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

S C Broome, A J Braakhuis, C J Mitchell, T L Merry

Journal: Journal of the International Society of Sports Nutrition 2021;18(1):58

PMID: 34419082

Plain Language Summary

Oxygen-derived radical and non-radical species, collectively referred to as reactive oxygen species (ROS), are continuously produced by skeletal muscle. High levels of ROS production in cells may overwhelm the endogenous antioxidant defence network resulting in damage to cellular proteins, lipids and DNA and impaired cellular function. The aim of this study was to investigate whether Mitochondria-targeted coenzyme Q10 (MitoQ), supplementation could improve the time taken to complete an 8 km cycling time trial. This study is a double-blind, placebo-controlled crossover design trial. Twenty-two healthy middle-aged, recreationally trained male cyclists were recruited via advertisements. They were randomised by an independent researcher to two groups, which would determine the order in which they received MitoQ and an identical placebo. Results show that oral supplementation of the mitochondria-targeted antioxidant MitoQ can improve cycling time trial performance in middle-aged, recreationally trained male cyclists. In fact, MitoQ may improve performance above the aerobic threshold by allowing for increased use of anaerobic metabolism, or by improving tolerance to lower pH in muscle. Authors conclude that further research is required to determine the mechanisms responsible for the ergogenic effect of MitoQ, understand the important factors that determine an individual’s response to MitoQ supplementation, and identify optimal dosing strategies.

Abstract

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: 58.5 ± 6.2 ml·kg·min, 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 followed by an 8 km time trial after 28 days of supplementation with MitoQ (20 mg·day) and a placebo. Free F-isoprostanes were measured in plasma samples collected at rest, after 45 min cycling at 70% VO 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-isoprostanes were lower on completion of the time trial following MitoQ supplementation (35.89 ± 13.6 pg·ml) compared to placebo (44.7 ± 16.9 pg·ml 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.

Address: Discipline of Nutrition, School of Medical Sciences, University of Auckland, Private Bag 92019, Auckland, New Zealand.; School of Kinesiology, University of British Columbia, Vancouver, Canada.; Discipline of Nutrition, School of Medical Sciences, University of Auckland, Private Bag 92019, Auckland, New Zealand. [email protected].; Maurice Wilkins Centre for Molecular Biodiscovery, University of Auckland, Auckland, New Zealand. [email protected].

DOI: 10.1186/s12970-021-00454-0