MitoQ supplementation does not impact redox responses to acute exercise in skeletal muscle of older individuals.

MitoQ supplementation reduced mitochondrial H2O2 emission capacity in skeletal muscle of older individuals.

• Participants were aged 65-80 years and received MitoQ 20 mg/day or placebo for 12 weeks
• Randomised, double-blind, placebo-controlled, parallel design with 10 males and 12 females
• H2O2 emission capacity was measured in vastus lateralis muscle biopsies
• The reduction in H2O2 emission capacity was observed without ADP present

MitoQ supplementation did not impact mitochondrial respiration in skeletal muscle of older individuals.

• Mitochondrial bioenergetics were assessed in vastus lateralis muscle biopsies collected before supplementation and before exercise
• No significant differences in mitochondrial respiration were detected between MitoQ and placebo groups
• The sensitivity for ADP to stimulate respiration (apparent Km) was also unaffected by MitoQ supplementation

MitoQ supplementation did not affect H2O2 emission in the presence of ADP or the sensitivity for ADP to attenuate H2O2 emission.

• H2O2 emission was measured both in the absence and presence of ADP
• The apparent IC50 for ADP to attenuate H2O2 emission was not altered by MitoQ supplementation
• These findings suggest MitoQ did not alter the relationship between energy demand and mitochondrial oxidative stress

Acute exercise-induced peroxiredoxin oxidation in skeletal muscle was not altered by MitoQ supplementation.

• Muscle biopsies were collected before, immediately post-, and 4 hours post-exercise
• Peroxiredoxin oxidation is a marker of cellular H2O2 levels and redox signalling
• No significant difference in peroxiredoxin oxidation was detected between MitoQ and placebo groups at any time point

MitoQ had no effect on the phosphorylation of redox-sensitive protein kinases AMPK, p38 MAPK, and ERK1/2 following acute exercise.

• Phosphorylation of AMPK, p38 MAPK, and ERK1/2 were measured as markers of redox-sensitive signalling responses to exercise
• Biopsies were collected before, immediately post-, and 4 hours post-exercise to capture temporal signalling responses
• No significant differences in kinase phosphorylation were found between MitoQ and placebo groups at any time point

MitoQ supplementation did not affect the upregulation of mitochondrial and antioxidant genes following acute exercise.

• Gene expression related to mitochondrial biogenesis and antioxidant defenses was assessed from vastus lateralis biopsies
• Biopsy samples were collected before exercise and 4 hours post-exercise to capture transcriptional responses
• No significant differences in gene expression were observed between MitoQ and placebo groups following exercise

The study employed a randomised, double-blind, placebo-controlled, parallel design to assess MitoQ supplementation effects in older adults.

• 22 participants aged 65-80 years (10 males and 12 females) were randomised to MitoQ or placebo groups
• MitoQ was administered at 20 mg/day for 12 weeks prior to an acute exercise bout
• Vastus lateralis muscle biopsies were collected at four time points: before supplementation and before, immediately post-, and 4 hours post-exercise