作者: Neil Kubica , Douglas R. Bolster , Peter A. Farrell , Scot R. Kimball , Leonard S. Jefferson
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摘要: The contribution of mammalian target rapamycin (mTOR) signaling to the resistance exercise-induced stimulation skeletal muscle protein synthesis was assessed by administering Sprague-Dawley rats 2 h prior a bout exercise. Animals were sacrificed 16 postexercise, and gastrocnemius synthesis, mTOR signaling, biomarkers translation initiation assessed. Exercise stimulated rate synthesis; however, this effect prevented pretreatment with rapamycin. mediated an increase in initiation, since exercise caused polysome aggregation that abrogated administration. Taken together, data suggest not reduced phosphorylation eukaryotic factor 4E (eIF4E) binding 1 (BP1), because did cause significant change 4E-BP1(Thr-70) phosphorylation, 4E-BP1-eIF4E association, or eIF4F complex assembly concomitant increased synthetic rates. Alternatively, there rapamycin-sensitive decrease relative eIF2Bepsilon(Ser-535) explained expression eIF2Bepsilon protein. proportion mRNA polysomes following exercise, treatment, suggesting mTOR-dependent encoding abundance occurred independent similar changes other eIF2B subunits. These novel link between could contribute acute