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

Ageing is associated with attenuated exercise responses in skeletal muscle, which may be related to a failure of muscle redox signalling. The attenuation of redox responses to exercise in aged muscle has been linked to perturbations in redox homeostasis induced by age-related increases in mitochondrial oxidative stress. Accordingly, we investigated the effects of supplementation with the mitochondria-targeted antioxidant MitoQ on mitochondrial bioenergetics and H(2)O(2) emission as well as acute exercise-induced redox responses in skeletal muscle of older individuals. In a randomised, double-blind, placebo-controlled, parallel design, 10 males and 12 females aged 65-80 years were randomised to receive either MitoQ (20 mg/day) or a placebo for 12 weeks before completing a single bout of exercise. Vastus lateralis muscle biopsies were collected before supplementation and before, immediately post- and 4 h post-exercise. MitoQ supplementation reduced mitochondrial H(2)O(2) emission capacity in skeletal muscle but did not impact mitochondrial respiration, H(2)O(2) emission in the presence of ADP, or the sensitivity for ADP to stimulate respiration (apparent K(m)) and attenuate H(2)O(2) emission (apparent IC50). Acute exercise-induced peroxiredoxin oxidation in skeletal muscle was not altered by MitoQ supplementation. Similarly, MitoQ had no effect on the phosphorylation of several redox-sensitive protein kinases (AMPK, p38 MAPK, and ERK1/2) or the upregulation of mitochondrial and antioxidant genes following exercise. Collectively, these findings indicate that MitoQ supplementation did not influence the basal myocellular redox state or redox responses to exercise in skeletal muscle of older individuals.