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1 Department of Health Sciences, Sargent College of Health and Rehabilitation Sciences, Boston University, Boston, MA, USA
2 Department of Health Sciences, Sargent College of Health and Rehabilitation Sciences, Boston University, Boston, MA, USA; Center for the Molecular Stress Response, Boston University School of Medicince, Boston, MA, USA
* To whom correspondence should be addressed. E-mail: fielding{at}bu.edu.
With age, skeletal muscle experiences substantial atrophy and weakness. While resistance training can increase muscle size and strength, the myogenic response to exercise and the capacity for muscle hypertrophy in older humans and animals is limited. In the present study, we assessed the ability of muscle contractile activity to activate cellular pathways involved in muscle cell growth and myogenesis in adult (6-month) and old(30-month) Fischer 344BN rats. A single bout of rat hindlimb muscle contractile activity was elicited by high frequency electrical stimulation (HFES) of the sciatic nerve. Plantaris (PLA) and tibialis anterior (TA) muscles were assayed for mTOR, p70S6K, and ERK 1/2 phosphorylation and total protein either at baseline, immediately after, or six hours after HFES. mTOR phosphorylation was elevated in PLA (1.3 ± 0.3-fold, p < 0.05) immediately after HFES and to a lesser extent six hours after HFES (0.6 ± 0.1-fold, p < 0.05) in old rats. Post-HFES, p70S6K phosphorylation increased 1.2 ± 0.3 fold in TA (p < 0.05, figure 3) and remained elevated six hours later (0.6 ± 0.2-fold, p < 0.05) in old rats. ERK phosphorylation was lower in old animals immediately after exercise in both TA (11.1 ± 2.9 vs. 2.1 ± 0.5-fold, p < 0.05) and PLA (6.5 ± 1.5 vs. 1.8 ± 0.5-fold, p < 0.05) and returned to baseline by six hours in both age groups. These results suggest that mTOR and ERK 1/2 signaling are attenuated following in situ muscle contractile activity in older animals and may reflect an impaired anabolic response to exercise.
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