Avaliação da remodelação cardíaca de ratos espontaneamente hipertensos submetidos ao treinamento intervalado de alta intensidade

Abstract

Introduction: Hypertension, is a serious public health problem, can lead to concentric hypertrophy - an important risk factor for heart failure, which is considered a predictor of greater cardiovascular morbidity and mortality. High Intensity Interval Training (HIIT) can be indicated for hypertensive patients. However, the potential effect of HIIT has controversial results and the molecular aspects of cardiac remodeling in hypertensive patients have not been fully elucidated. Objective: to analyze the effects of HIIT during the compensated phase of arterial hypertension on the possible parameters, give and myocardial remodeling molecules in spontaneously hypertensive rats (SHR). Methods: we evaluated the influence of HIIT on blood pressure, exercise tolerance and cardiac remodeling in spontaneously hypertensive rats (SHR). Methods: Male rats (12 months old) were divided into three groups: 1) Wistar Kyoto rats (WKY, n = 8); 2) spontaneously hypertensive sedentary rats (SED-SHR, n = 10) and 3) spontaneously hypertensive trained rats (HIIT-SHR, n = 10). The parameters of mean arterial pressure, maximum exercise capacity and echocardiographic profile were taken before and after HIIT; cardiac remodeling was assessed using echocardiography, isolated papillary muscle and gene expression quantified in relation to the MAPK pathway: Elk1, cJun, ATF2, MEF2. For comparison between the groups, ANOVA was used followed by Tukey or Kruskal-Wallis and Dunn’s (p <0.05). Results: HIIT decreased SBP (SED-SHR: 229 ± 5,93 mmHg vs HIIT-SHR: 198,6 ± 18,3 mmHg; p = 0,001), increased the distance covered, being 82.7% greater in the SHR- HIIT (SED-SHR = 183.0 ± 88.08m vs. HIIT-SHR = 1126.0 ± 187.1m; p <0.0001) and reduced the resting period of the papillary muscle (WKY = 0.77 ± 0.216 ; SED-SHR = 1.26 ± 0.20; HIIT-SHR = 0.67 ± 0.23; p = 0.0001) and in gene expression there was a decrease in the gene encoding ATF2 protein in hypertensive groups in relation to control group (WKY: 1.14 ± 0.62; SHR-SED: 0.39 ± 0.11; HIIT-SHR: 0.62 ± 0.21 p = 0.03) Conclusion: The HIIT applied in SHR models in the compensated hypertension phase, a technique to decrease blood pressure, functional capacity, generated an increase in cardiac hypertrophy, but attenuated myocardial diastolic dysfunction, without dissipating damage or altering the gene.