Mitochondria-targeted antioxidant supplementation improves 8 km time trial performance in middle-aged trained male cyclists.

Autor: Broome SC; Discipline of Nutrition, School of Medical Sciences, University of Auckland, Private Bag 92019, Auckland, New Zealand., Braakhuis AJ; Discipline of Nutrition, School of Medical Sciences, University of Auckland, Private Bag 92019, Auckland, New Zealand., Mitchell CJ; School of Kinesiology, University of British Columbia, Vancouver, Canada., Merry TL; Discipline of Nutrition, School of Medical Sciences, University of Auckland, Private Bag 92019, Auckland, New Zealand. t.merry@auckland.ac.nz.; Maurice Wilkins Centre for Molecular Biodiscovery, University of Auckland, Auckland, New Zealand. t.merry@auckland.ac.nz.
Jazyk: angličtina
Zdroj: Journal of the International Society of Sports Nutrition [J Int Soc Sports Nutr] 2021 Aug 21; Vol. 18 (1), pp. 58. Date of Electronic Publication: 2021 Aug 21.
DOI: 10.1186/s12970-021-00454-0
Abstrakt: Background: Exercise increases skeletal muscle reactive oxygen species (ROS) production, which may contribute to the onset of muscular fatigue and impair athletic performance. Mitochondria-targeted antioxidants such as MitoQ, which contains a ubiquinone moiety and is targeted to mitochondria through the addition of a lipophilic triphenylphosphonium cation, are becoming popular amongst active individuals as they are designed to accumulate within mitochondria and may provide targeted protection against exercise-induced oxidative stress. However, the effect of MitoQ supplementation on cycling performance is currently unknown. Here, we investigate whether MitoQ supplementation can improve cycling performance measured as time to complete an 8 km time trial.
Method: In a randomized, double-blind, placebo-controlled crossover study, 19 middle-aged (age: 44 ± 4 years) recreationally trained (VO 2peak : 58.5 ± 6.2 ml·kg - 1 ·min - 1 , distance cycled per week during 6 months prior to study enrollment: 158.3 ± 58.4 km) male cyclists completed 45 min cycling at 70% VO 2peak followed by an 8 km time trial after 28 days of supplementation with MitoQ (20 mg·day - 1 ) and a placebo. Free F 2 -isoprostanes were measured in plasma samples collected at rest, after 45 min cycling at 70% VO 2peak and after completion of the time trial. Respiratory gases and measures of rating of perceived exertion (RPE) were also collected.
Results: Mean completion time for the time trial was 1.3% faster with MitoQ (12.91 ± 0.94 min) compared to placebo (13.09 ± 0.95 min, p = 0.04, 95% CI [0.05, 2.64], d = 0.2). There was no difference in RPE during the time trial between conditions (p = 0.82) despite there being a 4.4% increase in average power output during the time trial following MitoQ supplementation compared to placebo (placebo; 270 ± 51 W, MitoQ; 280 ± 53 W, p = 0.04, 95% CI [0.49, 8.22], d = 0.2). Plasma F 2 -isoprostanes were lower on completion of the time trial following MitoQ supplementation (35.89 ± 13.6 pg·ml - 1 ) compared to placebo (44.7 ± 16.9 pg·ml - 1 p = 0.03).
Conclusion: These data suggest that MitoQ supplementation may be an effective nutritional strategy to attenuate exercise-induced increases in oxidative damage to lipids and improve cycling performance.
(© 2021. The Author(s).)
Databáze: MEDLINE
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