title: Oral administration of vitamin C decreases muscle mitochondrial biogenesis and hampers training-induced adaptations in endurance performance.
abstract: BACKGROUND
  Exercise practitioners often take vitamin C supplements because intense muscular contractile activity can result in oxidative stress, as indicated by altered muscle and blood glutathione concentrations and increases in protein, DNA, and lipid peroxidation. There is, however, considerable debate regarding the beneficial health effects of vitamin C supplementation.
  
  
  OBJECTIVE
  This study was designed to study the effect of vitamin C on training efficiency in rats and in humans.
  
  
  METHODS
  The human study was double-blind and randomized. Fourteen men (27-36 y old) were trained for 8 wk. Five of the men were supplemented daily with an oral dose of 1 g vitamin C. In the animal study, 24 male Wistar rats were exercised under 2 different protocols for 3 and 6 wk. Twelve of the rats were treated with a daily dose of vitamin C (0.24 mg/cm2 body surface area).
  
  
  RESULTS
  The administration of vitamin C significantly (P=0.014) hampered endurance capacity. The adverse effects of vitamin C may result from its capacity to reduce the exercise-induced expression of key transcription factors involved in mitochondrial biogenesis. These factors are peroxisome proliferator-activated receptor co-activator 1, nuclear respiratory factor 1, and mitochondrial transcription factor A. Vitamin C also prevented the exercise-induced expression of cytochrome C (a marker of mitochondrial content) and of the antioxidant enzymes superoxide dismutase and glutathione peroxidase.
  
  
  CONCLUSIONS
  Vitamin C supplementation decreases training efficiency because it prevents some cellular adaptations to exercise.
authors.affiliation: Department of Physiology, Faculty of Medicine, University of Valencia, Valencia, Spain.
authors.forename: Mari-Carmen
authors.initials: MC
authors.lastname: Gomez-Cabrera
authors.forename: Elena
authors.initials: E
authors.lastname: Domenech
authors.forename: Marco
authors.initials: M
authors.lastname: Romagnoli
authors.forename: Alessandro
authors.initials: A
authors.lastname: Arduini
authors.forename: Consuelo
authors.initials: C
authors.lastname: Borras
authors.forename: Federico V
authors.initials: FV
authors.lastname: Pallardo
authors.forename: Juan
authors.initials: J
authors.lastname: Sastre
authors.forename: Jose
authors.initials: J
authors.lastname: Viña
mesh_terms: D000222:Adaptation, Physiological / Q000187:drug effects* / Q000502:physiology; D000284:Administration, Oral; D000328:Adult; D000818:Animals; D000975:Antioxidants / Q000008:administration & dosage* / Q000494:pharmacology; D001205:Ascorbic Acid / Q000008:administration & dosage* / Q000494:pharmacology; D018592:Cross-Over Studies; D004268:DNA-Binding Proteins / Q000378:metabolism; D019587:Dietary Supplements; D004311:Double-Blind Method; D006801:Humans; D008297:Male; D008931:Mitochondria, Muscle / Q000187:drug effects* / Q000378:metabolism; D024101:Mitochondrial Proteins / Q000378:metabolism; D051266:Nuclear Respiratory Factor 1 / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects*; D010101:Oxygen Consumption; D047492:Peroxisome Proliferator-Activated Receptors / Q000378:metabolism; D010807:Physical Endurance / Q000187:drug effects / Q000502:physiology; D051381:Rats; D017208:Rats, Wistar; D017382:Reactive Oxygen Species; D014157:Transcription Factors / Q000378:metabolism
chemical_list: D000975:Antioxidants; D004268:DNA-Binding Proteins; D024101:Mitochondrial Proteins; D051266:Nuclear Respiratory Factor 1; D047492:Peroxisome Proliferator-Activated Receptors; D017382:Reactive Oxygen Species; D014157:Transcription Factors; C422562:mitochondrial transcription factor A; D001205:Ascorbic Acid