Arrhythmias and structural remodeling in lifelong and retired master endurance athletes

Abstract

Background: A greater prevalence of arrhythmias has been described in endurance athletes, but it remains unclear whether this risk persists after detraining. We aimed to evaluate the prevalence of arrhythmias and their relationship with cardiac remodeling in lifelong and retired master endurance athletes compared to non-athletic controls.

Methods: We performed a cross-sectional analysis of observational studies that used echocardiography and cardiac magnetic resonance to detail cardiac structure and function, and Holter monitors to identify atrial and ventricular arrhythmias in 185 endurance athletes and 81 non-athletic controls aged ≥40 years. Athletes were categorized as active lifelong (n = 144) or retired (n = 41) based on hours per week of high-intensity endurance exercise within 5 years of enrollment and validated by percentage of predicted maximal oxygen consumption (VO_2max). Athletes with overt cardiomyopathies, channelopathies, pre-excitation, and/or myocardial infarction were excluded.

Results: Lifelong athletes (median age = 55 years (interquartile range (IQR): 46-62), 79% male) were significantly fitter than retired athletes (median age = 66 years (IQR: 58-71), 95% male) and controls (median age = 53 years (IQR: 48-60), 96% male), respectively (predicted VO_2max: 131% ± 18% vs. 99% ± 14% vs. 98% ± 15%, p < 0.001). Compared to controls, athletes in our cohort had a higher prevalence of atrial fibrillation ((AF): 32% vs. 0%, p < 0.001) and non-sustained ventricular tachycardia ((NSVT): 9% vs. 1%, p = 0.007). There was no difference in prevalence of any arrhythmia between lifelong and retired athletes. Lifelong athletes had larger ventricular volumes than retired athletes, who had ventricular volumes similar to controls (left ventricular end-diastolic volume indexed to body surface area (LVEDVi): 101 ± 20 mL/m²vs. 86 ± 16 mL/m²vs. 94 ± 18 mL/m², p < 0.001; right ventricular end-diastolic volume indexed to body surface area (RVEDVi): 117 ± 23 mL/m²vs. 101 ± 19 mL/m²vs. 100 ± 19 mL/m², p < 0.001). Athletes had more scar (40% vs. 18%, p = 0.002) and larger left atria (median volume = 45 mL/m² (IQR: 38-52) vs. 31 mL/m² (IQR: 25-38), p < 0.001) than controls, with no difference in atrial volumes and non-ischaemic scar between the athlete groups.

Conclusion: Master endurance athletes have a higher prevalence of AF and NSVT than non-athletic controls. Whereas ventricular remodeling tends to reverse with detraining, the propensity to arrhythmias persists regardless of whether they are actively exercising or retired.

Keywords: Arrhythmias; Athletes; Atrial fibrillation; Detraining; Non-sustained ventricular tachycardia.

Graphical abstract

Fig. 1

Cardiac remodeling. (A) Left ventricular end-diastolic volume indexed to body surface area (LVEDVi), (B) Right ventricular end-diastolic volume indexed to body surface area (RVEDVi), (C) Left atrial volume indexed to body surface area (LAVi), and (D) Right atrial volume indexed to body surface area (RAVi).

Fig. 2

Examples of late gadolinium enhancement (LGE) in athletes. (A) 3 lifelong athletes and (B) 3 retired athletes are presented as examples of LGE. The abnormal LGE is signified with red arrows in each case. As can be seen, the volume of scar is limited and there is a variety of myocardial segments affected.