Selective breeding and improved nutritional management over the past 20–30 years has resulted in dramatic improvements in growth efficiency for pigs and poultry, particularly lean tissue growth. However, this has been achieved using high-quality feed ingredients, such as wheat and soya that are also used for human consumption and more recently biofuels production. Ruminants on the other hand are less efficient, but are normally fed poorer quality ingredients that cannot be digested by human subjects, such as grass or silage. The challenges therefore are to: (i) maintain the current efficiency of growth of pigs and poultry, but using more ingredients not needed to feed the increasing human population or for the production of biofuels; (ii) improve the efficiency of growth in ruminants; (iii) at the same time produce animal products (meat, milk and eggs) of equal or improved quality. This review will describe the use of: (a) enzyme additives for animal feeds, to improve feed digestibility; (b) known growth promoting agents, such as growth hormone, β-agonists and anabolic steroids, currently banned in the European Union but used in other parts of the world; (c) recent transcriptomic studies into molecular mechanisms for improved growth efficiency via low residual feed intake. In doing so, the use of genetic manipulation in animals will also be discussed.

Hypertension is a major risk factor for the development of CVD. Epidemiological studies have shown that low birth weight increases the risk of developing hypertension in adulthood. Hypertension increases the risk of suffering IHD and early findings provide evidence that hearts from prenatally protein-restricted, hypertensive, male offspring are more susceptible to cardiac dysfunction following ischaemic events. Hypertension and abnormalities in cardiac function following ischaemia–reperfusion in the human population are treated therapeutically with β-adrenergic antagonists. We hypothesised that increased susceptibility to myocardial ischaemia–reperfusion injury in prenatally programmed offspring may be due to sympathetic hyperactivity. Pregnant Wistar rats were fed control or low-protein (maternal low protein; MLP) diets throughout gestation. At age 6 months, hearts were rapidly excised and retro-perfused using the Langendorff apparatus, to assess isolated cardiac function following stimulation with increasing doses of the non-specific β-agonist isoproterenol. Baseline heart rates were similar in control and MLP-fed offspring. With significant diet × sex interactions (P < 0·01) maximum heart rate response following isoproterenol infusion was significantly longer in MLP than control. Prenatal diet had no effect on maximal left ventricular developed pressure (LVDP) response, but the LVDP isoproterenol response was significantly longer in duration in MLP-exposed male offspring (diet × sex P < 0·001). Myocardial mRNA expression of β2-adrenergic receptors was increased in 2-week-old female MLP offspring only (P < 0·049). In conclusion, maternal protein restriction programmes cardiac sympathetic activity in a sex-specific manner, and may explain increased susceptibility to ischaemia–reperfusion injury in males subject to fetal undernutrition.

In earlier studies with pigs the P-adrenergic agonist Ro 16·8714 ((3-AG) enhanced the efficiency of nitrogen (N) retention. Therefore effects of Ro 16·8714 were studied on growth rate, body composition, N, fat and energy retention in pigs fed isoenergetically, but given different amounts of protein (112 or 138 g/kg diet) without (groups LP and NP) or with 60 mg Ro 16·8714 per kg diet (groups LPP and NPP) from 60 to 100 kg live weight. Weight gain (898, 927, 855 and 810 g/day in NP, NPp, LP and LPp) decreased, whereas food: gain ratio (2·94, 2·82, 3·04 and 3·24 kg/kg in NP, NPP, LP and LPP) was increased by low protein intake (P < 0·05) and both weight gain and food conversion were modified by the interaction (P × P) of protein intake and Ro 16·8714 (P < 0·05). Killing-out proportion (820, 830, 830 and 830 g/kg in groups NP, NPp, LP and LPP) was modified by protein intake and Ro 16·8714 (P < 0·05). Carcass growth rate (760, 814, 748 and 723 g/day in NP, NPP, LP and LPP) was modified by protein intake and by P × p (P < 0·05), while non-carcass growth rate (90, 77, 76 and 56 g/day in NP, NPP, LP and LPP) was changed by protein intake and by Ro 16·8714 (P < 0·05). Compared with NP, weights of kidneys (−0·025 kg), small intestine (−0·26 kg) and large intestine (−0·17 kg) were decreased by low protein feeding, and weights of heart, spleen and stomach decreased in response to Ro 16·8714 (-002, -0·02 and -0·06 kg; P < 0·05) while both low protein intake and Ro 16·8714 reduced liver weight (−0·12 and −0·23 kg, respectively; P < 0·05) and blood volume obtained at slaughter (-0·12 and -0·23 kg; P < 0·05). Carcass N (1813, 1970, 1786 and 1825 g in NP NPp, LP and LPP) increased in response to Ro 16-8714, but was reduced by low protein intake (P < 0·05), while noncarcass N (330, 309, 312 and 285 g in NP, NPp, LP and LPP) was decreased by both low protein intake and Ro 16-8714 (P < 0·01). Carcass and non-carcass fat (22·1, 19·9, 23·4 and 23·0 kg, respectively 1·51, 1·41, 1·59 and 1·68 kg in NP, NPp, LP and LPP) increased with low protein feeding (P < 0·05), but were not significantly influenced by Ro 16·8714. The efficiency of N retention (295, 363, 321 and 327 g/kg N retained: N intake in NP, NPp, LP and LPP) was enhanced by Ro 16·8714 (P > 0·05) whereas the efficiency of energy retention was not influenced by Ro 16·8714 and protein intake. In conclusion, an adequate intake of protein is necessary for optimum expression of many, but not all, effects of the P-adrenergic agonist Ro 16·8714.