Left Ventricular Hypertrophy and Cardiomegaly in swimming exercised 10-11-week-old white experimental rats


Swimming exercise

How to Cite

Gogiberidze , A. ., Khetsuriani , R. ., Arabuli-Tchlikadze, M., Shvangiradze , E. ., & Kandelaki, S. . (2022). Left Ventricular Hypertrophy and Cardiomegaly in swimming exercised 10-11-week-old white experimental rats. GEORGIAN SCIENTISTS, 4(4), 199–207. https://doi.org/10.52340/gs.2022.04.04.22


The aim of the study was to assess the quality of hyperthrophy of the left ventricle in 10-11 week-old rats after a 6-week dosed swimming load. In general, rat swimming is considered one of the best physiological triggers for hypertrophy of the left ventricle and end-diastolic volume increase.  As part of our study, we ensured 10-11 week-old rats to undergo dosed swimming exercises for  6 weeks and afterward, we studied micro and macro-structural parameters of the heart in order to assess the quality of hypertrophy. The rats were divided into 3 groups: 1) a control group that did not receive any load (n=7); 2) The first study group was subjected to a daily 40-minute swimming load for 6 weeks with a weight in the amount of 2% of the body weight of the rat (n=7) attached to the tail, 3) The second study group, which was subjected to a daily 60-minute swimming exercise for 6 weeks, the weight of the load attached to the tail amounted to 4% of the weight of the rat (n=7). 3). Hypertrophy was observed only in rats of the experimental group (exercise load for 40 minutes with a load of 2% of body weight or exercise load for 60 minutes with a load of 4% of body weight). The ratio of heart weight to body weight is proportional to the intensity of load and to the increase in the duration of exercise. The increase in the mass of the heart was mainly due to an increase in the mass of the left ventricle. 60 minutes of histological exercise load induced hypertrophy in 7 of 7 rats. And a 40-minute load was sufficient for the development of left ventricular hypertrophy in 4 out of 7 rats included in the group. The mentioned study can be considered another step forward in the study of the pathogenetic mechanisms of myocardial hypertrophy and remodeling.



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