Effects of clenbuterol on growth in underfed cattle

This study examined the effects of clenbuterol on the growth of young cattle (160 kg) that were fed a restricted quantity of a low-quality hay to simulate dry-season pasture conditions in the tropics. Twenty Brahman steers were used. Ten control animals lost an average of 0.24 kg/day in the first 17 days, then maintained their liveweight for the remaining 21 days of the experiment. By contrast, 10 clenbuterol-treated animals lost 0.3 kg/day for the first 17 days of the experiment, then continued to lose weight at a steady rate of 0.15 kg/day. In control steers, plasma concentrations of urea-nitrogen decreased over the course of the experiment, and this effect was accelerated by clenbuterol treatment (P < 0.05). There were no marked changes in plasma concentrations of glucose, potassium, or Nt-methylhistidine in response to clenbuterol treatment. Clenbuterol had no effect on β2 -adrenoceptor density in the longissimus muscle, but there was a marked increase in β2-adrenoceptors in both groups of cattle over time. Despite their loss of liveweight, the carcasses of clenbuterol-treated cattle were not lighter than controls (74.3 v. 72 kg, respectively) and contained 10% more protein (P < 0.05). This was reflected by a trend towards increased weight of the biceps femoris muscle (9%; P < 0.1). These findings are consistent with clenbuterol causing a drive to deposit muscle protein at the expense of other tissues, even when dietary protein and energy are limited

Differential effects of dexamethasone and clenbuterol on rat growth and on beta(2)-adrenoceptors in lung and skeletal muscle

β-adrenergic agonists increase growth rate, but their efficacy is reduced over time as the number of β2-adrenoceptors in muscle decreases. Dexamethasone increases β2-adrenoceptor density in many tissues, but this effect has not been reported in skeletal muscle. In this study, male rats were treated daily for 10 d with either clenbuterol (4 mg/kg of feed), dexamethasone (.2 mg/kg BW, s.c.), or clenbuterol plus dexamethasone. Untreated rats served as controls. Dexamethasone caused a marked suppression of growth rate, which resulted in decreased (P < .001) body weight (−29%), carcass weight (−30%), hind-limb muscles (−22%), omental fat (−22%), and heart weight (−10%). Feed intake was reduced (−26%), but feed conversion efficiency was also impaired (P < .001). Clenbuterol caused a small increase in growth rate (+6%; P < .05), with an increase in leg muscle (+7%; P < .01) and heart mass (+8%; P < .05). Feed efficiency was improved (P < .001) by clenbuterol. Rats given the combined treatment still showed a reduction in growth rate (−81%). Clenbuterol caused only a mild attenuation of the effects of dexamethasone on feed intake, BW, and carcass weight, but reduced the catabolic effect of dexamethasone on hind-limb muscle to only −8%. Clenbuterol caused a slight increase in the affinity β2-adrenoceptors in lung for binding to the radioligand (−)[125I]iodocyanopindolol. Relative to control values, the density of β2-adrenoceptors in lung was +31% with dexamethasone treatment, −45% with clenbuterol, and −23% with the combined treatment. Clenbuterol also decreased β2-adrenoceptors in skeletal muscle (−35%), but so did dexamethasone (−13%), so the effects of the β-adrenergic agonist were not attenuated through use of the combined treatment (−40%). The results show that the inductive effect of glucocorticoids on β2-adrenoceptors is tissue-specific and that glucocorticoid treatment is not a useful adjunct to β-adrenergic agonist treatment in animal production