Left ventricular size and function in elite bodybuilders using anabolic steroids
Deutscher übersetzter Titel: | Groesse und Funktion des linken Ventrikels bei leistungssportlich trainierenden, anabole Steroide konsumierenden Bodybuildern |
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Autor: | Dickerman, R.D.; Schaller, F.; Zachariah, N.Y.; McConathy, W.J. |
Erschienen in: | Clinical journal of sport medicine |
Veröffentlicht: | 7 (1997), 2, S. 90-93, Lit. |
Format: | Literatur (SPOLIT) |
Publikationstyp: | Zeitschriftenartikel |
Medienart: | Gedruckte Ressource |
Sprache: | Englisch |
ISSN: | 1050-642X, 1536-3724 |
Schlagworte: | |
Online Zugang: | |
Erfassungsnummer: | PU199711208156 |
Quelle: | BISp |
Abstract des Autors
Objective: To investigate the relationship between resistance training, anabolic steroid use, and left ventricular function. Design: Sixteen competitive bodybuilders were recruited for an echocardiography study. Setting: University of North Texas Health Science Center (Fort Worth, TX, U.S.A.); the cardiologist and technician were blinded as to subjects' drug status. Subjects: Eight competitive heavyweight drug-free (DF) bodybuilders and eight competitive heavyweight bodybuilders on self-directed regimens of anabolic steroids. Results: Average body mass indexes (BMI; kg/m**2) for the drug-user (DU) and DF groups were not significantly different (34.1+/-2.8 and 32.0+/-4.3, respectively). Increases in left ventricular posterior wall and ventricular septal thickness were apparent in the DU group (p<0.05). The ratio of echocardiographic findings to BMI revealed a significantly smaller left ventricular end-diastolic dimension (LVDEd/BMI; p<0.05) in the DU group. The smaller LVDEd in DUs is coupled with a significantly disproportionate septal and posterior wall thickness in DUs when indexed to body mass compared to DFs. There was no direct evidence of diastolic dysfunction detected by mitral inflow velocity patterns. Conclusion: Anabolic steroids may potentiate concentric left ventricular hypertrophy with decreasing ventricular compliance without affecting cardiac function. Verf.-Referat