6533b839fe1ef96bd12a5b39

RESEARCH PRODUCT

Oral administration of vitamin C decreases muscle mitochondrial biogenesis and hampers training-induced adaptations in endurance performance

Elena DomenechJuan SastreFederico PallardóConsuelo BorrásAlessandro ArduiniMarco RomagnoliJose ViñaMa Carmen Gómez-cabrera

subject

VitaminAdultMalemedicine.medical_specialtyAntioxidantmedicine.medical_treatmentPeroxisome Proliferator-Activated ReceptorsMedicine (miscellaneous)Administration OralAscorbic AcidBiologymedicine.disease_causeAntioxidantsLipid peroxidationMitochondrial Proteinschemistry.chemical_compoundOxygen ConsumptionDouble-Blind MethodInternal medicinemedicineAnimalsHumansRats Wistarchemistry.chemical_classificationNutrition and DieteticsCross-Over StudiesVitamin CNuclear Respiratory Factor 1Glutathione peroxidaseAscorbic acidAdaptation PhysiologicalMitochondria MuscleRatsDNA-Binding ProteinsOxidative StressEndocrinologychemistryMitochondrial biogenesisDietary SupplementsPhysical EnduranceReactive Oxygen SpeciesOxidative stressTranscription Factors

description

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. Design 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. Conclusion Vitamin C supplementation decreases training efficiency because it prevents some cellular adaptations to exercise.

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