Anabolic beta-2-agonist clenbuterol fails to modify muscle atrophy due to femur fracture.

Unilateral femur fracture in rats resulted in a significant reduction in body weight gain and food intake. The former was reversed by addition of the beta 2-adrenoceptor agonist clenbuterol to the diet (4 mg/kg) but food intake was unaffected. Neither resting oxygen consumption (VO2) nor brown adipose tissue GDP binding (measured on day 4) was affected either by femur fracture or by administration of clenbuterol. Femur fracture caused reductions in the mass, protein, and RNA content of gastrocnemius muscle from the fractured leg but not from the intact leg. Clenbuterol did not modify the reduction in the mass or protein content of muscle from the fractured leg, but stimulated these parameters in the intact leg and in heart. The ratio of RNA to protein was enhanced by clenbuterol in gastrocnemius muscle from both legs and heart. These data confirm the anabolic effect of clenbuterol in intact limb muscle but suggest that this agent is unable to prevent muscle atrophy at the site of femur fracture in the rat.