期刊
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
卷 23, 期 17, 页码 -出版社
MDPI
DOI: 10.3390/ijms23179735
关键词
dexamethasone; muscle atrophy; essential amino acids; resistance exercise training; physical performance; mitochondrial biogenesis; neuromuscular junction stability; protein turnover; glucose metabolic flux
资金
- Basic Science Research Program through the National Research Foundation of Korea (NRF) - Ministry of Science and ICT [2020R1F1A106680913]
- National Research Foundation of Korea (NRF) - Korea government (MSIT) [2021R1A2C3005801]
- Basic Science Research Capacity Enhancement Project through the Korea Basic Science Institute (National research Facilities and Equipment Center) - Ministry of Education [2021R1A6C101A432]
- National Research Foundation of Korea [2021R1A2C3005801] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
In this study, it was found that essential amino acids (EAA) and resistance exercise training (RET) synergistically improved muscle mass and/or strength, endurance capacity, insulin sensitivity, and glucose metabolism in dexamethasone (DEX)-treated muscle. These improvements were achieved, in part, through enhancements in myofibrillar protein synthesis, neuromuscular junction stability, fiber type preservation, and/or mitochondrial biogenesis.
Our previous study shows that an essential amino acid (EAA)-enriched diet attenuates dexamethasone (DEX)-induced declines in muscle mass and strength, as well as insulin sensitivity, but does not affect endurance. In the present study, we hypothesized that the beneficial effects will be synergized by adding resistance exercise training (RET) to EAA, and diet-free EAA would improve endurance. To test hypotheses, mice were randomized into the following four groups: control, EAA, RET, and EAA+RET. All mice except the control were subjected to DEX treatment. We evaluated the cumulative rate of myofibrillar protein synthesis (MPS) using (H2O)-H-2 labeling and mass spectrometry. Neuromuscular junction (NMJ) stability, mitochondrial contents, and molecular signaling were demonstrated in skeletal muscle. Insulin sensitivity and glucose metabolism using C-13(6)-glucose tracing during oral glucose tolerance tests were analyzed. We found that EAA and RET synergistically improve muscle mass and/or strength, and endurance capacity, as well as insulin sensitivity, and glucose metabolism in DEX-treated muscle. These improvements are accomplished, in part, through improvements in myofibrillar protein synthesis, NMJ, fiber type preservation, and/or mitochondrial biogenesis. In conclusion, free EAA supplementation, particularly when combined with RET, can serve as an effective means that counteracts the adverse effects on muscle of DEX that are found frequently in clinical settings.
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