The role of mTOR signalling in the regulation of skeletal muscle mass in a rodent model of resistance exercise

Abstract

Resistance exercise (RE) activates signalling by the mammalian target of rapamycin (mTOR), and it has been suggested that rapamycin-sensitive mTOR signalling controls RE-induced changes in protein synthesis, ribosome biogenesis, autophagy, and the expression of peroxisome proliferator gamma coactivator 1 alpha (PGC-1α). However, direct evidence to support the aforementioned relationships is lacking. Therefore, in this study, we investigated the role of rapamycin-sensitive mTOR in the RE-induced activation of muscle protein synthesis, ribosome biogenesis, PGC-1α expression and hypertrophy. The results indicated that the inhibition of rapamycin-sensitive mTOR could prevent the induction of ribosome biogenesis by RE, but it only partially inhibited the activation of muscle protein synthesis. Likewise, the inhibition of rapamycin-sensitive mTOR only partially blocked the hypertrophic effects of chronic RE. Furthermore, both acute and chronic RE promoted an increase in PGC-1α expression and these alterations were not affected by the inhibition of rapamycin-sensitive mTOR. Combined, the results from this study not only establish that rapamycin-sensitive mTOR plays an important role in the RE-induced activation of protein synthesis and the induction of hypertrophy, but they also demonstrate that additional (rapamycin-sensitive mTOR-independent) mechanisms contribute to these fundamentally important events.

Searching for a mitochondrial root to the decline in muscle function with ageing

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Progressive resistance training prevents loss of muscle mass and strength in bile duct‐ligated rats

“…Myostatin deactivates the mammalian target of rapamycin (mTOR) resulting in decreased protein synthesis and increased autophagy, at least in part mediated through downstream molecules as p70S6K and 4E‐BP1 . Several physiological factors are triggered by resistance training, but among other, weight training activates protein synthesis trough the above mentioned mTOR pathway . This indicates exercise can counteract hyperammonaemia.…”

Activation of mTORC1 signalling in rat skeletal muscle is independent of the EC‐coupling sequence but dependent on tension per se in a dose‐response relationship

“…Once mTORC1 is activated, it is believed to activate downstream signalling through, eg, p70S6K and rpS6 and subsequently promote muscle protein translation initiation . Indeed, several studies have shown that mTORC1 signalling is activated following a mechanical stimulus, and moreover, the subsequent increases in protein synthesis and hypertrophy is dependent on mTORC1 signalling . Consequently, mTORC1 signalling is regarded as vital for transducing a mechanical stimulus into biochemical signalling for muscle protein synthesis.…”