PDF(Pubmed)
Abstract：
OBJECTIVE: 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.
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.
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.
摘要：
目的：心肌梗死（MI）常导致心脏重构和衰竭，降低生活质量，在心血管死亡中起着重要作用。虽然体育锻炼是公认的有效的非药物治疗心血管疾病，力量训练(ST)对心脏重构的结构和功能方面的影响需要进一步记录.在这项研究中,我们旨在研究线性阻断ST方案在大鼠MI模型中的作用.
结果：MI诱导或假手术6周后，雄性成年大鼠在接下来的12周内进行ST。以阶梯为基础的ST计划在4周的三个周期内组织，根据最大承载载荷试验，每个块有一个载荷增量。12周后,梗塞训练的大鼠表现出提高的表现，与未训练组相比，心脏肥大和肺充血减少。尽管没有改变MI大小，通过超声心动图和血流动力学评估，ST程序部分预防了心脏扩张和心室功能障碍，和间质纤维化通过组织学评估。此外,来自梗塞训练大鼠的离体心肌在稳定状态下改善了收缩性参数，并响应钙或刺激暂停。
结论：梗死大鼠的ST增加了携带肿块的能力，与心脏重塑和肺充血的衰减相关，可归因于改善心脏功能，至少在某种程度上,改善心肌收缩力。
结果：MI诱导或假手术6周后，雄性成年大鼠在接下来的12周内进行ST。以阶梯为基础的ST计划在4周的三个周期内组织，根据最大承载载荷试验，每个块有一个载荷增量。12周后,梗塞训练的大鼠表现出提高的表现，与未训练组相比，心脏肥大和肺充血减少。尽管没有改变MI大小，通过超声心动图和血流动力学评估，ST程序部分预防了心脏扩张和心室功能障碍，和间质纤维化通过组织学评估。此外,来自梗塞训练大鼠的离体心肌在稳定状态下改善了收缩性参数，并响应钙或刺激暂停。
结论：梗死大鼠的ST增加了携带肿块的能力，与心脏重塑和肺充血的衰减相关，可归因于改善心脏功能，至少在某种程度上,改善心肌收缩力。
