Abstract

Background In elite athletes left ventricular morphologic changes are predicted to alter passive pressure/volume characteristics by reducing myocardial stiffness and increasing compliance.

Aim We investigated the utility of a new Doppler tissue index based on the pressure volume relation ((E/Ea)/LVEDD), which provides a measure of myocardial stiffness, and assessed its usefulness in detecting cardiac adaptation in elite rowers.

Methods Thirty-six international rowers (mean age 27±7 years,) who had trained intensively for 15-20 hours per week for more than 5 years and a control group of 30 sedentary but otherwise normal subjects (mean age 26±8 years,) were consented and enrolled into the study. The groups were similar in age and gender. Left ventricular (LV) septal and posterior wall thickness, mass, chamber size, transmitral Doppler peak early (E) and late (A) diastolic filling velocities and isovolumic relaxation times were measured. Early diastolic myocardial velocities (Ea) were averaged from 4 sites at the mitral annulus; Diastolic stiffness was assessed with the use of three indices E, Ea, and the left ventricular end diastolic diameter in diastole (LVEDD). The ratio, [(E/Ea)/LVEDD], represents a pressure/volume relationship and provides a novel index of diastolic stiffness. Rowers were further divided into 2 groups based on the presence or absence of left ventricular hypertrophy (LVH), ≤ 12mm and > 12mm.

Results There was no significant difference in Ea (4 site average) between the two groups, but there was a difference in the stiffness index, with rowers having significantly more compliant ventricles (p=0.0003). When compared with controls and adjusted for body surface area (BSA) and heart rate this difference remained statistically significant (p= 0.016). When the rowers were divided into 2 groups based on the presence or absence of LVH there was no difference in the stiffness index (p = 0.68)

Conclusions The key distinguishing feature of intense training is a reduction of myocardial stiffness despite the development of left ventricular hypertrophy.