Physical Activity in Arrhythmogenic Cardiomyopathy: From Trigger to Therapeutic Dilemma

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  Fig. 1.. Potential benefits of low-intensity physical activity in patients with arrhythmogenic cardiomyopathy. In contrast to high-intensity or endurance exercise, carefully selected low-intensity physical activity may confer beneficial systemic and functional effects in patients with arrhythmogenic cardiomyopathy. These include improvements in cardiorespiratory fitness, endothelial function, lipid and glycemic profiles, and overall quality of life. Additional potential benefits comprise anti-inflammatory and antioxidative effects, preservation of musculoskeletal function, and reductions in frailty, sarcopenia, and fall risk. Such activity does not modify the underlying genetic disease substrate but may support long-term cardiovascular health and functional capacity when integrated into an individualized exercise prescription that avoids vigorous or competitive sports.

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  Fig. 2.. Exercise-related mechanisms promoting disease progression and arrhythmogenesis in arrhythmogenic cardiomyopathy. Endurance exercise imposes repetitive mechanical and hemodynamic stress on the myocardium, resulting in desmosomal stretch and dysfunction that promote cardiomyocyte detachment and cellular injury. In genetically predisposed individuals, pathogenic variants affecting desmosomal and cytoskeletal proteins create a vulnerable myocardial substrate that amplifies these effects. Exercise-related myocardial injury may be further exacerbated by inflammatory and autoimmune responses, leading to myocardial inflammation and progressive fibro-fatty replacement. In parallel, systemic exercise-related factors, including dehydration, electrolyte and acid–base disturbances, and adrenergic hyperactivity, act as dynamic modulators that lower arrhythmic thresholds. The interaction of structural remodelling and transient systemic stressors culminates in ventricular arrhythmias and sudden cardiac death, illustrating how endurance exercise may contribute to disease progression and arrhythmogenesis in ACM. PKP2, plakophilin-2; DSP, desmoplakin; DSG2, desmoglein-2; DSC2, desmocollin-2; FLNC,…