Document Detail


Oral administration of vitamin C decreases muscle mitochondrial biogenesis and hampers training-induced adaptations in endurance performance.
MedLine Citation:
PMID:  18175748     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
Authors:
Mari-Carmen Gomez-Cabrera; Elena Domenech; Marco Romagnoli; Alessandro Arduini; Consuelo Borras; Federico V Pallardo; Juan Sastre; Jose Viña
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Publication Detail:
Type:  Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  The American journal of clinical nutrition     Volume:  87     ISSN:  0002-9165     ISO Abbreviation:  Am. J. Clin. Nutr.     Publication Date:  2008 Jan 
Date Detail:
Created Date:  2008-01-07     Completed Date:  2008-02-28     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0376027     Medline TA:  Am J Clin Nutr     Country:  United States    
Other Details:
Languages:  eng     Pagination:  142-9     Citation Subset:  AIM; IM    
Affiliation:
Department of Physiology, Faculty of Medicine, University of Valencia, Valencia, Spain.
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MeSH Terms
Descriptor/Qualifier:
Adaptation, Physiological / drug effects*,  physiology
Administration, Oral
Adult
Animals
Antioxidants / administration & dosage*,  pharmacology
Ascorbic Acid / administration & dosage*,  pharmacology
Cross-Over Studies
DNA-Binding Proteins / metabolism
Dietary Supplements
Double-Blind Method
Humans
Male
Mitochondria, Muscle / drug effects*,  metabolism
Mitochondrial Proteins / metabolism
Nuclear Respiratory Factor 1 / metabolism
Oxidative Stress / drug effects*
Oxygen Consumption
Peroxisome Proliferator-Activated Receptors / metabolism
Physical Endurance* / drug effects,  physiology
Rats
Rats, Wistar
Reactive Oxygen Species
Transcription Factors / metabolism
Chemical
Reg. No./Substance:
0/Antioxidants; 0/DNA-Binding Proteins; 0/Mitochondrial Proteins; 0/Nuclear Respiratory Factor 1; 0/Peroxisome Proliferator-Activated Receptors; 0/Reactive Oxygen Species; 0/Transcription Factors; 0/mitochondrial transcription factor A; 50-81-7/Ascorbic Acid

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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