Abstract
BackgroundSarcopenia, the loss of skeletal muscle mass during aging, increases the risk for falls and dependency. Resistance exercise (RE) training is an effective treatment to improve muscle mass and strength in older adults, but aging is associated with a smaller amount of training-induced hypertrophy. This may be due in part to an inability to stimulate muscle-protein synthesis (MPS) after an acute bout of RE. We hypothesized that older adults would have impaired mammalian target of rapamycin complex (mTORC)1 signaling and MPS response compared with young adults after acute RE.MethodsWe measured intracellular signaling and MPS in 16 older (mean 70 ± 2 years) and 16 younger (27 ± 2 years) subjects. Muscle biopsies were sampled at baseline and at 3, 6 and 24 hr after exercise. Phosphorylation of regulatory signaling proteins and MPS were determined on successive muscle biopsies by immunoblotting and stable isotopic tracer techniques, respectively.ResultsIncreased phosphorylation was seen only in the younger group (P< 0.05) for several key signaling proteins after exercise, including mammalian target of rapamycin (mTOR), ribosomal S6 kinase (S6K)1, eukaryotic initiation factor 4E-binding protein (4E-BP)1 and extracellular signal-regulated kinase (ERK)1/2, with no changes seen in the older group (P >0.05). After exercise, MPS increased from baseline only in the younger group (P< 0.05), with MPS being significantly greater than that in the older group (P <0.05).ConclusionsWe conclude that aging impairs contraction-induced human skeletal muscle mTORC1 signaling and protein synthesis. These age-related differences may contribute to the blunted hypertrophic response seen after resistance-exercise training in older adults, and highlight the mTORC1 pathway as a key therapeutic target to prevent sarcopenia.
Highlights
Maintenance of skeletal muscle mass is largely dependent on the dynamic relationship of muscle-protein balance, which is the relationship between protein synthesis and protein breakdown
We found that muscle-protein synthesis (MPS) and associated translational signaling through the mTORC1 and mitogen-activated protein kinase (MAPK) pathways are upregulated at multiple post-exercise time points in younger subjects, with a depressed response in both intracellular signaling and MPS after an acute bout of resistance exercise in older subjects
High-intensity resistance exercise is well established as a potent stimulus for MPS and hypertrophy in young adults [13,14,16,19,32,33,34], and we have shown that a single bout of resistance exercise at 70% 1 repetition maximum (1RM) increases MPS during exercise recovery [15]
Summary
Maintenance of skeletal muscle mass is largely dependent on the dynamic relationship of muscle-protein balance, which is the relationship between protein synthesis and protein breakdown. Resistance exercise is capable of increasing muscle mass through direct stimulation of MPS, which, over time, induces contractile protein accumulation and hypertrophy of individual muscle fibers. The fractional synthetic rate (FSR) of muscle proteins has been shown to be increased in as little as 1 hour [15] and for as long as 48 hours [16,17,18] after an unaccustomed, acute bout of resistance exercise. Resistance exercise (RE) training is an effective treatment to improve muscle mass and strength in older adults, but aging is associated with a smaller amount of training-induced hypertrophy. This may be due in part to an inability to stimulate muscle-protein synthesis (MPS) after an acute bout of RE. We hypothesized that older adults would have impaired mammalian target of rapamycin complex (mTORC) signaling and MPS response compared with young adults after acute RE
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