Strength training improves heart function, collagen and strength in rats with heart failure

医学 收缩性 心力衰竭 心脏病学 内科学 心功能曲线 心肌梗塞 肌肉肥大 射血分数 心室重构 纤维化 力量训练 物理疗法
作者
Leisiane G. Dias,Carlos H. O. Reis,Leonardo dos Santos,Walter Krause Neto,Ana Paula Lima‐Leopoldo,Julien S. Baker,André Soares Leopoldo,Danilo Sales Bocalini
出处
期刊:Journal of Physiological Sciences [Springer Nature]
卷期号:74 (1)
标识
DOI:10.1186/s12576-024-00899-3
摘要

Abstract Background/objectives Myocardial infarction (MI) frequently leads to cardiac remodeling and failure with impaired life quality, playing an important role in cardiovascular deaths. Although physical exercise is a well-recognized effective non-pharmacological therapy for cardiovascular diseases, the effects of strength training (ST) on the structural and functional aspects of cardiac remodeling need to be further documented. In this study, we aimed to investigate the role of a linear block ST protocol in the rat model of MI. Methods and results After 6 weeks of MI induction or sham surgery, male adult rats performed ST for the following 12 weeks. The ladder-based ST program was organized in three mesocycles of 4 weeks, with one load increment for each block according to the maximal carrying load test. After 12 weeks, the infarcted-trained rats exhibited an increase in performance, associated with reduced cardiac hypertrophy and pulmonary congestion compared with the untrained group. Despite not changing MI size, the ST program partially prevented cardiac dilatation and ventricular dysfunction assessed by echocardiography and hemodynamics, and interstitial fibrosis evaluated by histology. In addition, isolated cardiac muscles from infarcted-trained rats had improved contractility parameters in a steady state, and in response to calcium or stimuli pauses. Conclusions The ST in infarcted rats increased the capacity to carry mass, associated with attenuation of cardiac remodeling and pulmonary congestion with improving cardiac function that could be attributed, at least in part, to the improvement of myocardial contractility.

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