Abstract
The reactive oxygen species (ROS) produced during exercise act as a double-edged sword because they may cause oxidative damage but also play a role in the signaling pathways. A supplementation of exogenous antioxidants can reduce the total amount of ROS during exercise while it may also affect the ROS’ role in the signaling pathways of mitochondrial biogenesis. It has been suggested that hydrogen gas, as an antioxidant, can selectively scavenge hydroxyl radicals but does not affect superoxide anion’s signal transduction. The aim of this study was to compare the effects of 1-h hydrogen gas inhalation 30min prior to a treadmill exercise on the key biomarkers of mitochondrial biogenesis and related signaling pathways, and the activities of endogenous antioxidant enzymes, with those of vitamin C, in the rat skeletal muscle. Eighty-one 8-week-old male Sprague–Dawley (SD) rats were randomly assigned to three interventions (exercise-only, exercise+4%H2, and exercise+vitamin C at 500mg/kg weight, with 27 rats under each intervention), and sampled at pre-, immediately post and 4h post a 60-min treadmill exercise at speed of 27m/min and flat inclination, with nine rats in each sub-group. Expression of mitochondrial biogenetic markers and related signaling molecules in gastrocnemius muscle, and concentrations of oxidative stress markers in serum were measured. Two-way ANOVA or Kruskal–Wallis analyses showed that both hydrogen inhalation and vitamin C supplementation significantly reduced serum levels of MDA immediately after exercise and AGEs 4h after exercise. The pre-exercise supplement of vitamin C significantly reduced mitochondrial complex IV concentrations and PGC-1α, NRF-1, TFAM gene expression levels compared to the pre-exercise group, but the hydrogen gas intervention did not result in a reduction in these measurements. Unlike vitamin C, hydrogen inhalation did not blunt post-exercise mitochondrial biogenetic signals, but resulted in an increase in complex IV concentration, activation of PGC-1α, and TFAM and NRF-2 gene transcription, and up-regulation of PGC-1α protein expression. The findings indicated that hydrogen gas inhalation could play the role as an effective antioxidant in response to the exercise, whilst it did not significantly affect mitochondrial biogenesis. The dose–response relationship and antioxidant effects in different types of exercise for hydrogen inhalation require further investigation.
Highlights
There has been evidence that high intensity exercise, either prolonged or short-duration, can cause an increase in reactive oxygen species (ROS) level in skeletal muscle (Powers et al, 2016)
Mitochondrial cytochrome C oxidase concentration and expression of mitochondrial biogenetic signal-related proteins and genes (PGC-1α, TFAM, NRF-1, etc.) in gastrocnemius muscle of each group were measured to reflect the level of mitochondrial biogenesis
The activity and gene expression of antioxidant enzymes (SOD, CAT, and GPx) in the gastrocnemius muscle were assessed to reflect the effects of vitamin C and hydrogen on the antioxidant system
Summary
There has been evidence that high intensity exercise, either prolonged or short-duration, can cause an increase in reactive oxygen species (ROS) level in skeletal muscle (Powers et al, 2016). A meta-analysis of 11 studies, including humans and rodent models and various exercise modalities, reported that supplementation with vitamins C and E for three or more weeks produced inconsistent results, with six studies showing no effect and two studies reporting negative effects on mitochondrial metabolism and exercise performance (Nikolaidis et al, 2012). This means exogenous antioxidant supplementation may blunt exercise-induced beneficial adaptations (Strobel et al, 2011; Paulsen et al, 2014; Ristow, 2014). Further research is required to explore the pros and cons of various antioxidant supplementation regimes for optimizing adaptations to exercise and benefits to health
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