Abstract
PurposeLeft ventricular (LV) enlargement has been linked to sudden cardiac death among young athletes. This study aimed to model the effect of long-term incessant endurance training on LV dimensions in female adolescent runners.MethodsJapanese female adolescent competitive distance runners (n = 36, age: 15 years, height: 158.1 ± 4.6 cm, weight: 44.7 ± 6.1 kg, percent body fat: 17.0 ± 5.2%) underwent echocardiography and underwater weighing every 6 months for 3 years. Since the measurement occasions varied across subjects, multilevel analysis was used for curvilinear modeling of changes in running performance (velocities in 1500 m and 3000 m track race), maximal oxygen uptake (VO2max), body composition, and LV dimensions.ResultsInitially, LV end-diastolic dimension (LVEDd) and LV mass were 47.0 ± 3.0 mm and 122.6 ± 15.7 g, respectively. Running performance and VO2max improved along with the training duration. The trends of changes in fat-free mass (FFM) and LVEDd were similarly best described by quadratic polynomials. LVEDd did not change over time in the model including FFM as a covariate. Increases in LV wall thicknesses were minimal and independent of FFM. LV mass increased according to a quadratic polynomial trend even after adjusting for FFM.ConclusionsFFM was an important factor determining changes in LVEDd and LV mass. Although running performance and VO2max were improved by continued endurance training, further LV cavity enlargement hardly occurred beyond FFM gain in these adolescent female runners, who already demonstrated a large LVEDd.
Highlights
Many cross-sectional studies have indicated that young trained endurance athletes have larger left ventricles than sedentary controls [1,2,3,4,5]
The trends of changes in fat-free mass (FFM) and LV end-diastolic dimension (LVEDd) were best described by quadratic polynomials
LVEDd did not change over time in the model including FFM as a covariate
Summary
Many cross-sectional studies have indicated that young trained endurance athletes have larger left ventricles than sedentary controls [1,2,3,4,5] This enlargement, referred to as “athlete’s heart,” has been regarded as a consequence of physiologic adaptation of the left ventricles to realize larger cardiac output and sustain the higher oxygen demand of exercised skeletal muscles [1] [2]. This training-induced adaptation has been reported to occur in female athletes [3] or adolescent populations [4]. Long-term observational evidence is scarce for female adolescent distance runners
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