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Persistent strength training can increase ventricular blood pressure and volume and the resultant loading in ventricles of the human heart. It is proved that pressure overload can increase ventricular thickness and volume. In this article, we modeled athlete’s heart syndrome macroscopically arising from pressure overload using continuum mechanics and finite elements methods. We tried to improve previous results by using a more precise geometry and loading and by modifying previous equations. Firstly, we saw that because the left ventricular pressure was more than the right ventricular pressure, increase in myocardium thickness started from the left ventricle and secondly, this increase in myocardium thickness started from lower regions that located far from the right ventricle. Then, it was shown that thicker regions with greater values of the growth multiplier had less stress than regions with less values of the growth multiplier. As time passed and more loading cycles were applied to the endocardium, myocardium thickness increased gradually until the growth multiplier reached its maximum threshold value. Finally, we demonstrated that when the ventricular pressure rises and hypertrophy occurs, residual stresses remain in the myocardium after unloading.

Keywords: Athlete’s heart syndrome, Finite growth, Continuum mechanics, Stem cells

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