk of exercise. There were no differences in the magnitudes of any of these adaptive responses between the control and antioxidant groups. These results show that very large doses of antioxidant vitamins do not prevent the exercise-induced adaptive responses of muscle mitochondria, GLUT4, and insulin action to exercise and have no effect on the level of these proteins in sedentary rats.

From the paper:

TWO ARTICLES HAVE BEEN PUBLISHED RECENTLY reporting that taking the vitamin ascorbic acid (vitamin C) or the combination of ascorbic acid and α-tocopherol (vitamin E) prevents the adaptive responses of skeletal muscle to endurance exercise. In the first study, Gomez-Cabrera et al. (6) reported that men taking 1.0 g/day ascorbic acid (vitamin C) had a markedly reduced increase in maximal oxygen uptake (V̇O2 max) in response to 8 wk of endurance training. They also reported that giving rats ascorbic acid prevented adaptive increases in enzyme levels in skeletal muscle and severely reduced the increase in endurance induced by a treadmill-running program. In the other study, Ristow et al. (23) evaluated the effects of taking ascorbic acid and α-tocopheral on adaptive responses to a 4-wk-long exercise program, the major component of which was circuit training. The study involved two groups of men, one trained and the other untrained, at the start of the study. Ristow et al. (23) interpreted their findings as evidence that antioxidant vitamins prevent exercise training-induced increases in insulin sensitivity and in skeletal muscle peroxisome proliferator-activated receptor-γ (PPARγ) coactivator-1α PGC-1α, PPARγ, and superoxide dismutases (SOD), which they referred to as “the health-promoting effects of physical exercise.” More recently, Strobel et al. (30) reported that oral administration of the antioxidants vitamin E and α-lipoic acid for 14 wk had no effect on the adaptive increases in mitochondrial proteins in response to exercise training but lowered the baseline levels of mitochondrial enzymes.

A large proportion of endurance athletes, including elite athletes, take vitamin supplements, often in large amounts (28). If taking ascorbic acid and α-tocopherol markedly reduced the effects of training on V̇O2 max and endurance (6) and prevented the adaptations in skeletal muscle that mediate increased endurance and the enhancement of insulin action responsible for glycogen supercompensation (6, 23), taking antioxidant vitamins would make competitive athletes noncompetitive. It seems unlikely that a phenomenon of this magnitude would not have been noticed over the long period that these vitamins have been available. It also seems improbable that an effect of this magnitude would not have been recognized in the numerous training studies that have been reported. Training studies conducted to determine whether antioxidant vitamins improve exercise performance and/or enhance the effects of training on V̇O2 max and exercise capacity have generally not shown an improvement in performance (4, 14, 18). However, they have also not shown any reduction of the adaptive response, which argues against the conclusions of Gomez-Cabrera et al. (6), Ristow et al. (23), and Strobel et al. (30). Antioxidant vitamins do have a protective effect against exercise-induced oxidative stress (27), and therefore, it is possible that antioxidant vitamins could have a protective effect against cumulative effects of strenuous exercise-induced free radical damage to heart and skeletal muscle.

Conclusion:

We conclude on the basis of our findings in this study and the results of the studies by Yfanti and colleagues (36, 37) that, contrary to the reports by Gomez-Cabrera et al. (6) and Ristow et al. (23), antioxidant vitamin supplementation does not have an inhibitory effect on the adaptive responses of skeletal muscle to exercise. We also conclude that antioxidant vitamin supplementation does not lower the mitochondrial content of muscle in sedentary animals. Supplementation with antioxidant vitamins has the potentially beneficial effect of protecting against exercise-induced oxidative stress.

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