Department of Cardiac Rehabilitation, Zhejiang Hospital, Hangzhou, 310013, Zhejiang, China.
Zhejiang Provincial Key Laboratory of Geriatrics & Geriatrics Institute of Zhejiang Province, Hangzhou, 310013, Zhejiang, China.
Biomed Pharmacother. 2020 Nov;131:110690. doi: 10.1016/j.biopha.2020.110690. Epub 2020 Sep 2.
Exercise training is beneficial for cardiac rehabilitation. Nevertheless, few study focused on the role of high-intensity interval training (HIIT) in cardiac repair. The current study aimed to elucidate the effect of HIIT on cardiac rehabilitation and the involved mechanisms after acute myocardial infarction (MI).
A total of 65 male rats underwent coronary ligation or sham operation and were randomly assigned to 4 groups: sham (n = 10), sedentary (MI-Sed, n = 12), moderate-intensity continuous training (MI-MCT, n = 12) and HIIT (MI-HIIT, n = 12). One week after MI induction, adaptive training starts follow by formal training. After the experiment, cardiac functions were determined by echocardiography and hemodynamic measurements. Changes in infarct size, collagen accumulation, myofibroblasts, angiogenesis, inflammation level, endothelin-1 (ET-1), and renin-angiotensin-aldosterone system (RAAS) activities were measured. Data were analyzed by one-way ANOVA.
After MI, cardiac structure and function were significantly deteriorated. However, post-MI HIIT for 8 weeks had significantly ameliorated left ventricular end-diastolic pressure (LVEDP), LV systolic pressure (LVSP), and maximum peak velocities of relaxation (-dP/dtmax). Moreover, it preserved cardiac functions, reduced infarct size, protected the myocardium structure, increased angiogenesis and decreased the myofibroblasts and collagen accumulation. HIIT for 4 weeks had no effect on LVEDP, -dP/dtmax, infarct size and angiogenesis. Additionally, it induced inflammation response and repressed ET-1 and RAAS activities were found in myocardium and peripheral circulation after HIIT.
Our results suggested that post-MI HIIT had a positive role in cardiac repair, which might be linked with the induction of inflammation and inhibition of ET-1 and RAAS activities.
运动训练有益于心脏康复。然而，很少有研究关注高强度间歇训练（HIIT）在心脏修复中的作用。本研究旨在阐明 HIIT 对急性心肌梗死（MI）后心脏康复的作用及其涉及的机制。
共 65 只雄性大鼠行冠状动脉结扎或假手术，并随机分为 4 组：假手术组（n=10）、安静组（MI-Sed，n=12）、中等强度持续训练组（MI-MCT，n=12）和 HIIT 组（MI-HIIT，n=12）。MI 诱导后 1 周开始适应性训练，然后进行正式训练。实验结束后，通过超声心动图和血流动力学测量来评估心功能。测量梗死面积、胶原沉积、肌成纤维细胞、血管生成、炎症水平、内皮素-1（ET-1）和肾素-血管紧张素-醛固酮系统（RAAS）活性的变化。数据采用单因素方差分析进行分析。
MI 后，心脏结构和功能明显恶化。然而，MI 后 8 周进行 HIIT 可显著改善左室舒张末期压（LVEDP）、左室收缩压（LVSP）和最大舒张速度（-dP/dtmax）。此外，它还能维持心脏功能，减小梗死面积，保护心肌结构，增加血管生成，减少肌成纤维细胞和胶原沉积。MI 后 4 周进行 HIIT 对 LVEDP、-dP/dtmax、梗死面积和血管生成无影响。此外，在 HIIT 后心肌和外周循环中发现炎症反应增加，ET-1 和 RAAS 活性受到抑制。
我们的结果表明，MI 后 HIIT 对心脏修复具有积极作用，这可能与诱导炎症反应以及抑制 ET-1 和 RAAS 活性有关。
