1. Male and female broiler chickens (144 in total) were given diets supplemented with clenbuterol (CB) at 0 (control) and at 1 mg/kg between 28 and 49 d of age to study the effect of CB on growth, carcase and skeletal muscle. 2. CB improved growth in males by increasing daily weight gain and final live weight and by lowering food conversion ratio. In females it changed the carcase composition by reducing abdominal fat pad and by increasing the proportion of protein. Consequently, carcase protein gain was increased in both sexes (11% and 16%, respectively). 3. Skeletal muscle weights were enhanced by between 6% and 22%. Muscle fibre diameters were increased in extensor hallucis longus (EHL) but not in gastrocnemius (GAS) muscle. This increase was more pronounced in females. EHL total muscle fibre number remained unchanged. The proportion of fast-twitch glycolytic fibres was increased at the expense of fast-twitch oxidative fibres in males only. Nuclear/cytoplasm and DNA/protein ratios tended to be decreased by CB. 4. From the elevated EHL muscle RNA/DNA, unchanged protein/RNA and translation activity it is suggested that CB stimulated protein synthesis at the pretranslational level. Reduced protein degradation is deduced from decreased neutral calcium-dependent proteolytic activity. 5. It is concluded that broiler chickens respond to long-term CB treatment as has been shown in various mammals. However, the sex-specific response in growth, carcase composition and skeletal muscle cellularity is more clearly apparent in broiler chickens.

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The effects of clenbuterol (CB) on the weights of 6 hindleg muscles as well as on structural and biochemical characteristics of extensor digitorum longus muscle (EDL) were studied on Wistar rats. Different CB-doses (5 vs. 18 mg/kg diet) were tested and rats of different sex were used. The 12 days treatment accelerated the growth of the 6 hindleg muscles by 13 to 24% without predominant response of fast twitch or slow twitch muscles. The higher muscle weights were achieved by fibre hypertrophy as demonstrated by increased fibre diameters (+13 to +16%), and not by fibre multiplication. There was no evidence for a selective fibre hypertrophy of one of the metabolic fibre types. Fibre type composition shifted to the fast glycolytic fibres (FTG +0.7 to +4.9%-units). There were no significant differences in responses between the sexes of CB-doses. Clenbuterol decreased the nucleus/cytoplasm ratio, measured as nuclei number/mm2 fibre area, between 24 and 28% and the DNA/protein ratio by 17%. RNA content and RNA/DNA ratio were enhanced by 25 and 22%, respectively; the protein/RNA ratio remained unchanged. The results suggest that clenbuterol changes fibre type composition and stimulates fibre growth in a pretranslational stage of protein synthesis without addition of nuclei by satellite cell proliferation.

In 3 experimental groups 9 female Wistar rats (initial live weight 150 g) were fed either the control diet, the control diet supplemented with 5 mg clenbuterol or the combination of 5 mg clenbuterol and 500 mg propranolol per kg diet over a 12-day period. The N-balance was estimated over days 6 to 10 followed by a 15N-tracer experiment for determining the influence of the feed additives on characteristics of protein metabolism on day 12. All differences in the means were concluded to be significant for P < 0.05. Live weight gain and feed efficiency were improved by clenbuterol. The animals treated with clenbuterol had 18%-24% higher muscle weights whereas the combined treatment increased the muscle weights by 10%-16% only. The good correlation between the increase of muscle weights and the total protein content indicates that clenbuterol does not change the relation between protein- and water accumulation. Histological-histochemical investigations showed that the higher muscle weights were achieved through muscle fibre hypertrophy. The number of muscle fibres remained constant. Concerning the distribution of the fibre types, clenbuterol increased the proportion of FTG-fibres (white, fast-twitch, glycolytic) on the expense of the FTO-fibres (fast-twitch, oxidative). While the number of nuclei per muscle fibre did not change, the nucleus-cytoplasm relation decreased by 24%. Compared to the animals fed the control diet, the N-balance in the clenbuterol-treated group was increased by 41%. Feeding the combination of clenbuterol and propranolol resulted in an increase of 24% only. Clenbuterol increased the N-content of the carcass by 6% and reduced the carcass fat content by 30%. In the group fed clenbuterol and propranolol, the N-content of the carcass only tended to be increased and the influence on carcass fat reduction was only 16%. The stimulated N-deposition in the carcass of clenbuterol-treated rats was obtained, since the calculated protein degradation rates were more reduced than protein synthesis rates. In-vitro investigations of the muscle protein synthesis and -protease activities support these results. The clenbuterol-induced increase in muscle protein was accompanied by an inhibition of the Ca-dependent protease activity and an increase of muscle DNA- and RNA-content. The additional application of propranolol reduced these effects of clenbuterol again. Since propranolol partly prevented the effects of clenbuterol on protein metabolism it is suggested that not only the lipolytic but also protein anabolic effects are caused by the beta-adrenergic action of clenbuterol.