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Skeletal muscle mitochondrial DNA content in exercising humans

¹Department of Biochemistry, Molecular and Cell Biology, University of Zaragoza, Zaragoza, Spain; ²The Copenhagen Muscle Research Centre, Rigshospitalet, University of Copenhagen, Denmark; and ³Department of Physical Education, University of Las Palmas de Gran Canaria, Canary Islands, Spain

Submitted 10 March 2005 ; accepted in final form 30 May 2005

Several weeks of intense endurance training enhances mitochondrial biogenesis in humans. Whether a single bout of exercise alters skeletal muscle mitochondrial DNA (mtDNA) content remains unexplored. Double-stranded mtDNA, estimated by slot-blot hybridization and real time PCR and expressed as mtDNA-to-nuclear DNA ratio (mtDNA/nDNA) was obtained from the vastus lateralis muscle of healthy human subjects to investigate whether skeletal muscle mtDNA changes during fatiguing and nonfatiguing prolonged moderate intensity [2.0–2.5 h; 60% maximal oxygen consumption (O_{2 max})] and short repeated high-intensity exercise (5–8 min; 110% O_{2 max}). In control resting and light exercise (2 h; 25% O_{2 max}) studies, mtDNA/nDNA did not change. Conversely, mtDNA/nDNA declined after prolonged fatiguing exercise (0.863 ± 0.061 vs. 1.101 ± 0.067 at baseline; n = 14; P = 0.005), remained lower after 24 h of recovery, and was restored after 1 wk. After nonfatiguing prolonged exercise, mtDNA/nDNA tended to decline (n = 10; P = 0.083) but was reduced after three repeated high-intensity exercise bouts (0.900 ± 0.049 vs. 1.067 ± 0.071 at baseline; n = 7; P = 0.013). Our findings indicate that prolonged and short repeated intense exercise can lead to significant reductions in human skeletal muscle mtDNA content, which might function as a signal stimulating mitochondrial biogenesis with exercise training.

human skeletal muscle; mtDNA content; exercise

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