English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

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.

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