期刊
MEDICINE AND SCIENCE IN SPORTS AND EXERCISE
卷 47, 期 9, 页码 1922-1931出版社
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1249/MSS.0000000000000605
关键词
RESISTANCE TRAINING; SKELETAL MUSCLE; MITOCHONDRIA; BIOENERGETICS
资金
- National Institutes of Health [RO1 AR049877, P30 AG024832]
- Shriners Hospitals for Children [84090]
- National Center for Advancing Translational Sciences, National Institutes of Health [UL1TR000071]
- National Institute for Disabilities and Rehabilitation Research [H133P110012]
- Department of Education
Introduction Loss of mitochondrial competency is associated with several chronic illnesses. Therefore, strategies that maintain or increase mitochondrial function will likely be of benefit in numerous clinical settings. Endurance exercise has long been known to increase mitochondrial function in the skeletal muscle. Comparatively little is known regarding the effect of resistance exercise training (RET) on skeletal muscle mitochondrial respiratory function. Purpose The purpose of the current study was to determine the effect of chronic resistance training on skeletal muscle mitochondrial respiratory capacity and function. Methods Here, we studied the effect of a 12-wk RET program on skeletal muscle mitochondrial function in 11 young healthy men. Muscle biopsies were collected before and after the 12-wk training program, and mitochondrial respiratory capacity was determined in permeabilized myofibers by high-resolution respirometry. Results RET increased lean body mass and quadriceps muscle strength by 4% and 15%, respectively (P < 0.001). Coupled mitochondrial respiration supported by complex I, and complex I and II substrates increased by 2- and 1.4-fold, respectively (P < 0.01). The ratio of coupled complex I-supported respiration to maximal respiration increased with RET (P < 0.05), as did complex I protein abundance (P < 0.05), whereas the substrate control ratio for succinate was reduced after RET (P < 0.001). Transcripts responsible for proteins critical to electron transfer and NAD(+) production increased with training (P < 0.05), whereas transcripts involved in mitochondrial biogenesis were unaltered. Conclusions Collectively, 12 wk of RET resulted in qualitative and quantitative changes in skeletal muscle mitochondrial respiration. This adaptation was accompanied by modest changes in mitochondrial proteins and transcript expression. RET seems to be a means to augment the respiratory capacity and intrinsic function of skeletal muscle mitochondria.
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