Abstract Background The wide-ranging benefits of frequent and moderate exercise are well recorded in the literature. Chronic deleterious remodelling in response to exercise is less well described. We describe an amateur endurance cyclist who, in addition to developing a heart failure syndrome and electrocardiographic evidence of arrhythmia, also developed severe functional tricuspid regurgitation. Case summary After developing palpitations during long distance cycle rides as part of his fitness regimen, a 69-year-old male presented to emergency services but was discharged. While continuing to enjoy long-distance cycling, he began to develop peripheral swelling and presented for a second time to hospital. Subsequent investigation found he had a dilated right heart, exercise-induced arrhythmia, and mid-wall myocardial fibrosis. A diagnosis of exercise-induced cardiomyopathy was made. He was managed with diuretics and immediate cessation of exercise. His symptoms improved and he remains symptom free. Discussion The volume of blood passing through the right heart increases during exercise. In vulnerable individuals undertaking frequent endurance exercise, this can promote structural remodelling and fibrotic change. It is unclear if cessation of exercise can reverse the remodelled heart. There are some early advances in predictive biomarkers and imaging techniques in categorizing those in the population who would be at risk of developing this cardiomyopathy, and those who can undergo intense exercise regimens without concern. If those at risk of developing an exercise-induced cardiomyopathy can be accurately identified, the next dilemma is how can their risk of heart failure or sudden death be acceptably minimized.