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Arrhythmias are a prevalent cardiovascular condition, frequently seen in athletes and fitness enthusiasts due to their high-intensity physical activities, which can complicate or be secondary to heart failure, myocardial hypoxia, ischemia, and in severe cases, lead to sudden death. In the context of athletic and fitness-oriented lifestyles, myocardial hypoxia—often a result of intense physical exertion—can significantly impact endoplasmic reticulum stress and mitochondrial autophagy. The endoplasmic reticulum (ER) plays a crucial role in cellular protein synthesis. Disruptions in ER homeostasis, due to various factors including strenuous physical activity, can lead to an accumulation of misfolded proteins in the ER, triggering ER stress. This stress has been identified in various diseases and is of particular interest in the athletic population, where the body's systems, including the heart, are often pushed to their limits. Furthermore, mitochondrial autophagy, a process vital for maintaining cellular health by degrading and recycling mitochondrial components, has been linked to arrhythmia. This connection is especially pertinent in athletes, as their hearts undergo considerable physiological stress and adaptation in response to ongoing physical demands. This study aims to explore the mechanisms by which myocardial hypoxia induces ER stress and mitochondrial autophagy, and how these processes contribute to the development of cardiac arrhythmias in athletes and fitness enthusiasts. By focusing on this specific group, the research seeks to provide a deeper understanding of the cardiac risks associated with high levels of physical activity and to inform preventative and therapeutic strategies tailored to this population.
