期刊
JOURNAL OF PHYSIOLOGY-LONDON
卷 596, 期 18, 页码 4413-4426出版社
WILEY
DOI: 10.1113/JP275308
关键词
muscle memory; myonuclei; mitochondrial biogenesis; resistance training
资金
- American Heart Association (AHA) [12SDG12070327] Funding Source: Medline
- HHS | National Institutes of Health (NIH) [R01HL126952] Funding Source: Medline
- National Research Foundation of Korea (NRF) [NRF-2011-356-G00013] Funding Source: Medline
- NHLBI NIH HHS [R01 HL126952] Funding Source: Medline
Muscle hypertrophy induced by resistance training is accompanied by an increase in the number of myonuclei. The acquired myonuclei are viewed as a cellular component of muscle memory by which muscle enlargement is promoted during a re-training period. In the present study, we investigated the effect of exercise preconditioning on mitochondrial remodelling induced by resistance training. Sprague-Dawley rats were divided into four groups: untrained control, training, pre-training or re-training. The training groups were subjected to weight loaded-ladder climbing exercise training. Myonuclear numbers were significantly greater (up to 20%) in all trained muscles compared to untrained controls. Muscle mass was significantly higher in the re-training group compared to the training group (similar to 2-fold increase). Mitochondrial content, mitochondrial biogenesis gene expression levels and mitochondrial DNA copy numbers were significantly higher in re-trained muscles compared to the others. Oxidative myofibres (type I) were significantly increased only in the re-trained muscles. Furthermore, in vitro studies using insulin-like growth factor-1-treated L6 rat myotubes demonstrated that myotubes with a higher myonuclear number confer greater expression levels of both mitochondrial and nuclear genes encoding for constitutive and regulatory mitochondrial proteins, which also showed a greater mitochondrial respiratory function. These data suggest that myonuclei acquired from previous training facilitate mitochondrial biogenesis in response to subsequent retraining by (at least in part) enhancing cross-talk between mitochondria and myonuclei in the pre-conditioned myofibres.
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