Introduction and objective:
While endurance training confers significant cardiovascular benefits, emerging evidence suggests that prolonged high-volume exercise may promote myocardial fibrosis in some athletes. The aim of the review is to examine the prevalence, underlying mechanisms, imaging characteristics, and clinical significance of fibrotic remodelling in the athlete’s heart – emphasizing its dual role as both physiological adaptation and potential arrhythmogenic substrate.

Review methods:
The review draws on literature published between 2017- 2024, focusing on studies involving cardiac magnetic resonance imaging (CMR), myocardial fibrosis biomarkers, and structural cardiac adaptations in endurance-trained individuals. Particular attention is given to prospective and comparative research relevant to athletic populations.

Brief description of the state of knowledge:
Myocardial fibrosis has been observed in up to 21% of endurance athletes, most commonly at right ventricular insertion points. Suggested mechanisms include repetitive mechanical stress, subclinical myocarditis, and sustained inflammatory activation. While certain fibrosis patterns may reflect benign remodelling, others – such as mid-wall or ischemic late gadolinium enhancement (LGE) – have been linked to increased arrhythmic risk. Newer imaging techniques, e.g. T1 mapping and extracellular volume (ECV) analysis, offer promise but require further standardization in athletes.

Summary:
Fibrotic remodelling in athletes spans a clinical spectrum. Its relevance depends on distribution, extent, and co-existing structural or electrical changes. Distinguishing physiological from pathological fibrosis remains a diagnostic challenge, underscoring the need for improved risk stratification and long-term data from athletic cohorts.