Vitamin C and E Supplementation Inhibits Acute Exercise-induced Skeletal Muscle Signaling but does not Alter Maker of Muscle Adaptations
Koichi Yada *
Faculty of Sport Sciences, Waseda University, Tokorozawa, Saitama 359-1192, Japan
Tsubasa Mizokami
Graduate School of Sport Sciences, Waseda University, Tokorozawa, Saitama 359-1192, Japan
Hiroyuki Niihara
Graduate School of Sport Sciences, Waseda University, Tokorozawa, Saitama 359-1192, Japan
Katsuhiko Suzuki
Faculty of Sport Sciences, Waseda University, Tokorozawa, Saitama 359-1192, Japan
*Author to whom correspondence should be addressed.
Abstract
Aim: The aim of this study was to investigate the effects of vitamin C and E supplementation on acute exercise-induced changes of makers of skeletal muscle adaptation and its signaling pathways in mice.
Methodology: 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.
Results: Vitamin C and supplementation attenuated exercise-induced oxidative stress (P<0.01). However, vitamin C and E supplementation with vitamins C and E 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) following the treadmill running (P<0.05).
Conclusion: 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.
Keywords: Vitamin C, vitamin E, reactive oxygen species, mitochondrial biogenesis, angiogenesis