Background/Introduction Longitudinal studies of cardiac detraining in former athletes are sparse, though studies of master endurance athletes have documented increased risk of atrial fibrillation[1]. Cardiac adaptations to exercise are characterized by uniform dilation of cardiac chambers due to increased volume load[2]. Examinations of finishers at long-duration events have demonstrated examples of acute right ventricular dilation and dysfunction[3]. This raises concerns regarding the susceptibility of thin-walled cardiac chambers to repetitive acute overload, posing a potential risk for the development of left atrial fibrosis and cardiac rhythm disorders over the long term. Purpose The aim of this investigation was to assess the pattern of inverse cardiac remodelling in retired elite athletes. Methods In this longitudinal study of elite athletes from sports of high cardiac demands we performed a 10-year follow-up examination, including a standard resting echocardiogram. Baseline echocardiograms was performed in 2009-2014. All measures of size were indexed to body surface area (BSA). Age adjusted ratios of left atrium maximum (maxLAVi), right ventricle end systolic area (RVEDVi) and left ventricle end diastolic volume (LVEDVi) were compared between baseline follow-up. Analysis of Covariance models was used to allow for adjustments for categorical variables and continuous covariates. Results are presented with 95% confidence intervals. Results MaxLAVi was increased at the time for follow-up examination compared to baseline (31.39ml/m2 CI: 29.28 -33.51ml/m2 to 33.32 ml/m2 CI: 31.06-35.58 ml/m2; p=0.04), while RVEDVi (14,57cm2 CI: 13.90-15.23 to 12.79 CI: 12.21-13.37cm2; p<0.01) and LVEDVi both dropped significantly (82.40ml/m2 CI: 79.34-85.45ml/m2 to 74.35ml/m2 71.50-77.21ml/m2; p<0.01). A comparison of cardiac chamber size ratios showed a significant increase in maxLAVi/RVEDVi ratio from baseline to follow-up examination (baseline: 2.21 CI: 2.05-2.38; follow-up: 2.63 CI: 2.47-2.79; p<0.01), this difference persisted when adjusting for age (p<0.01). MaxLAVi/LVEDVi ratio also increased (baseline: 0.38 CI: 0.36-0.41; follow-up: 0.45 CI: 0.42-0.47; p<0.01), however, when we adjusted for age, this difference was no longer significant (p=0.15). A comparison of ventricular size (RVEDVi/LVEDVi) showed no difference over the course of the study period (baseline: 5.80 CI: 5.47-6.13; follow-up: 5.91 CI: 5.63-6.19; p=0.31), adjusting for age did not affect this difference (p=0.12). Conclusion In our population of elite endurance athletes, both ventricles were smaller after the end of their sporting career, while LA increased in size. Cardiac chamber size ratios showed similarly a relative increase in LA size compared to either ventricle, though after adjusting for age no significant change was present between LA and LV.
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Aarøe et al. (2024) studied this question.
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