The responses of dwarf mice to dietary administration of clenbuterol (3 mg/kg diet), daily injections of growth hormone (15 μg/mouse per d) or both treatments combined were investigated and their actions, and any interactions, on whole-body growth, composition and protein metabolism, and muscle, liver and heart growth and protein metabolism, were studied at days 0, 4 and 8 of treatment. Growth hormone, with or without clenbuterol, induced an increase in body-weight growth and tail length growth; clenbuterol alone did not affect body-weight or tail length. Both growth hormone and clenbuterol reduced the percentage of whole-body fat and increased the protein:fat ratio. They also increased protein synthesis rates of whole body and muscle, although the magnitude of the increase was greater in response to growth hormone than to clenbuterol. Clenbuterol specifically induced growth of muscle, with a decrease in liver protein content, whereas growth hormone exhibited more general anabolic effects on tissue protein. Previous reports have suggested that effects of clenbuterol on skeletal muscle are mediated, at least in part, via decreased rates of protein degradation; we could find little evidence of any decrease in whole-body or tissue protein degradation and anabolic effects were largely due to increases in protein synthesis rates. However, small increases in muscle protein degradation rate were observed in response to growth hormone. Growth hormone induced a progressive increase in serum insulin-like growth factor-1 concentration, whereas there was no change with clenbuterol administration. Anabolic effects on whole-body and skeletal muscle protein metabolism, therefore, appear to be initially via independent mechanisms but are finally mediated by a common response (increased protein synthesis) in dwarf mice.

Twenty-three British Friesian bull calves at approximately 7 d of age were allocated to one of four treatments: controls untreated (five calves), a group (Clen) given 1 mg clenbuterol/kg diet (five calves), a group (GH) given a daily subcutaneous injection of 3.5 mg bovine pituitary growth hormone (GH) (five calves) and a group (Clen + GH) given a combination of clenbuterol as in the Clen group with GH as in the GH group (seven calves). All calves were given milk-substitute at levels adjusted weekly according to metabolic live weight. The animals were slaughtered over the weight range 150–170 kg. Samples of semimembranosus and triceps muscles were excised a t slaughter. Treatment with GH produced approximately a threefold increase in mean daily serum GH concentration. Calves given Clen + GH were heaviest a t slaughter and the combined treatment produced a significantly higher (P < 0-01) feed conversion ratio. Administration of clenbuterol either alone or in combination with GH increased the cross-sectional area of both fast twitch glycolytic (FG), and fast twitch oxidative glycolytic (FOG) fibres in both muscles. In contrast GH produced little change in fibre size in semimembranosus muscle, although FOG fibres in triceps were slightly larger than in controls. Neither Clen nor GH resulted in any change in fibre percentage frequency in either muscle. Treatments involving clenbuterol produced a significant decrease in muscle glycogen concentration. Muscles from all three treatment groups tended to show small increases in protein and RNA concentration compared with the controls. Muscles from animals treated with GH alone exhibited an increase in DNA concentration not seen in muscles from the two other treatment groups. Overall, the differential response to the two agents suggested that clenbuterol does not mediate its effects via the GH axis, and that an additive response in terms of protein anabolism may be achieved from the use of a combination of clenbuterol plus GH.

The influence of subchronic application of the β-adrenergic agonist clenbuterol on plasma norepinephrine (NE), epinephrine (E) and β-receptors on lymphocytes was investigated in 8 male, healthy volunteers. Treatment with clenbuterol (0.04 mg/day) for 6 days induced significant reduction of β-receptor specific binding in 7 of the 8 subjects with a mean decrease of 40% (p < 0.01) with no changes in affinity. Concomitantly an increase in the plasma NE concentration was observed (mean 50%, p < 0.01), but no significant overall alteration of E concentration. Our results suggest that β-adrenergic agonists exercise a similar effect on the peripheral adrenergic system and on the adrenergic system in the brain.