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Skeletal muscle anabolic response to resistance exercise and essential amino acids is delayed with aging
Author(s) -
Drummond Micah J,
Dreyer Hans C,
Pennings Bart,
Fry Christopher S,
Dhanani Shaheen,
Dillon Edgar L,
SheffieldMoore Melinda,
Volpi Elena,
Rasmussen Blake B
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.959.17
Subject(s) - sarcopenia , anabolism , ampk , medicine , skeletal muscle , endocrinology , ingestion , p70 s6 kinase 1 , insulin resistance , pi3k/akt/mtor pathway , phosphorylation , signal transduction , biology , insulin , microbiology and biotechnology , protein kinase a
The loss of skeletal muscle during aging (sarcopenia) leads to an increased risk of falls, fractures and eventually loss of independence. Resistance exercise (RE) is a useful intervention to prevent sarcopenia, however, the response to RE is less when compared to young subjects. Essential amino acids (EAA) increase muscle protein synthesis (MPS) equally in both young and old subjects. We hypothesized that EAA ingestion following RE would restore anabolic signaling and MPS in aging muscle. Young and old men ingested 20g of EAA 1hr following a bout of leg‐RE. Muscle biopsies were obtained before, 1, 3, and 6hr post‐exercise to measure MPS and signaling pathways which regulate translation initiation. MPS increased early in young (1–3hr post‐exercise) and later in old (3–6hr post‐exercise). RE activated ERK1/2 and eIF2α signaling only in the young 1hr post‐exercise. mTOR/S6K1 signaling was similar between groups at all time points and AMPKα phosphorylation was higher in old 1–3hr post‐exercise. We conclude that MPS after RE and EAA ingestion is similar between young and old but delayed with aging. Unresponsive ERK1/2 signaling and AMPK activation in aging may explain the delayed activation of MPS. Notwithstanding, the combination of RE and EAA should be a useful strategy to combat sarcopenia. Supported by NIH/NIAMS grant # R01 AR049877 and NIH/NIA P30 AG024832