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This study aimed to determine whether aerobic exercise could ameliorate pressure overload\u2010induced heart hypertrophy through M<jats:sub>2<\/jats:sub>AChR, and to elucidate the underlying mechanisms of action. Mice were used to establish the myocardial hypertrophy model by transverse aortic constriction (TAC), and subjected to 2, 4, and 8 weeks of moderate\u2010intensity aerobic exercise and choline intervention (14\u2009mg\/kg\/day). Our results showed that 4 and 8 weeks of exercise and choline intervention reduced excessive mitochondrial fission and autophagy of myocardial mitochondria, thereby improving the ultrastructure and function of mitochondria after TAC. Moreover, 8\u2010week exercise and choline intervention have enhanced parasympathetic function and promoted the expression of M<jats:sub>2<\/jats:sub>AChR. In addition, 8\u2010week exercise and choline intervention also inhibited the protein expression of myocardial MFN2, PERK\/eIF2\u03b1\/ATF4, and NLRP3\/caspase\u20101\/IL\u20101\u03b2 signaling pathways, thereby effectively reducing mitochondrial fusion, endoplasmic reticulum stress, and inflammation. Taken together, these data suggest that pressure overload led to cardiac hypertrophy, cardiac dysfunction, and decreased parasympathetic function in cardiac tissues. Aerobic exercise attenuated cardiac dysfunction by modulating the expression of proteins involved in mitochondrial quality control, and induced endoplasmic reticulum stress and inflammation, thereby reducing cardiac hypertrophy and improving cardiac function in impaired heart tissues following TAC, which was likely mediated by M<jats:sub>2<\/jats:sub>AChR activation.<\/jats:p>","DOI":"10.1002\/jcp.30342","type":"journal-article","created":{"date-parts":[[2021,2,22]],"date-time":"2021-02-22T07:46:54Z","timestamp":1613980014000},"page":"6581-6596","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":50,"title":["Aerobic exercise ameliorates cardiac hypertrophy by regulating mitochondrial quality control and endoplasmic reticulum stress through M<sub>2<\/sub>AChR"],"prefix":"10.1002","volume":"236","author":[{"given":"Mei","family":"Ma","sequence":"first","affiliation":[{"name":"Institute of Sports and Exercise Biology, School of 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