{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,11,3]],"date-time":"2026-11-03T15:57:41Z","timestamp":1793721461796,"version":"4.6.1"},"reference-count":42,"publisher":"American Physiological Society","issue":"2","funder":[{"DOI":"10.13039\/501100012226","name":"MOE | Fundamental Research Funds for the Central Universities","doi-asserted-by":"publisher","award":["GK202103121"],"award-info":[{"award-number":["GK202103121"]}],"id":[{"id":"10.13039\/501100012226","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["31671240"],"award-info":[{"award-number":["31671240"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["journals.physiology.org"],"crossmark-restriction":true},"short-container-title":["American Journal of Physiology-Cell Physiology"],"published-print":{"date-parts":[[2022,2,1]]},"abstract":"<jats:p>\n                    Myocardial infarction (MI)-induced heart failure (HF) is commonly accompanied with profound effects on skeletal muscle. With the process of MI-induced HF, perturbations in skeletal muscle contribute to muscle atrophy. Exercise is viewed as a feasible strategy to prevent muscle atrophy. The aims of this study were to investigate whether exercise could alleviate MI-induced skeletal muscle atrophy via insulin-like growth factor 1 (IGF-1) pathway in mice. Male C57\/BL6 mice were used to establish the MI model and were divided into three groups: sedentary MI group (MI), MI with aerobic exercise group, and MI with resistance exercise group; sham-operated group was used as control. Exercise-trained animals were subjected to 4 wk of aerobic exercise (AE) or resistance exercise (RE). Cardiac function, muscle weight, myofiber size, levels of IGF-1 signaling and proteins related to myogenesis, protein synthesis, and degradation and apoptosis in gastrocnemius muscle were detected. H\n                    <jats:sub>2<\/jats:sub>\n                    O\n                    <jats:sub>2<\/jats:sub>\n                    -treated C2C12 cells were intervened with recombinant human IGF-1, IGF-1 receptor (IGF-1R) inhibitor NVP-AEW541, and PI3K inhibitor LY294002 to explore the mechanism. Exercises upregulated the IGF-1\/IGF-1R-phosphatidylinositol 3-kinase (PI3K)\/protein kinase B (Akt) signaling; increased the expressions of Pax7, myogenic regulatory factors (MRFs), and protein synthesis; and reduced protein degradation and cell apoptosis in MI mice. In vitro, IGF-1 upregulated the levels of Pax7, MRFs, mTOR, and P70S6K; reduced MuRF1 and MAFbx; and inhibited cell apoptosis via IGF-1R-PI3K\/Akt pathway. AE and RE, safely and effectively, alleviate skeletal muscle atrophy by regulating the levels of myogenesis, protein degradation, and cell apoptosis in mice with MI via activating IGF-1\/IGF-1R-PI3K\/Akt signaling pathway.\n                  <\/jats:p>","DOI":"10.1152\/ajpcell.00344.2021","type":"journal-article","created":{"date-parts":[[2021,12,1]],"date-time":"2021-12-01T17:42:36Z","timestamp":1638380556000},"page":"C164-C176","update-policy":"https:\/\/doi.org\/10.1152\/aps-crossmark-policy","source":"Crossref","is-referenced-by-count":144,"title":["Aerobic exercise and resistance exercise alleviate skeletal muscle atrophy through IGF-1\/IGF-1R-PI3K\/Akt pathway in mice with myocardial infarction"],"prefix":"10.1152","volume":"322","author":[{"given":"Lili","family":"Feng","sequence":"first","affiliation":[{"name":"Institute of Sports Biology, College of Physical Education, Shaanxi Normal University, Xi\u2019an, People\u2019s Republic of 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