Arrhythmogenic cardiomyopathy (AC) is a rare genetic disorder characterised by progressive fibrous and fatty replacement of, predominantly, the right ventricular myocardium. It has a prevalence of at least 1 in 1000 and is a common cause of sudden cardiac death within the young athlete population. It has been observed that exercise increases the disease expression and progression of AC but there is limited evidence to support this. This pilot study aimed to investigate this effect in greater detail. This study utilised a retrospective and observational design using a questionnaire directed at a cohort of clinically affected (n=40) and unaffected (n=13) pathogenic desmosomal gene mutation carriers. The questionnaire aimed to quantify participation of sport throughout life in average hours/year. An independent variable was utilised that measured the total life-hours playing sports greater than Class IA (sports with both a low dynamic and static component) prior to diagnosis of AC (according to 2010 Task Force Criteria (TFC)) in affected carriers, and until current age in unaffected carriers; the variable was adjusted for age. The hours/year of sports greater than Class IA was then compared to the following endpoints: age of TFC diagnosis, age of fulfilling the combined arrhythmia endpoint (CAE), age of onset of symptoms and age of onset of heart failure. Participants were separated into three groups: those who participated in less than 20 hours/year sport > Class IA (g20), more than 100 hours/year (G100) and more than 300 hours/year (G300). Age of onset was compared between the 3 groups using a Student t test and the percentage of each group reaching each endpoint was compared using a Chi-Square test. Results – TFC diagnosis: There was a significantly larger proportion of participants in G100 fulfilling TFC than in g20 (p=0.016). Of those fulfilling TFC, the average age of diagnosis was significantly lower in G300 at 39 years (p=0.0155) and G100 at 40.5 years (p=0.011) than in g20 (55.5 years) CAE: There was a significantly larger proportion of participants fulfilling CAE in group G100 (p=0.008) and G300 (p=0.019) than in g20. Of those fulfilling CAE, the average age of fulfilment of CAE was significantly lower in G300 at 33.7 years (p=0.001) and G100 at 38 years (p=0.008) than in g20 (57 years). There were no significant differences in the prevalence of symptoms or heart failure between each group, or between the average ages of onset of symptoms or heart failure. Overall, these results support the hypothesis that exercise increases disease expression in AC. These results provide support for the introduction of specific sporting guidelines for both affected and unaffected pathogenic desmosomal gene mutation carriers. Further investigation is needed to provide further evidence in order to give more credence to this hypothesis.