No role for early IGF-1 signalling in stimulating acute 'muscle building' responses.

摘要

The molecular controls governing load-induced changes in rates of muscle protein synthesis muscle protein synthesis leading to fibre hypertrophy involve a multitude of signals. It appears that many of these signals converge at the mammalian target of rapamycin complex 1 (mTORCl), a kinase directly downstream of the protein kinase B (Akt). Acute activation of mTORCl signalling has been reported to be essential for mediating increased rates of muscle protein synthesis after resistance exercise (Drummond et a. 2009); however, the upstream intramuscular signalling events that serve to phosphorylate and activate mTORC 1 after an anabolic stimulus to muscle, such as after resistance exercise in humans or synergist ablation-induced overload in rodents, remain enigmatic.