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on February 4, 2002

A more recent version of this article appeared on February 26, 2002

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Submitted on October 19, 2001
Revised on December 18, 2001
Accepted on December 21, 2001

Remodeling of Left Ventricular Hypertrophy in Elite Athletes After Long-Term Deconditioning

Antonio Pelliccia MD^*, Barry J. Maron MD, Rosanna De Luca MD, Fernando M. Di Paolo MD, Antonio Spataro MD, and Franco Culasso PhD

From the Institute of Sports Science, Department of Medicine (A.P., R.D.L., F.M.D.P., A.S.), Rome, Italy; Minneapolis Heart Institute Foundation (B.J.M.), Minneapolis, Minn; and Department of Experimental Medicine, University La Sapienza (F.C.), Rome, Italy.

^* To whom correspondence should be addressed. E-mail: ant.pelliccia{at}libero.it.

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

Methods and Results—We prospectively evaluated 40 elite male athletes who had shown marked LV cavity enlargement of 60 mm, wall thickness of 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 (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.

Conclusions—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.

Key words: athlete • hypertrophy • remodeling • ventricles • deconditioning

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