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Introduction Endurance sport participation has many health benefits including improved cardiovascular fitness and longer life expectancy. It is a paradox that endurance sport participation is also associated with cardiac arrhythmias. The true prevalence and incidence of arrhythmias in endurance athletes is difficult to define due to variable definitions of endurance sport participation and identifying athletes with arrhythmias. There are several proposed mechanisms by which endurance sport may predispose athletes to arrhythmias. Aims The aim of this thesis is to characterise what electrophysiologic changes are normal in endurance athletes, define the risk of arrhythmias attributable to endurance sport participation and investigate the mechanistic causes for an increased burden of arrhythmias. Results To characterise normal electrophysiologic changes in endurance athletes we recruited 223 current and former athletes as well as fifty-two nonathletic control participants. We found that bradycardia and notably ventricular pauses are very common in athletes and rare in non-athletes. We found no significant association of ectopic burden with endurance sport. To investigate the mechanisms by which endurance sport leads to bradycardia in athletes we performed an experimental study in thirty volunteers split equally between nonathletes, endurance athletes and endurance athletes with extreme bradycardia. By administering autonomic blockade, we confirmed that bradycardia in athletes is not due to autonomic influence. Furthermore, this is the first study which has shown high vagal tone does not explain extreme resting bradycardia in athletes. To better define the risk of atrial fibrillation attributable to endurance sport, we performed a case control study which strictly defined past endurance sport participation. We recruited 121 former elite rowers who competed at a national, world championship or Olympic level and compared them to an age, gender and ethnicity matched cohort from the UK Biobank at a ratio of 100:1. Despite less traditional risk factors we found the prevalence of atrial fibrillation 6.7 times higher in the athlete cohort and incidence was 2.8 times higher over two years of follow up. Using a polygenic risk score we were able to show that genetic risk plays a role in which athletes develop atrial fibrillation in a similar manner to non-athletes. In our last study we attempted to identify why some athletes develop atrial fibrillation. In our previous study we demonstrated that genetic risk plays a role in which athletes develop atrial fibrillation but does not appear to explain the excess burden of atrial fibrillation in endurance athletes. For this study we performed a case control study with fifty-three current and former endurance athletes with atrial fibrillation age and gender matched to fifty-three athletes without atrial fibrillation. We found that endurance sports athletes with atrial fibrillation have similar risk factor profiles, body composition, training history, physical fitness and electrophysiologic remodelling to endurance athletes without atrial fibrillation. Conclusion Endurance sport training leads to profound electrophysiologic remodelling which is not explained by autonomic tone. The risk of atrial fibrillation in markedly increased in endurance athletes but the mechanisms which lead to the excess burden of atrial fibrillation in endurance athletes remain elusive.

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