期刊
MEDICINE AND SCIENCE IN SPORTS AND EXERCISE
卷 43, 期 6, 页码 1017-1024出版社
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1249/MSS.0b013e318203afa3
关键词
alpha-LIPOIC ACID; EXERCISE TRAINING; MITOCHONDRIA; Nfe2l2; PGC-1 alpha; VITAMIN E
资金
- University of Queensland
STROBEL, N. A., J. M. PEAKE, A. MATSUMOTO, S. A. MARSH, J. S. COOMBES, and G. D. WADLEY. Antioxidant Supplementation Reduces Skeletal Muscle Mitochondrial Biogenesis. Med. Sci. Sports Exerc., Vol. 43, No. 6, pp. 1017-1024, 2011. Purpose: Exercise increases the production of reactive oxygen species (ROS) in skeletal muscle, and athletes often consume antioxidant supplements in the belief they will attenuate ROS-related muscle damage and fatigue during exercise. However, exercise-induced ROS may regulate beneficial skeletal muscle adaptations, such as increased mitochondrial biogenesis. We therefore investigated the effects of long-term antioxidant supplementation with vitamin E and alpha-lipoic acid on changes in markers of mitochondrial biogenesis in the skeletal muscle of exercise-trained and sedentary rats. Methods: Male Wistar rats were divided into four groups: 1) sedentary control diet, 2) sedentary antioxidant diet, 3) exercise control diet, and 4) exercise antioxidant diet. Animals ran on a treadmill 4 d.wk(-1) at similar to 70% V (over dot)O(2max) for up to 90 min.d(-1) for 14 wk. Results: Consistent with the augmentation of skeletal muscle mitochondrial biogenesis and antioxidant defenses, after training there were significant increases in peroxisome proliferator-activated receptor F coactivator 1 alpha (PGC-1 alpha) messenger RNA (mRNA) and protein, cytochrome C oxidase subunit IV (COX IV) and cytochrome C protein abundance, citrate synthase activity, Nfe2l2, and SOD2 protein (P < 0.05). Antioxidant supplementation reduced PGC-1 alpha mRNA, PGC-1 alpha and COX IV protein, and citrate synthase enzyme activity (P < 0.05) in both sedentary and exercise-trained rats. Conclusions: Vitamin E and alpha-lipoic acid supplementation suppresses skeletal muscle mitochondrial biogenesis, regardless of training status.
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