Vitamin C and E supplementation prevents some of the cellular adaptations to endurance-training in humans.
BACKGROUND
It is clear that reactive oxygen species (ROS) produced during skeletal muscle contraction have a regulatory role in skeletal muscle adaptation to endurance exercise. However, there is much controversy in the literature regarding whether attenuation of ROS by antioxidant supplementation can prevent these cellular adaptations. Therefore, the aim of this study was to determine whether vitamin C and E supplementation attenuates performance and cellular adaptations following acute endurance exercise and endurance training.


METHODS
A double-blinded, placebo-controlled randomized control trial was conducted in eleven healthy young males. Participants were matched for peak oxygen consumption (VO 2peak) and randomly allocated to placebo or antioxidant (vitamin C (2 × 500 mg/day) and E (400 IU/day)) groups. Following a four-week supplement loading period, participants completed acute exercise (10 × 4 min cycling at 90% VO 2peak, 2 min active recovery). Vastus lateralis muscle samples were collected pre-, immediately-post- and 3h-post-exercise. Participants then completed four weeks of training (3 days/week) using the aforementioned exercise protocol while continuing supplementation. Following exercise training, participants again completed an acute exercise bout with muscle biopsies.


RESULTS
Acute exercise tended to increase skeletal muscle oxidative stress as measured by oxidized glutathione (GSSG) (P=0.058) and F2-isoprostanes (P=0.056), with no significant effect of supplementation. Acute exercise significantly increased mRNA levels of peroxisome proliferator-activated receptor gamma coactivator 1α (PGC-1α), mitochondrial transcription factor A (TFAM) and PGC related coactivator (PRC), with no effect of supplementation. Following endurance training, supplementation did not prevent significantly increased VO 2peak, skeletal muscle levels of citrate synthase activity or mRNA or protein abundance of cytochrome oxidase subunit 4 (COX IV) (P<0.05). However, following training, vitamin C and E supplementation significantly attenuated increased skeletal muscle superoxide dismutase (SOD) activity and protein abundance of SOD2 and TFAM.


CONCLUSIONS
Following acute exercise, supplementation with vitamin C and E did not attenuate skeletal muscle oxidative stress or increased gene expression of mitochondrial biogenesis markers. However, supplementation attenuated some (SOD, TFAM) of the increased skeletal muscle adaptations following training in healthy young men.
Centre for Physical Activity and Nutrition (C-PAN) Research, School of Exercise and Nutrition Sciences, Deakin University, 221 Burwood Highway, Burwood, Victoria, Australia.
Dale
D
Morrison
Centre for Physical Activity and Nutrition (C-PAN) Research, School of Exercise and Nutrition Sciences, Deakin University, 221 Burwood Highway, Burwood, Victoria, Australia.
Jed
J
Hughes
Centre for Physical Activity and Nutrition (C-PAN) Research, School of Exercise and Nutrition Sciences, Deakin University, 221 Burwood Highway, Burwood, Victoria, Australia.
Paul A
PA
Della Gatta
Centre for Physical Activity and Nutrition (C-PAN) Research, School of Exercise and Nutrition Sciences, Deakin University, 221 Burwood Highway, Burwood, Victoria, Australia.
Shaun
S
Mason
Centre for Physical Activity and Nutrition (C-PAN) Research, School of Exercise and Nutrition Sciences, Deakin University, 221 Burwood Highway, Burwood, Victoria, Australia.
Séverine
S
Lamon
Centre for Physical Activity and Nutrition (C-PAN) Research, School of Exercise and Nutrition Sciences, Deakin University, 221 Burwood Highway, Burwood, Victoria, Australia.
Aaron P
AP
Russell
Centre for Physical Activity and Nutrition (C-PAN) Research, School of Exercise and Nutrition Sciences, Deakin University, 221 Burwood Highway, Burwood, Victoria, Australia. Electronic address: glenn.wadley@deakin.edu.au.
Glenn D
GD
Wadley
D000222:Adaptation, Physiological / Q000187:drug effects; D000293:Adolescent; D000328:Adult; D000975:Antioxidants / Q000627:therapeutic use*; D001205:Ascorbic Acid / Q000627:therapeutic use*; D019587:Dietary Supplements; D004311:Double-Blind Method; D015444:Exercise / Q000502:physiology*; D006801:Humans; D015151:Immunoblotting; D008297:Male; D018482:Muscle, Skeletal / Q000187:drug effects / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects*; D010807:Physical Endurance / Q000502:physiology; D017382:Reactive Oxygen Species / Q000032:analysis / Q000378:metabolism; D059467:Transcriptome / Q000187:drug effects; D014810:Vitamin E / Q000627:therapeutic use*; D055815:Young Adult
D000975:Antioxidants; D017382:Reactive Oxygen Species; D014810:Vitamin E; D001205:Ascorbic Acid
Antioxidants; Endurance exercise; Mitochondrial biogenesis; Oxidative stress; Reactive oxygen species; Vitamin C; Vitamin E