Recent studies demonstrated that resistance exercise not only leads to muscle hypertrophy, but also improves mitochondrial function. Since it has been suggested that calorie restriction (CR) induces 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/week) increased gastrocnemius muscle weight in ad libitum-fed (AL) rats by 14%. The degree of muscle-weight increase by resistance training was lower in CR rats (7.4%). CR showed no effect on phosphorylation of mammalian target of rapamycin (mTOR) signaling proteins rpS6 and ULK1. Our results revealed that CR elevated the levels of peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α) protein, a known master regulator of mitochondrial biogenesis. Resistance training alone also increased PGC-1α levels in skeletal muscle. The magnitude of the increase in PGC-1α was similar in both CR and AL rats. Moreover, we found that resistance training with CR elevated the levels of proteins involved in mitochondrial fusion, Opa1 and Mfn1, and oxidative phosphorylation, whereas there was no effect of CR on fission regulatory proteins Fis1 and Drp1. These results indicate that CR attenuates resistance training-induced muscle hypertrophy, but may enhance mitochondrial adaptations in skeletal muscle.
- energy intake
- muscle hypertorphy
- mitochondrial dynamics
- Copyright © 2016, Journal of Applied Physiology