EVALUATION OF PHYSICAL EXERCISE BY SWIMMING PREVIOUSLY TO MYOCARDIAL INFARCTION

Abstract

Physical exercise prior to myocardial infarction (MI) protects against the IM scar, prevents cardiac remodeling and attenuates systolic dysfunction and diastolic activity in rats. Evaluate the influence of physical training by swimming, performed prior to MI, on the growth of cardiac masses, pulmonary and hepatic water content. Characterize the echocardiographic changes indicative of cardioprotection induced by physical training prior to myocardial infarction. Young rats weighing between 170 and 190 grams, from the Experimental Models Development Center (CEDEME) of the Federal University of São Paulo, were used. The animals were kept in boxes with water and rations in a temperature controlled environment. They were distributed in four experimental groups: non‐infarcted sedentary (SS); Sedentary infarcted (IMS); Trained non‐infarcted (SE); Infarcted Training (IME) The animals were submitted to a period of adaptation to the swimming exercise, later those belonging to the SE and IME groups swam for 90 minutes, this time was maintained until five weeks were completed. After this period the maximum physical capacity (MCF) was again evaluated and then the rats were submitted to myocardial infarction (MI) surgery. The method of production of IM was based on the work of Johns and Olson (1954). After three weeks of infarction the animals were submitted to Doppler echocardiography and were sacrificed for the analysis of the wet and dry weight of the heart, lungs and liver. The data were statistically evaluated, one‐way ANOVA followed by Tukey's test, and significant values of (p<0,05) were considered. After the training period prior to MI, the animals exercised SE (2,317 ± 275 seconds) and IME (3,104 ± 281 seconds) had an increase (p ≤ 0.001) in MCF compared to SS sedentary animals (378 ± 43 seconds) and IMS (341 ± 25 seconds), respectively. These results indicate that the protocol was effective in increasing the cardiorespiratory capacity of the exercised animals. The atrial masses of the infarcted animals were higher than those of the non‐infarcted animals (p ≤ 0.001). The right ventricular (RV) mass values of SE, IMS and IME animals were higher than the values for the SS group (p ≤ 0.001). There was hypertrophy (12%) of the left ventricle (LV) of the SE rats in relation to the SS (p = 0.008). The results of the IMS and IME groups related to the cardiac morphology indicated significant LV dilation and decreased LV wall thickness (p ≤ 0.001) in relation to SS and SE animals. No significant differences were observed in the comparisons of aortic diameters, left atrial and LV posterior wall thickness between groups. The water contents of the lungs and liver did not differ significantly between the four experimental groups. The results related to the systolic function indicated that there was a significant loss (p ≤ 0.001) of the shortening fraction and the shortening fraction of the transverse area indicating clear systolic dysfunction, not prevented by physical exercise. Values for diastolic function in infarcted animals were significantly worse than those recorded in non‐infarcted animals (p<0,05). The protocol of physical training per swimming, imposed prior to MI, did not prevent the cardiac remodeling of infarcted rats and does not prevent cardiac remodeling or systolic and diastolic dysfunction evaluated by Doppler echocardiography.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.