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Antioxidant Supplementation Reduces Skeletal Muscle Mitochondrial Biogenesis

STROBEL, NATALIE A.1; PEAKE, JONATHAN M.1; MATSUMOTO, AYA1; MARSH, SUSAN A.2; COOMBES, JEFF S.1; WADLEY, GLENN D.3,4

Medicine & Science in Sports & Exercise: June 2011 - Volume 43 - Issue 6 - pp 1017-1024
doi: 10.1249/MSS.0b013e318203afa3
Basic Sciences

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 α-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 γ coactivator 1α (PGC-1α) 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-1α mRNA, PGC-1α and COX IV protein, and citrate synthase enzyme activity (P < 0.05) in both sedentary and exercise-trained rats.

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

1School of Human Movement Studies, The University of Queensland, St. Lucia, Queensland, AUSTRALIA; 2Program in Nutrition and Exercise Physiology, Washington State University, Spokane, WA; 3Department of Physiology, The University of Melbourne, Parkville, Victoria, AUSTRALIA; and 4Centre for Physical Activity and Nutrition, School of Exercise and Nutrition Sciences, Deakin University, Burwood, Victoria, AUSTRALIA

Address for correspondence: Glenn D. Wadley, Ph.D., Centre for Physical Activity and Nutrition, School of Exercise and Nutrition Sciences, Deakin University, 221 Burwood Hwy, Burwood, 3125, Australia; E-mail: glenn.wadley@deakin.edu.au.

Submitted for publication August 2010.

Accepted for publication October 2010.

©2011The American College of Sports Medicine