Department of Physical Medicine and Rehabilitation, Tianjin Medical University General hospital, Tianjin, China.
Department of Physical Medicine and Rehabilitation, Tianjin Medical University General hospital, Tianjin, China.
Heart Lung Circ. 2021 May;30(5):773-780. doi: 10.1016/j.hlc.2020.08.004. Epub 2020 Sep 19.
High-intensity interval training (HIIT) and aerobic training (AT) both improve cardiac function; however, their effects on cardiac function after myocardial infarction (MI) and the molecular mechanisms are unclear. In this study, HIIT, AT and sedentary (SED) interventions were performed for 4 weeks to compare the effects on cardiac function after MI and explore a more suitable approach for clinical application and the potential mechanisms.
Twenty-four (24) male rats were randomly divided into a control group (CON), MI-sedentary group (MI-SED), MI-aerobic training group (MI-AT), and MI-high-intensity interval training group (MI-HIIT). After 4 weeks of intervention the exercise capacity, heart rate (HR), left ventricular end-diastolic diameter (LVEDD), left ventricular end systolic diameter (LVESD), left ventricular ejection fraction (LVEF), AMP-activated protein kinase α1 (AMPKα1), cardiomyocyte morphology, and cardiac mitochondria were assessed.
After intervention: 1) exercise capacity in the MI-AT (49.08±3.141 m; p<0.001) and MI-HIIT (51.70±7.572 m; p<0.001) groups was significantly more increased than the MI-SED group; there was no significant difference between the MI-AT and MI-HIIT group (p=0.33). 2) LVEDD and LVESD in the MI-SED (p<0.01) and MI-HIIT (p<0.01) groups was significantly more increased than the CON group; the MI-AT group showed no significant difference in LVEDD and LVESD compared with the CON group; LVEF in the MI-AT (53.47±7.913%; p=0.03) and MI-HIIT (56.20±7.224%; p=0.006) groups was significantly more increased than the MI-SED group, and there was no statistical difference between the MI-AT and MI-HIIT groups. 3) AMPKα1 expression was significantly increased in the MI-AT (1.15±0.264; p=0.001) and MI-HIIT (1.04±0.238; p=0.003) groups and decreased in the MI-SED group (0.71±0.257; p<0.001) when compared with the CON group. 4) The MI-SED group exhibited sarcoplasmic dissolution and fibrous hyperplasia in the myocardium, cardiac mitochondrial damage and reduced mitochondrial numbers; the MI-HIIT group displayed swollen and vacuolated cardiac mitochondria with disrupted cristae; the MI-AT and MI-HIIT groups had significantly increased cardiac mitochondrial numbers than the MI-SED group; there was no statistical difference between the MI-AT and MI-HIIT groups.
Aerobic training and HIIT for 4 weeks had similar cardioprotection and were superior to SED intervention. Both AT and HIIT improved cardiac function and exercise capacity by upregulating AMPKα1 expression. However, 4 weeks of intervention resulted in left ventricular dilation and cardiac myocardial mitochondrial injury in the MI-HIIT group.
高强度间歇训练（HIIT）和有氧运动（AT）均可改善心功能；然而，它们对心肌梗死（MI）后的心脏功能的影响及其分子机制尚不清楚。在这项研究中，我们进行了 4 周的 HIIT、AT 和久坐（SED）干预，以比较它们对 MI 后心功能的影响，并探索更适合临床应用的方法和潜在机制。
将 24 只雄性大鼠随机分为对照组（CON）、MI-SED 组、MI-AT 组和 MI-HIIT 组。干预 4 周后，评估运动能力、心率（HR）、左室舒张末期直径（LVEDD）、左室收缩末期直径（LVESD）、左室射血分数（LVEF）、AMP 激活蛋白激酶α1（AMPKα1）、心肌细胞形态和心脏线粒体。
干预后：1）MI-AT（49.08±3.141 m；p<0.001）和 MI-HIIT（51.70±7.572 m；p<0.001）组的运动能力明显高于 MI-SED 组；MI-AT 组和 MI-HIIT 组之间无显著差异（p=0.33）。2）MI-SED 组和 MI-HIIT 组的 LVEDD 和 LVESD 明显高于 CON 组（p<0.01）；MI-AT 组与 CON 组的 LVEDD 和 LVESD 无显著差异；MI-AT 组（53.47±7.913%；p=0.03）和 MI-HIIT 组（56.20±7.224%；p=0.006）的 LVEF 明显高于 MI-SED 组，且 MI-AT 组和 MI-HIIT 组之间无统计学差异。3）MI-AT（1.15±0.264；p=0.001）和 MI-HIIT（1.04±0.238；p=0.003）组的 AMPKα1 表达明显高于 CON 组，而 MI-SED 组则明显低于 CON 组（0.71±0.257；p<0.001）。4）MI-SED 组心肌出现肌浆溶解和纤维增生、心肌线粒体损伤和数量减少；MI-HIIT 组心肌线粒体肿胀、空泡化，嵴断裂；MI-AT 组和 MI-HIIT 组的心肌线粒体数量明显多于 MI-SED 组；MI-AT 组和 MI-HIIT 组之间无统计学差异。
4 周的有氧运动和 HIIT 具有相似的心脏保护作用，优于 SED 干预。AT 和 HIIT 均可通过上调 AMPKα1 表达来改善心功能和运动能力。然而，4 周的干预导致 MI-HIIT 组左心室扩张和心肌线粒体损伤。
