Reduced ventricular flow propagation velocity in elite athletes is augmented with the resumption of exercise training

Abstract

Chronic exercise induces physiological enlargement of the left ventricle ('athlete's heart'), but the effects of current and long-term exercise training on diastolic function have not been investigated. Echocardiography and Doppler imaging were used to assess left ventricular (LV) dimensions and indices of diastolic filling in 22 elite athletes at the end of their 'off-season' (baseline) and, subsequently, following 3 and 6 months of training. Twelve matched controls were also studied at baseline, 3 and 6 months. Compared to controls at baseline, athletes exhibited significantly higher LV mass (235.7 +/- 7.1 g versus 178.1 +/- 14.5 g, P < 0.01) and reduced flow propagation velocity (V(P): 50.21 +/- 1.7 versus 72.2 +/- 3.6 cm s(-1), P < 0.01), a measure of diastolic function. Three months of training further increased LV mass in athletes (253.2 +/- 7.1 g; P < 0.01 versus baseline), and significantly increased their V(P) (66.7 +/- 2.5 cm s(-1); P < 0.05 versus baseline). These trends for increased mass and diastolic filling persisted following 6 months of training (LV mass 249.0 +/- 8.7 g P < 0.05 versus baseline; V(P) 75.7 +/- 3.0 cm s(-1); P < 0.01 versus baseline, and P = 0.01 versus 3 months). This study suggests that following a period of relative inactivity the rate of ventricular relaxation during early diastole may be slowed in athletes who exhibit ventricular hypertrophy, whilst resumption of training increases the speed of ventricular relaxation in the presence of further hypertrophy of the left ventricle.

Figure 1. Mean left ventricular mass (LV mass, grams) in the athlete (filled bars, n = 22) and controls (open bars, n = 12) at baseline, 3 and 6 months

Values are means ± s.e.m. The athletes possessed significantly increased LV mass (all P < 0.001) compared to the controls at all three time points. Compared to baseline measures, LV mass increased following 3 and 6 months training in the athlete group (P < 0.01, P < 0.05, respectively), but no changes occurred in LV mass in controls with time. *P < 0.001; †P < 0.01; ‡P < 0.05.

Figure 2. Mean colour flow propagation velocity (V_P, in cm s⁻¹) in the athlete (filled bars, n = 22) and controls (open bars, n = 12) at baseline, 3 and 6 months

Values are means ± s.e.m. The athletes possessed impaired V_P compared to the controls at baseline (P < 0.001). V_P improved with 3 months of training (P < 0.05 compared to controls), and normalized (NS, compared to controls) following 6 months of training. There were significant improvements in V_P in the athlete group from baseline to 3 months (P < 0.001) and 6 months (P < 0.001), and from 3 to 6 months (P < 0.001). *P < 0.001; †P < 0.01; ‡P < 0.05.