Interactions between protein supply and the anabolic response to exogenous bovine (b) GH have been examined in two experiments using 28-35 kg lambs sustained entirely by intragastric infusion of volatile fatty acids (700 kJ/kg W 0.75 per day) into the rumen and the casein (600 mg (low protein; LP) or 1200 mg (high protein; HP)/kg W 0.75 per day) into the abomasum. Sheep received continuous i.v. infusions of bGH for 6 days in experiment 1 and for 18 days in experiment 2. Nitrogen balances were determined daily throughout both experiments and blood samples, from indwelling catheters, were assayed for GH, insulin-like growth factor-I (IGF-I), insulin and glucose. Infusion of bGH increased plasma GH concentration by five- to sixfold in all animals. There was an increase in N retention in both HP and LP animals over the first 2-3 days of GH administration. HP animals sustained higher N retentions (31%; P less than 0.05) throughout the GH administration but LP animals did not. In contrast, plasma IGF-I concentrations increased progressively over the first 72 to 96 h of GH administration in all sheep and thereafter remained significantly (P less than 0.05) elevated until termination of the GH infusion. In lambs which received both HP and LP infusion in experiment 1 the increase in IGF-I and LP infusions in experiment 1 the increase in IGF-I concentration by day 6 of GH administration was significantly (P less than 0.05) greater when they received the higher protein intake.(ABSTRACT TRUNCATED AT 250 WORDS)

Seven measurements of the effect of clenbuterol on basal nitrogen excretion (UN,), and protein turnover were made in six female sheep. The sheep were sustained by the intraruminal infusion of energy as volatile fatty acids to provide maintenance, but given no protein (N-free) for 12 d (6 d control, 6 d clenbuterol). Clenbuterol reduced UN, by 20%, but only on day 2 of the 6 d subperiod. Protein flux (equivalent to degradation on N-free nutrition), measured on day 6 by the irreversible loss of leucine was significantly increased (12 %) by clenbuterol. Amino-N oxidation measured by N excretion was unchanged and, therefore, protein synthesis was also increased. During the 12 d N-free period, the recovery of urinary total N (Kjeldahl) as the sum of urea, ammonia, creatinine and purine derivatives, declined from 87.7 to 74.2 %. The form of this missing N was not identified. The effect of clenbuterol of increasing both degradation and synthesis is unlike that reported in the literature for animals receiving protein when, in general, synthesis is unchanged and degradation reduced. This could be due to a different effect of clenbuterol in the N-free state, or to unchanged effects on protein pools other than muscle whose relative contribution to protein metabolism is different in the N-free state.Clenbuterol : Protein turnover: Nitrogen loss : SheepWe have reported (Hovel1 et al. 1989) that the P,-adrenergic agonist clenbuterol reduced the endogenous nitrogen loss of sheep. That experiment was based on the hypothesis that the increase in N retention caused by the P,-agonists in animals given dietary protein is mediated by a decrease in body protein degradation Buttery & Dawson, 1987). We had, therefore, reasoned that the /3,-agonists might reduce the endogenous N loss of animals given energy, but no protein, and found that clenbuterol did significantly reduce endogenous N losses. Clearly, such an effect could be mediated by the drug modifying either protein synthesis, or degradation, or both, with the net effect that a reduced amount of amino acid would be lost to oxidation. The objective of the work to be reported here was to extend our observations on the effect of clenbuterol on basal N loss to measurements of protein turnover. M A T E R I A L S A N D METHODS Treatments and designSeven measurements were made of the daily endogenous N loss (UN,) during a 12 d period in six sheep (one sheep measured twice) given energy as an infusion of volatile fatty acids (VFA) into the rumen, but no protein (N-free period). The 12 d N-free period was divided into two 6 d subperiods either with or without the abomasal infusion of clenbuterol (6 10 pg/kg per d). On the last day of each 6 d subperiod, protein turnover was estimated from the irreversible loss rate of ~-[4,5-~H]leucine given by jugular infusion. For three of the * For reprints.

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