Acute endurance exercise induces the generation of reactive oxygen species (ROS) in muscle (Davies et al., 1982). It has been shown that exercise-induced production of ROS also regulates skeletal muscle adaptations. First, Gomez-Cabrera et al. (2008) have reported that antioxidant vitamin C supplementation prevents the mitochondrial biogenesis induced by exercise training in rat skeletal muscle. Since then, evidence supporting that antioxidant supplementation attenuates exercise training-induced adaptations in human and rodent skeletal muscle has been published (Meier et al., 2013; Ristow et al., 2009). On the other hand, we and another research group have shown that antioxidant supplementation does not alter exercise training-induced adaptations (Higashida et al., 2011; Strobel et al., 2011). Accordingly, the effects of antioxidant supplementation on endurance exercise training-induced skeletal muscle adaptations are still not definitive.
The aim of this study was to investigate the effects of vitamin C and E supplementation on acute exercise-induced changes of markers of skeletal muscle adaptation and its signaling pathways in mice. Male C57BL/6 mice were assigned to one of four groups: a control group; exercise group; vitamin C and E supplemented group; and vitamin C and E supplemented exercise group. Mice in vitamin C and E supplemented group were given vitamin C (750 mg/kg weight/day) and vitamin E (150 mg/kg weight/day) for two weeks. One hour after the last supplementation, exercise group mice ran on a treadmill at 25 m/min, 8% grade for 120 min. Vitamin C and E supplementation attenuates exercise-induced oxidative stress. However, vitamin C and E supplementation did not alter the acute exercise-induced increase in gene expression of peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α), citrate synthase (CS) and vascular endothelial growth factor (VEGF). On the other hand, vitamin C and E supplementation prevented the phosphorylation of AMP activated kinase (AMPK) and p38 mitogen-activated protein kinase (p38 MAPK). These results suggest that reactive oxygen species (ROS) inhibits exercise-induced skeletal muscle signaling but does not alter mitochondrial biogenesis and angiogenesis in skeletal muscle.
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Higashida K, Kim SH, Higuchi M, Holloszy JO, Han DH. (2011). Normal adaptations to exercise despite protection against oxidative stress. American Journal of Physiology. Endocrinology and Metabolism 301: E779-784.
Meier P, Renga M, Hoppeler H, Baum O. (2013). The impact of antioxidant supplements and endurance exercise on genes of the carbohydrate and lipid metabolism in skeletal muscle of mice. Cell Biochemistry and Function 31: 51-59.
Ristow M, Zarse K, Oberbach A, Kloting N, Birringer M, Kiehntopf M, Stumvoll M, Kahn CR, Bluher M. (2009). Antioxidants prevent health-promoting effects of physical exercise in humans. Proceedings of the National Academy of Science USA 106: 8665-8670.
Strobel NA, Peake JM, Matsumoto A, Marsh SA, Coombes JS, Wadley GD. (2011). Antioxidant supplementation reduces skeletal muscle mitochondrial biogenesis. Medicine & Science in Sports & Exercise 43: 1017-1024.