Sixty pigs were used to investigate the effects of two levels of dietary ractopamine (RAC; 0 and 20 mg/kg) and three sex types (SEX; boars, gilts, and barrows) on performance over the live weight range 60 to 90 kg. Pigs were housed in individual pens and allowed ad libitum access to a diet containing 3.466 Mcal of DE and 10.7 g of lysine/kg. Control boars exhibited faster and more efficient growth and deposited more protein and less fat than gilts or barrows. The RAC increased ADG by 17 and 21% in gilts and barrows but not in boars. Feed intake was not altered by dietary RAC. Dietary RAC increased the rate of protein deposition by 15, 42, and 41% in boars, gilts, and barrows, respectively. Nevertheless, the daily rate of protein deposition was greatest in RAC-treated boars. The RAC tended to reduce the daily rate of fat deposition by 21% in boars but not in gilts or barrows. Carcass protein content increased by 5% and fat content decreased by 8% in response to RAC. These improvements in carcass composition occurred without compromising meat quality. Results show that RAC is a potent stimulator of protein deposition in finishing pigs. However, increased protein deposition is not necessarily at the expense of fat deposition.

Interactions between the beta-adrenoceptor agonist cimaterol and beta-adrenoceptors on rat skeletal muscle membranes were examined in two studies. In Exp. 1, muscle samples from eight Sprague-Dawley rats (female, approximately 200 g) were used for competition binding and autoradiographic studies using [125I]cyanopindolol (ICYP) as a radioligand. The affinities or dissociation constants for binding (KD values) for cimaterol in plantaris and soleus muscles were .68 and .92 microM, respectively. Muscle areas stained for succinic dehydrogenase had propranolol-resistant ICYP binding sites; cimaterol did not seem to compete for these sites. In Exp. 2, 60 Sprague-Dawley rats (female, approximately 218 g) were fed 0 or 10 ppm of cimaterol in rat diet that was ground. Groups were killed after 1, 3, 7, 14, or 28 d of treatment. Cimaterol increased BW gain up to 14 d after commencement of treatment, with little or no improvement thereafter. Enhanced weight gain in skeletal muscles also occurred up to 14 d of cimaterol treatment. Densities of beta-adrenoceptors in plantaris and soleus muscle membrane homogenates were estimated using a radioligand binding assay with ICYP. A significant reduction in the number of binding sites (Bmax) was observed after 3 d of cimaterol treatment in plantaris muscle without a change in the KD of ICYP binding. The percentage reductions in Bmax were 26.8, 42.2, 37.7, and 37.8% at 3, 7, 14, and 28 d after cimaterol administration, respectively. In the soleus muscle, significant reductions (44.1 and 29.8%) in Bmax were observed after 3 and 14 d of cimaterol treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

The chapter elaborates on the factors that affect the efficiency of feed utilization by lambs, their body composition in terms of lean and fat content, and aspects of carcass quality including fat content and meat yield. Predictive mathematical models that would aid in making decisions in relation to nutritional management for sheepmeat production are presented. Aspects of growth and metabolism, the influence of genotype, and the effects of diet on composition of gain are discussed.

The goal of this modelling exercise was to evaluate genetic, nutritional and other factors affecting the distribution of fat in growing and finishing beef cattle. The model had the following objectives: (i) to predict the accretion of total body fat as a function of genotype, sex, implant status and nutrition; (ii) to predict the partition of fat in different depots throughout the animal's lifetime; and (iii) to examine the possible mechanisms for genetic and nutritional differences in fat distribution. This model appears to adequately describe normal growth and accretion fat in the whole body and in the four main depots. It represents a first step in the development of an analytical tool for the study of factors affecting fat deposition and distribution.

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