4.7 Article

Interval exercise training increases LIF expression and prevents myocardial infarction-induced skeletal muscle atrophy in rats

Journal

LIFE SCIENCES
Volume 193, Issue -, Pages 77-86

Publisher

PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.lfs.2017.12.009

Keywords

Interval exercise training; Myocardial infarction; Skeletal muscle atrophy; Leukemia inhibitory factor

Funding

  1. National Natural Science Foundation of China [31371199, 31171141]

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Aims: Myocardial infarction (MI) is commonly associated with body weight loss and skeletal muscle atrophy. Studies have shown that exercise training could give beneficial effects on skeletal muscle growth. Leukemia inhibitory factor (LIF) is a key regulator of muscle growth and regeneration. The aim of this study was to investigate the effects of interval exercise training (IET) on the expression of LIF and the MI-induced skeletal muscle atrophy. Main methods: Male Sprague-Dawley rats were used to establish the MI model by ligation of the left anterior descending coronary artery. Infarcted Rats were divided into two groups: sedentary MI group (MI) and MI with interval exercise group (ME), and compared to sham-operated group (Sham). Exercise-trained animals were subjected to eight weeks of IET. Cardiac function, collagen volume fraction, expression of LIF and its receptor LIFR, myofiber size, apoptosis and proliferation in gastrocnemius muscle were analyzed. Key findings: IET increased heart functional performance and was accompanied with reversing cardiac pathological remodeling. Moreover, IET increased the expression of LIF and LIFR, activated signal transducer and activator of transcription (STAT3), reduced apoptosis and promoted proliferation in gastrocnemius muscle compared with the MI group. In addition, there was a significant negative correlation between skeletal muscle atrophy and LIF expression which was stimulated by IET in infarcted rats. Significance: IET reverses MI-induced cardiac dysfunction and skeletal muscle atrophy. In addition, IET upregulates the expression of muscle LIF/LIFR and activates the STAT3.

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