Send to

Choose Destination
Circulation. 2002 Feb 26;105(8):944-9.

Remodeling of left ventricular hypertrophy in elite athletes after long-term deconditioning.

Author information

Institute of Sports Science, Department of Medicine, Rome, Italy.



The clinical significance and long-term consequences of left ventricular (LV) hypertrophy associated with intensive athletic conditioning remain unresolved.


We prospectively evaluated 40 elite male athletes who had shown marked LV cavity enlargement of > or = 60 mm, wall thickness of > or = 13 mm, or both in a longitudinal fashion with serial echocardiograms, initially at peak training (age 24 +/- 4 years) and subsequently after a long-term deconditioning period (1 to 13 years; mean, 5.6 +/- 3.8). After detraining, LV cavity dimension decreased by 7% (61.2 +/- 2.9 to 57.2 +/- 3.1 mm; P<0.001), maximum wall thickness by 15% (12.0 +/- 1.3 to 10.1 +/- 0.8 mm; P<0.001), and mass normalized to height by 28% (194 +/- 25 to 140 +/- 21 g/m; P<0.001). However, individual subject analysis showed persistent substantial cavity dilatation (> or = 60 mm) in 9 athletes (22%); in contrast, wall thickness returned to normal in each athlete. Multiple regression analysis demonstrated that approximately 50% of the incomplete reduction in cavity dimension was explained by increased body weight and recreational physical activity performed during the follow-up period. No athlete had developed cardiac symptoms, impaired exercise performance, or evidence of LV dysfunction.


LV remodeling was evident after long-term detraining, with significant reduction in cavity size and normalization of wall thickness. Resolution of cavity enlargement was, however, incomplete in most cases, and substantial chamber dilatation persisted in >20% of athletes. The possibility that this residual LV hypertrophy, apparently part of the athlete's heart syndrome, may have future long-term clinical implications in some individuals cannot be excluded with certainty.

[Indexed for MEDLINE]

Supplemental Content

Loading ...
Support Center