Background: There is a considerable commercial market, especially within the sports community, claiming the need for antioxidant supplementation. One argument for antioxidant supplementation in sports is that physical exercise is associated with increased reactive oxygen and nitrogen species (RONS) production, which may cause cell damage. However, RONS production may also activate redox-sensitive signaling pathways and transcription factors, which subsequently, may promote training adaptation.
Purpose: Our aim was to investigate the effects of combined vitamin C and E supplementation to healthy individuals on different measures of exercise performance after endurance training.
Methods: Using a double-blinded placebo-controlled design, moderately trained young men received either oral supplementation with vitamins C and E (n = 11) or placebo (n = 10) before and during 12 wk of supervised, strenuous bicycle exercise training of a frequency of 5 d·wk−1. Muscle biopsies were obtained before and after training.
Results: After the training period, maximal oxygen consumption, maximal power output, and workload at lactate threshold increased markedly (P < 0.01) in both groups. Also, glycogen concentration, citrate synthase, and β-hydroxyacyl-CoA dehydrogenase activity in the muscle were significantly higher in response to training (P < 0.01) in both groups. However, there were no differences between the two groups concerning any of the physiological and metabolic variables measured.
Conclusions: Our results suggest that administration of vitamins C and E to individuals with no previous vitamin deficiencies has no effect on physical adaptations to strenuous endurance training.
1Center of Inflammation and Metabolism at Department of Infectious Diseases, Rigshospitalet, University of Copenhagen, Copenhagen, DENMARK; 2Institut Cochin, Université Paris Descartes, Paris, FRANCE; 3INSERM, Paris, FRANCE; 4Cellular and Metabolic Research Section, Department of Biomedical Sciences, University of Copenhagen, Copenhagen, DENMARK; 5Section of Biomedicine, Department of Disease Biology, Faculty of Life Sciences, University of Copenhagen, Copenhagen, DENMARK; and 6Molecular Physiology Group, Department of Exercise and Sport Sciences, Section of Human Physiology, University of Copenhagen, Copenhagen, DENMARK
Address for correspondence: Christina Yfanti, Center of Inflammation and Metabolism, Rigshospitalet M7641, Blegdamsvej 9, DK-2100 Copenhagen, Denmark; E-mail: firstname.lastname@example.org.
Submitted for publication June 2009.
Accepted for publication December 2009.