Douglas P S, O'Toole M L, Hiller W D, Reichek N
Am J Cardiol. 1986 Oct 1;58(9):805-9. doi: 10.1016/0002-9149(86)90358-9.
To determine left ventricular (LV) structural and functional changes induced by ultraendurance exercise training, M-mode LV echograms and Doppler recordings of LV inflow velocity in 26 triathletes and 17 normal subjects were studied. All triathletes trained 20 to 40 hours/week in swimming, cycling and running for more than 2 years. Structurally, triathletes had normal LV systolic and diastolic cavity dimensions, but increased wall thickness (1.05 +/- 0.26 vs 0.80 +/- 0.27 cm in normal subjects, p less than 0.001), increased relative wall thickness, or h/R ratio (0.41 +/- 0.10 cm vs 0.33 +/- 0.11 cm in normal subjects, p less than 0.001), and increased LV mass (226 +/- 60 vs 143 +/- 54 g in normal subjects, p less than 0.001). LV mass correlated closely with mean exercise blood pressure during an 8-hour exercise test in 14 triathletes (r = 0.88). Systolic function at rest was similar in both groups, with no differences in fractional shortening or end-systolic stress. Diastolic LV function measured by digitized M-mode echo was similar in normal subjects and triathletes, with no differences in peak rates of cavity enlargement and wall thinning by echocardiogram. In contrast, the Doppler-derived ratio of early-to-late LV inflow velocities was slightly increased in triathletes (p less than 0.05). It is concluded that ultraendurance training produces a physiologic pattern of moderate pressure overload LV hypertrophy, in proportion to the hemodynamic load imposed during prolonged exercise. Unlike the abnormal hypertrophy of systemic hypertension, early diastolic function remains normal in the triathlete heart.
