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Mechanism of Skeletal Muscle Contraction: Intracellular Signaling in Skeletal Muscle Contraction

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Musculoskeletal Disease Associated with Diabetes Mellitus
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Abstract

Regular exercise contributes to maintaining the skeletal muscle mass and quality, which may prevent type II diabetes, hypertension, coronary heart disease, and/or sarcopenia. Exercise/muscle contraction induces activation or inactivation of the intracellular molecules for a short period, which results in an increased glucose uptake, fatty acid oxidation, and protein synthesis. Exercise also affects transcription factors and coactivators, which change the target gene expression and are related to muscle adaptations such as increasing glucose transport-related protein, mitochondrial biogenesis, and the muscle fiber type transition over a long period. Alterations of these molecules are mediated by changes in the intracellular Ca2+ level, energy status level, and/or the activated mitogen-activated protein kinase (MAPK) signaling pathway. In this section, the intracellular signaling pathway induced by skeletal muscle contraction is discussed.

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Manabe, Y. (2016). Mechanism of Skeletal Muscle Contraction: Intracellular Signaling in Skeletal Muscle Contraction. In: Inaba, M. (eds) Musculoskeletal Disease Associated with Diabetes Mellitus. Springer, Tokyo. https://doi.org/10.1007/978-4-431-55720-3_10

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