Antioxidant Supplementation Reduces Skeletal Muscle Mitochondrial Biogenesis

• Autores: Natalie A. Strobel, Jonathan M. Peake, Aya Matsumoto, Susan A. Marsh, Jeff S. Coombes
• Localización: Medicine & Science in Sports & exercise: Official Journal of the American College of Sports Medicine, ISSN 0195-9131, Vol. 43, Nº. 6, 2011, págs. 1017-1024
• Idioma: inglés
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• Dialnet Métricas: 2 Citas
• Resumen

  • 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 a-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 ~70%V?O2max 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 ? coactivator 1a (PGC-1a) 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-1a mRNA, PGC-1a and COX IV protein, and citrate synthase enzyme activity (P < 0.05) in both sedentary and exercise-trained rats.

    Conclusions: Vitamin E and a-lipoic acid supplementation suppresses skeletal muscle mitochondrial biogenesis, regardless of training status.