Skeletal muscle mitochondrial DNA content in exercising humans

• Published in: Journal of applied physiology (1985) 2005-10, Vol.99 (4), p.1372-1377
• Main Authors: Marcuello, A, Gonzalez-Alonso, J, Calbet, J. A. L, Damsgaard, R, Lopez-Perez, M. J, Diez-Sanchez, C
• Format: Article
• Language: English
• Subjects: Adult; Bicycling - physiology; Biological and medical sciences; Cell Nucleus - metabolism; DNA - antagonists & inhibitors; DNA - metabolism; DNA, Mitochondrial - antagonists & inhibitors; DNA, Mitochondrial - metabolism; Exercise; Exercise - physiology; Female; Fundamental and applied biological sciences. Psychology; Gene expression; Humans; Male; Mitochondrial DNA; Muscular system; Oxygen Consumption; Quadriceps Muscle - metabolism; Time Factors
• ISSN: 8750-7587; 1522-1601
• DOI: 10.1152/japplphysiol.00289.2005

1 Department of Biochemistry, Molecular and Cell Biology, University of Zaragoza, Zaragoza, Spain; 2 The Copenhagen Muscle Research Centre, Rigshospitalet, University of Copenhagen, Denmark; and 3 Department 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 Address for reprint requests and other correspondence: C. Díez-Sánchez, Dept. of Biochemistry, Molecular and Cell Biology, Univ. of Zaragoza, Miguel Servet 177, 50013 Zaragoza, Spain (e-mail: cardisan{at}unizar.es )