Effects of -lipoic Acid on mtDNA Damage after Isolated Muscle Contractions

FOGARTY, MARK C.1; DEVITO, GIUSEPPE2; HUGHES, CIARA M.3; BURKE, GEORGE4; BROWN, JOHN C.5; MCENENY, JANE6; BROWN, DAVID7; MCCLEAN, CONOR5; DAVISON, GARETH W.5

Medicine & Science in Sports & Exercise:
doi: 10.1249/MSS.0b013e31828bf31e
Basic Sciences
Abstract

Introduction: Although pharmacological antioxidants have previously been investigated for a prophylactic effect against exercise oxidative stress, it is not known if α-lipoic acid supplementation can protect against DNA damage after high-intensity isolated quadriceps exercise. This randomized controlled investigation was designed to test the hypothesis that 14 d of α-lipoic acid supplementation can attenuate exercise-induced oxidative stress.

Methods: Twelve (n = 12) apparently healthy male participants (age = 28 ± 10 yr, stature = 177 ± 12 cm and body mass = 81 ± 15 kg) were randomly assigned to receive either a daily supplement of 1000 mg of α-lipoic acid (2 × 500-mg tablets) for 14 d (n = 6) or receive no supplement (n = 6) in a double-blinded experimental approach. Blood and muscle biopsy tissue samples were taken at rest and after the completion of 100 isolated and continuous maximal knee extension (minimum force = 200 N, speed of contraction = 60°·s−1).

Results: Exercise increased mitochondrial 8-hydroxy-2-deoxyguanosine (8-OHdG) concentration in both groups (P < 0.05 vs rest) with a concomitant decrease in total antioxidant capacity (P < 0.05 vs rest). There was a marked increase in blood total antioxidant capacity after oral α-lipoic acid supplementation (P < 0.05 vs nonsupplemented), whereas DNA damage (Comet assay and 8-OHdG), lipid peroxidation, and hydrogen peroxide increased after exercise in the nonsupplemented group only (P < 0.05 vs supplemented). Exercise increased protein oxidation in both groups (P < 0.05 vs rest).

Conclusions: These findings suggest that short-term α-lipoic acid supplementation can selectively protect DNA (but not in muscle mitochondria) and lipids against exercise-induced oxidative stress.

Author Information

1Department of Sport, Health & Exercise Science, University of Hull, Cottingham Road, Kingston-upon-Hull, UNITED KINGDOM; 2Institute for Sport and Health, University College Dublin, Belfield, Dublin, IRELAND; 3School of Health Science, University of Ulster, Jordanstown, County Antrim, UNITED KINGDOM; 4School of Electrical and Mechanical Engineering, University of Ulster, Jordanstown, County Antrim, UNITED KINGDOM; 5Sport and Exercise Sciences Research Institute, University of Ulster, Jordanstown, County Antrim, UNITED KINGDOM; 6Centre for Public Health, Queen’s University Belfast, Belfast, UNITED KINGDOM; and 7School of Life Sciences, Heriot-Watt University, Edinburgh, UNITED KINGDOM

Address for correspondence: Gareth W. Davison, Ph.D., Sport and Exercise Sciences Research Institute, University of Ulster, Jordanstown, County Antrim BT37 0QB, Northern Ireland; E-mail: gw.davison@ulster.ac.uk.

Submitted for publication August 2012.

Accepted for publication February 2013.

© 2013 American College of Sports Medicine