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Oct 24, 2018

7th Congress of the European Academy of Paediatric Societies

10 - A NEW APPROACH TO CORRECT THE STRUCTURAL AND FUNCTIONAL MYOCARDIAL CHANGES, MEDIATED BY AN INTENSIVE PHYSICAL TRAINING IN YOUNG FOOTBALLERS

pathological cardiac remodeling

over-training syndrome

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pathological cardiac remodeling

over-training syndrome

Abstract

Intensive and prolonged physical exertion causes pathological cardiac remodeling in 30-55% of young athletes. In some of them these changes are significant, associated with over-training syndrome and impede continuation of sport competition. Aim. To study the mechanisms and findings of exercise-induced cardiac remodeling and develop the approaches to its pathogenetic correction. Material and methods. Probability of cardiac remodeling development due to stress and overtraining in mice was studied in an experimental model of swimming “till exertion” with the body mass of mice being burdened to 10%. The myocardial ultrastructure of over-training mice was studied by electron microscopy. The dynamics of cardiac disturbances was determined by a 14-day course of phosphocreatine (PC) intake. The state of the cardiovascular system in 189 young football players (12-18 years old) was studied in clinic by standard ECG, echo-cardiography, Holter-monitoring, veloergometry tests and by biochemical tests. The dynamics of these indicators were reanalyzed after the course of PC. Results. The findings of stress- and overtraining-induced myocardial dystrophy by day 14 of experiment developed in all the mice. It manifested in marked cell polymorphism (prevalence of the share of "dark cardiomyocytes") and cell damage in the form of enlarged invaginations of the nucleolemma, expansion of the perinuclear space, damage the plasmolemma with development of intracellular edema, myofibril degradation and mitochondrial destruction. 30% of the animals died during the experiment. The course intake of PC prolonged the duration of the training by 37-153%, it also increased the level of epinephrine in the myocardium, and limited the damage of myocardium ultrastructure, preserving the number and structure of mitochondria, and preventing lethality in tested mice. In 40 of 189 young footballers stress- and overtraining mediated myocardial remodeling was identified. It manifested in rhythm disturbances, heart cavities dilatation, myocardial hypertrophy, systolic and diastolic function impairment, elevation of myocardial enzymes level, autonomous dysfunction. In young athletes the use of PC contributed to a rise of physical working capacity by 9% to the original level and reduced (by 32-87%) or eliminated the structural and functional signs of myocardial damage. Conclusion. PC can reduced myocardial damage mediated by stress and over-training.

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All rights reserved.