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Inhibited longitudinal growth of bones in young male rats by clenbuterol


Medicine & Science in Sports & Exercise: February 2002 - Volume 34 - Issue 2 - p 267-273
BASIC SCIENCES: Original Investigations

KITAURA, T., N. TSUNEKAWA, and W. J. KRAEMER. Inhibited longitudinal growth of bones in young male rats by clenbuterol. Med. Sci. Sports Exerc., Vol. 34, No. 2, pp. 267–273, 2002.

Purpose Clenbuterol is one of the beta-2 adrenergic receptor agonists with potent anabolic properties in muscles, yet the concomitant effects on muscle and bone in young animals remain to be resolved. Therefore, the purpose of this study was to determine the effects of clenbuterol administration on muscles and bones of young rats.

Methods Twelve male Sprague-Dawley rats (9-wk-old) were randomly assigned to either a control (CON, N = 6) or clenbuterol group (CLE, N = 6). Clenbuterol of 2 mg·kg body wt·d−1 was administered subcutaneously for 4 wk. After treatment, the soleus (SOL), extensor digitorum longus (EDL), and ventricle (VENT) muscles and the femurs (FE) and tibiae (TI) bones were excised and analyzed. The bone mineral content (BMC), area, and bone mineral density (BMD) of FE and TI were measured by dual-energy x-ray absorptiometry (DXA). The longitudinal lengths of bones were measured with the Vernier calipers.

Results CLE showed smaller body weight than CON (P < 0.05) after the treatment. The muscle wet weights in CLE tended (P = 0.08) to be higher than CON in SOL (9%) and EDL (12%), but the ratio of muscle wet weight-to-body weight were higher (SOL:P < 0.05, EDL:P < 0.01) than CON. VENT of CLE showed increases in both the wet weight and the ratio (P < 0.01). FEs in CLE showed smaller values in BMC (P < 0.01), area (P < 0.01), and length (P < 0.05) than CON but not in BMD. TIs showed significant decreases (P < 0.01) in BMC, area, and length but not in BMD.

Conclusion These results indicated that clenbuterol induced the muscular hypertrophy but inhibited the longitudinal growth of bones in young male rats, which may be a serious concern in any ergogenic use.

Faculty of Pharmaceutical Sciences, University of Kanazawa, Kakuma, Kanazawa 920-1192, JAPAN; and The Human Performance Laboratory, The University of Connecticut, Storrs, CT 06269-1110

Submitted for publication March 2001.

Accepted for publication June 2001.

© 2002 Lippincott Williams & Wilkins, Inc.