Rodrigues Eder Anderson, Lima Aline Regina Ruiz, Gomes Mariana Janini, Souza Lidiane Moreira, Pontes Thierres Hernani Dias, Pagan Luana Urbano, Murata Gilson Masahiro, Damatto Felipe Cesar, Carvalho Depra Igor, Rego Amanda Bergamo Gonçalves Castro, Reyes David Rafael Abreu, Zornoff Leonardo Antonio Mamede, Okoshi Katashi, Okoshi Marina Politi
Department of Internal Medicine, Botucatu Medical School, Sao Paulo State University (UNESP), Botucatu 18618-687, SP, Brazil.
Department of Kinesiology and Sport Management, Texas A&M University, College Station, TX 77845, USA.
Antioxidants (Basel). 2023 Apr 7;12(4):896. doi: 10.3390/antiox12040896.
Exercise is an important therapeutic strategy for preventing and treating myocardial infarction (MI)-induced cardiac remodeling and heart failure. However, the myocardial effects of resistance exercise on infarcted hearts are not completely established. In this study, we investigated the effects of resistance exercise on structural, functional, and molecular cardiac alterations in infarcted rats.
Three months after MI induction or simulated surgery, Wistar rats were assigned into three groups: Sham ( = 14); MI ( = 9); and exercised MI (MI-Ex, = 13). Exercised rats performed, 3 times a week for 12 weeks, four climbs on a ladder with progressive loads. Cardiac structure and left ventricle (LV) function were analyzed by echocardiogram. Myocyte diameters were evaluated in hematoxylin- and eosin-stained histological sections as the smallest distance between borders drawn across the nucleus. Myocardial energy metabolism, lipid hydroperoxide, malondialdehyde, protein carbonylation, and antioxidant enzyme activities were evaluated by spectrophotometry. Gene expressions of NADPH oxidase subunits were evaluated by RT-PCR. Statistical analyses were performed using ANOVA and Tukey or Kruskal-Wallis and Dunn's test.
Mortality did not differ between the MI-Ex and MI groups. MI had dilated left atrium and LV, with LV systolic dysfunction. Exercise increased the maximum load-carrying capacity, with no changes in cardiac structure or LV function. Myocyte diameters were lower in MI than in Sham and MI-Ex. Lactate dehydrogenase and creatine kinase activity were lower in MI than in Sham. Citrate synthase and catalase activity were lower in MI and MI-Ex than in Sham. Lipid hydroperoxide concentration was lower in MI-Ex than in MI. Nox2 and p22phox gene expressions were higher in MI-Ex than in Sham. Gene expression of Nox4 was higher in MI and MI-Ex than in Sham, and p47phox was lower in MI than in Sham.
Late resistance exercise was safe in infarcted rats. Resistance exercise improved maximum load-carrying capacity, reduced myocardial oxidative stress, and preserved myocardial metabolism, with no changes in cardiac structure or left ventricle function in infarcted rats.
运动是预防和治疗心肌梗死（MI）诱发的心脏重塑和心力衰竭的重要治疗策略。然而，抗阻运动对梗死心脏的心肌影响尚未完全明确。在本研究中，我们调查了抗阻运动对梗死大鼠心脏结构、功能和分子变化的影响。
在诱导心肌梗死或模拟手术后三个月，将Wistar大鼠分为三组：假手术组（n = 14）；心肌梗死组（n = 9）；运动心肌梗死组（MI-Ex，n = 13）。运动大鼠每周进行3次，共12周，每次在有递增负荷的梯子上攀爬四次。通过超声心动图分析心脏结构和左心室（LV）功能。在苏木精和伊红染色的组织切片中评估心肌细胞直径，即穿过细胞核绘制的边界之间的最小距离。通过分光光度法评估心肌能量代谢、脂质过氧化氢、丙二醛、蛋白质羰基化和抗氧化酶活性。通过RT-PCR评估NADPH氧化酶亚基的基因表达。使用方差分析和Tukey检验或Kruskal-Wallis检验和Dunn检验进行统计分析。
MI-Ex组和MI组的死亡率无差异。MI导致左心房和左心室扩张，伴有左心室收缩功能障碍。运动增加了最大承载能力，心脏结构或左心室功能无变化。MI组的心肌细胞直径低于假手术组和MI-Ex组。MI组的乳酸脱氢酶和肌酸激酶活性低于假手术组。MI组和MI-Ex组的柠檬酸合酶和过氧化氢酶活性低于假手术组。MI-Ex组的脂质过氧化氢浓度低于MI组。MI-Ex组的Nox2和p22phox基因表达高于假手术组。MI组和MI-Ex组的Nox4基因表达高于假手术组，MI组的p47phox低于假手术组。
晚期抗阻运动对梗死大鼠是安全的。抗阻运动提高了最大承载能力，降低了心肌氧化应激，并维持了心肌代谢，梗死大鼠的心脏结构或左心室功能无变化。
