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1 Department of Health Sciences, Boston University, Boston, MA, USA
2 Department of Health Sciences, Boston University, Boston, MA, USA; Center for the Molecular Stress Response, Boston University School of Medicine, Boston, MA, USA
* To whom correspondence should be addressed. E-mail: fielding{at}bu.edu.
The cellular mechanisms by which contractile activity stimulates skeletal muscle hypertrophy are beginning to be elucidated and appear to include the activation of the PI3 kinase signaling substrate, mammalian target of rapamycin (mTOR). In the present study, we examined the time course and location of mTOR phosphorylation in response to an acute bout of contractile activity. Rat hindlimb muscle contractile activity was elicited by high frequency electrical stimulation (HFES) of the sciatic nerve. Plantaris (PLA), tibialis anterior (TA), and soleus (SOL) muscles from stimulated and control limbs were collected immediately after or 6 hr after stimulation. HFES resulted in mTOR phosphorylation immediately after (3.4 ± 0.9-fold, p < 0.01) contractile activity in PLA whereas the TA was unchanged compared to controls. mTOR phosphorylation remained elevated in the PLA (3.6 ± 0.6-fold) and increased in the TA (4.6 ± 0.9-fold, p < 0.05) 6 hr following HFES. Interestingly, mTOR activation occurred predominantly in fibers expressing the type IIa but not type I MHC isoform. Further, HFES induced modest p70S6K phosphorylation immediately after exercise in PLA (0.4 ± 0.1-fold, p < 0.05) but not TA, and more markedly 6 hr after in both the PLA and TA (1.4 ± 0.4 vs. 2.4 ± 0.3-fold, respectively, p < 0.01). Akt/PKB phosphorylation was similar to controls at both time points. These results suggest that mTOR signaling is increased after a single bout of muscle contractile activity. Despite reports that mTOR is activated downstream of Akt/PKB, in this study, HFES induced mTOR signaling independent of Akt/PKB phosphorylation. Fiber type-dependent mTOR phosphorylation may be a molecular basis by which some fiber types are more susceptible to contraction-induced hypertrophy.
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