Journal
JOURNAL OF APPLIED PHYSIOLOGY
Volume 121, Issue 3, Pages 806-810Publisher
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/japplphysiol.00465.2016
Keywords
energy intake; muscle hypertrophy; mitochondrial dynamics; PGC-1 alpha
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Funding
- Japan Society for the Promotion of Science [26702028, 26750304]
- Grants-in-Aid for Scientific Research [26702028, 26750304] Funding Source: KAKEN
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Recent studies have demonstrated that resistance exercise leads not only to muscle hypertrophy, but it also improves mitochondrial function. Because calorie restriction (CR) has been suggested as a way to induce mitochondrial biogenesis, we examined the effects of resistance training with or without CR on muscle weight and key mitochondrial parameters in rat skeletal muscle. Four weeks of resistance training (thrice/wk) resulted in increased gastrocnemius muscle weight by 14% in rats fed ad libitum (AL). The degree of muscle-weight increase via resistance training was lower in rats with CR (7.4%). CR showed no effect on phosphorylation of mammalian target of rapamycin (mTOR) signaling proteins rpS6 and ULK1. Our results revealed that CR resulted in elevated levels of peroxisome proliferator-activated receptor-gamma coactivator-1 alpha (PGC-1 alpha) protein, a known master regulator of mitochondrial biogenesis. Resistance training alone also resulted in increased PGC-1 alpha levels in skeletal muscle. The magnitude of the increase in PGC-1 alpha was similar in rats in both the CR and AL groups. Moreover, we found that resistance training with CR resulted in elevated levels of proteins involved in mitochondrial fusion (Opa1 and Mfn1), and oxidative phosphorylation, whereas there was no effect of CR on the fission-regulatory proteins Fis1 and Drp1. These results indicate that CR attenuates resistance training-induced muscle hypertrophy, and that it may enhance mitochondrial adaptations in skeletal muscle.
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