IntroductionThe increase in body fat and decrease in muscle mass during aging are associated with physical deterioration and degenerative diseases and cause obesity via the accumulation of abdominal fat. This increases insulin resistance as well as the production of cytokines (tumor necrosis factor-α, TNF-α; interleukin-4, IL-4; monocyte chemoattractant protein-1, MCP-1), which cause inflammation, and adipocytokines, which promote catabolism in muscles, thereby reducing muscle/ myo-function. These processes lead to obesity and ultimately to insulin resistance syndrome, diabetes, and cardiovascular diseases. Considering the recent domestic trend characterized by a rapidly aging population owing to an extension in the average life span and change in the population composition, it is necessary to analyze sarcopenic obesity and insulin resistance and to develop strategies for active prevention.In this review, the effects of aerobic exercise training, one of the major preventative methods for obesity, on endoplasmic reticulum (ER) stress and sarcopenic obesity caused by obesity and aging as well as insulin resistance syndrome were determined to analyze the correlations between these phenotypes. Asian J Kinesiol 2018; 20(3):1-10· DOI: https://doi.org/10.15758/ajk.2018.20.3 Endoplasmic reticulum (ER) stress associated with sarcopenic obesity in obesity and aging, which is a key factor in insulin resistance, are highly related. Long-term exercise training reduces ER stress via the activation of JUN N-terminal kinase (JNK) and reduction of nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, alpha (IκBα) decomposition and improves insulin resistance. Sarcopenia is associated with multiple factors, including increased pro-inflammation cytokine, oxidative stress, ER stress and fat infiltration as well as reduced mitochondrial function. Interaction between unfold protein response (UPR) and autophagy may play an important role to maintain the muscle protein quality control. The key factor in protein synthesis pathway for protein quality control is mammalian target of rapamycin complex 1 (mTORC1), indeed aging impairs contraction-induced human skeletal muscle mTORC1 signaling and protein synthesis. During exercise, mTOR pathway might be decreased that may result in an increase autophagy, because mTOR is a negative feedback factor for autophagy. Particularly, increased mTOR after exercise will be decrease autophagy. However, the effects of specific exercise training programs (type, intensity, time, frequency, etc.) and the mechanisms underlying these relationships are unclear. Therefore, it is necessary to establish the mechanisms of diabetes mellitus, focusing on sarcopenic obesity in obesity and aging, ER stress, and insulin resistance, and to analyze the effects of exercise training from a molecular biological perspective.
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