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1
Ulster University, Sport and Exercise Research Institute, Newtownabbey, Northern Ireland, UK.
2
Ulster University, Nursing and Health Research Institute, Newtownabbey, Northern Ireland, UK.
3
Free Radical Research Group, University of the Highlands and Islands, Centre for Health Sciences, Inverness, IV2 3JH, UK.
4
Ulster University, Sport and Exercise Research Institute, Newtownabbey, Northern Ireland, UK. Electronic address: [email protected].
1
Ulster University, Sport and Exercise Research Institute, Newtownabbey, Northern Ireland, UK.
2
Ulster University, Nursing and Health Research Institute, Newtownabbey, Northern Ireland, UK.
3
Free Radical Research Group, University of the Highlands and Islands, Centre for Health Sciences, Inverness, IV2 3JH, UK.
4
Ulster University, Sport and Exercise Research Institute, Newtownabbey, Northern Ireland, UK. Electronic address: [email protected].
High-intensity exercise damages mitochondrial DNA (mtDNA) in skeletal muscle. Whether MitoQ - a redox active mitochondrial targeted quinone - can reduce exercise-induced mtDNA damage is unknown. In a double-blind, randomized, placebo-controlled design, twenty-four healthy male participants consisting of two groups (placebo; n = 12, MitoQ; n = 12) performed an exercise trial of 4 x 4-min bouts at 90-95% of heart rate max. Participants completed an acute (20 mg MitoQ or placebo 1-h pre-exercise) and chronic (21 days of supplementation) phase. Blood and skeletal muscle were sampled immediately pre- and post-exercise and analysed for nuclear and mtDNA damage, lipid hydroperoxides, lipid soluble antioxidants, and the ascorbyl free radical. Exercise significantly increased nuclear and mtDNA damage across lymphocytes and muscle (P < 0.05), which was accompanied with changes in lipid hydroperoxides, ascorbyl free radical, and α-tocopherol (P < 0.05). Acute MitoQ treatment failed to impact any biomarker likely due to insufficient initial bioavailability. However, chronic MitoQ treatment attenuated nuclear (P < 0.05) and mtDNA damage in lymphocytes and muscle tissue (P < 0.05). Our work is the first to show a protective effect of chronic MitoQ supplementation on the mitochondrial and nuclear genomes in lymphocytes and human muscle tissue following exercise, which is important for genome stability.
Heart rate (b·min
−1
) across high-intensity intermittent exercise. Note: HIIE 1 refers to exercise completed during the acute phase, whereas HIIE 2 refers to exercise completed during the chronic phase. Heart rate across both trials was similar (P > 0.05). Average workload across work- and rest-intervals was 380 ± 137 W and 156 ± 102 W, respectively.
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