Hypertrophy Essay

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INTRODUCTION

Cardiac muscle hypertrophy has been found to be a typical physiological response to extensive training. Athletes most commonly experience nonpathological cardiac hypertrophy in response to a regular increased demand for cardiac output by the muscles in their bodies. Cardiac myocytes use growth signals from wall stress to increase thickness and normalize systolic pressure; this physiological condition is known as Left Ventricular Hypertrophy (LVH) because of its effect on the left ventricle which pumps oxygenated blood to the muscles. Hypertrophy of cardiac muscles becomes deleterious when the muscles can no longer beat in sync causing fibrillations or arrhythmias or when the muscles thicken to the point of constricting or obstructing blood flow.
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LVH is not itself a pathological condition, and is promoted by physiological growth signals, however the literature indicates that the physical activity that also causes LVH may leave athlete’s susceptible to myocardial infarction (MI) and the subsequent pathological cardiac hypertrophy (18). A five-week study done by Bajwa et al (1) showed that failure to heal properly from a myocardial infarct promoted the growth of porcine left ventricles. HCM is also understood to have a genetic origin, specifically involving mutations of genes regulating cardiac growth. The degree to which the myocardium hypertrophies designates whether it is obstructive or non-obstructive HCM, obstructive referring to the ability of blood to flow through the ventricles and atria. The thickening of the myocardium, the effect on blood flow and the sites of myocardial disarray is the source of mortality in HCM (17). The asymmetrical addition of sarcomeres to either the ventricles, the septum or the atria can cause atrial or ventricular fibrillations, arrhythmias in the heart that can be detrimental to one’s health and

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