Exercise-induced increases in left ventricular mass in elite athletes are not associated with extracellular volume, indicating LVM rise occurs independent of ECV changes.
Is left ventricular mass associated with myocardial extracellular volume in elite athletes?
In elite athletes, exercise-induced increases in left ventricular mass are not independently associated with lower myocardial extracellular volume after adjusting for sex and sport category.
Abstract Background Myocardial extracellular volume (ECV) has been reported to correlate with left ventricular mass (LVM), with higher levels of ECV observed in pathological increases in LVM (e.g. cardiomyopathies). In contrast, in healthy athletes, it has been hypothesized that increases in LVM due to myocardial hypertrophy compress the extracellular matrix, resulting in lower ECV. However, the latter association has only been observed in limited study populations of male endurance athletes and has not been validated in non-endurance or female athletes, nor in extreme phenotypes of elite athletes. Purpose To investigate the association between LVM and ECV in an elite athlete, extreme phenotype cohort, stratified by biological sex and sport-specific subgroups. Methods Cross-sectional analysis of elite athletes (national, international and Olympic level athletes, 16 years and older, and more than 10 hours of exercise/week), without a history of cardiovascular disease, enrolled in our longitudinal elite athlete prospective cohort study. Athletes underwent contrast-enhanced cardiac magnetic resonance imaging as part of standardize pre-participation cardiac screening. Native -and post-contrast T1 mapping, along with hematocrit levels, were used to quantify ECV. Spearman correlation and regression analysis were performed to examine the association between LVM and ECV, in the total athlete population, and in subgroups (sex; mixed-, endurance-, power/skill- sports). Results In 188 athletes (42% female; median age 29 (interquartile range IQR 25-32.2); 43.6% endurance, 43.6% mixed, 12.8% power/skill athletes, median ECV was 23.1% 21.8-24.7 Table 1. ECV was higher in female compared to male athletes (25.0% 23.6-26.0 vs. 22.1% 21.8-24.7, p .001). Mean indexed LVM was 57.2 ± 11.2 g/m² and was higher in men than in women. Spearman correlation analysis revealed an inverse relationship between ECV and LVM in the overall athlete population (rho = -0.378, R² = 0.143, P .001), as well as in endurance (rho = 0.367, R² = 0.135, p .001) and mixed athletes (rho = 0.510, R² = 0.26, p .001) Figure 1. No statistically significant correlations were found after stratification for sex, or in power/skill athletes. Multivariate regression analysis adjusting for sex and sport category showed no significant effect of ECV on LVM (Estimate = -0.274, p = 0.462). Conclusion In elite athletes with extreme phenotypes, LVM is not associated with ECV. This indicates that exercise-induced increases in LVM are not accompanied by the expected lower ECV. Given these findings, further investigations are needed before ECV may be considered a potential biomarker for differentiating pathological from physiological increases in LVM.Table 1.Study Characteristics Figure 1.Spearman correlation analysis
Leusden et al. (2025) studied this question. Exercise-induced increases in left ventricular mass in elite athletes are not associated with extracellular volume, indicating LVM rise occurs independent of ECV changes.