title: Antioxidant supplementation reduces skeletal muscle mitochondrial biogenesis.
abstract: OBJECTIVE
  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 at ∼ 70%VO2max for up to 90 min · d 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.
authors.affiliation: School of Human Movement Studies, The University of Queensland, St Lucia, Queensland, Australia. glenn.wadley@deakin.edu.au
authors.forename: Natalie A
authors.initials: NA
authors.lastname: Strobel
authors.forename: Jonathan M
authors.initials: JM
authors.lastname: Peake
authors.forename: Aya
authors.initials: A
authors.lastname: Matsumoto
authors.forename: Susan A
authors.initials: SA
authors.lastname: Marsh
authors.forename: Jeff S
authors.initials: JS
authors.lastname: Coombes
authors.forename: Glenn D
authors.initials: GD
authors.lastname: Wadley
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000494:pharmacology*; D015415:Biomarkers / Q000378:metabolism; D002950:Citrate (si)-Synthase / Q000235:genetics / Q000378:metabolism; D045304:Cytochromes c / Q000235:genetics / Q000378:metabolism; D003576:Electron Transport Complex IV / Q000235:genetics / Q000378:metabolism; D015227:Lipid Peroxidation; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D008931:Mitochondria, Muscle / Q000187:drug effects* / Q000378:metabolism; D018482:Muscle, Skeletal / Q000187:drug effects* / Q000378:metabolism; D051267:NF-E2-Related Factor 2 / Q000235:genetics / Q000378:metabolism; D000071248:Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha; D010805:Physical Conditioning, Animal; D016133:Polymerase Chain Reaction; D012333:RNA, Messenger / Q000378:metabolism; D016601:RNA-Binding Proteins / Q000235:genetics / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D013482:Superoxide Dismutase / Q000235:genetics / Q000378:metabolism; D008063:Thioctic Acid / Q000494:pharmacology; D014157:Transcription Factors / Q000235:genetics / Q000378:metabolism; D014810:Vitamin E / Q000494:pharmacology; D000099156:Superoxide Dismutase 2
chemical_list: D000975:Antioxidants; D015415:Biomarkers; D002950:Citrate (si)-Synthase; D045304:Cytochromes c; D003576:Electron Transport Complex IV; D008315:Malondialdehyde; D051267:NF-E2-Related Factor 2; D000071248:Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha; D012333:RNA, Messenger; D016601:RNA-Binding Proteins; D013482:Superoxide Dismutase; D008063:Thioctic Acid; D014157:Transcription Factors; D014810:Vitamin E; D000099156:Superoxide Dismutase 2; C495637:Nfe2l2 protein, rat; C501429:Ppargc1a protein, rat