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Plant secondary metabolites are a natural resource that is largely unexploited in ‘conventional’ animal production systems. They have in the past been generally considered as a source of anti-nutritional factors, and not as a source of exploitable performance-enhancing compounds. Recent and continuing changes to legislation controlling the use of animal feed additives have stimulated interest in bioactive secondary metabolites as alternative performance enhancers. They are broadly compatible with current thinking on the future of agriculture and food in Europe, and with consumer opinion. Interest has been largely on their manipulative role in the digestive and absorptive processes of the hindgut. The present paper will review the use of plants and their extracts to manipulate the rumen microbial ecosystem to improve the efficiency of rumen metabolism. The bioavailability of secondary metabolites and their actions on peripheral metabolism will be considered with a view to improving animal performance. The challenge of delivering plants and their extracts to animals outdoors in a controlled manner will be discussed. Much of what is known about the beneficial roles of plant secondary metabolites on animal performance is circumstantial and is based on tenuous data. In order to more fully exploit their bioactive properties for the benefit of animal performance, modes of action need to be understood. Uptake will be dependent on proven efficacy and consumer acceptance of assurances relating to safety, welfare and the environment.

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1. The effects of fasting for 12, 36 and 72 h were examined in 19 normal subjects. Each subject was studied before and during a euglycaemic (4 mmol/l) hyperinsulinaemic (100 m-units min-1 m-2) clamp. Measurements were made of palmitate turnover and oxidation, glucose disposal, thermogenesis, intermediary metabolites and cardiovascular variables. 2. Basal respiratory exchange ratio fell from 0.78 +/- 0.01 to 0.75 +/- 0.01 to 0.72 +/- 0.01 with fasting (P < 0.001). In response to the clamp it rose to 0.91 +/- 0.02, 0.83 +/- 0.01 and 0.77 +/- 0.01 after 12, 36 and 72h respectively. Metabolic rate rose during the clamp by 0.41 +/- 0.06, 0.11 +/- 0.03 and 0.14 +/- 0.04 kJ/min respectively (P < 0.001 for 36- and 72-h values versus that at 12h). 3. Fasting reduced total insulin-mediated glucose disposal rates from 42.6 +/- 2.5, to 31.0 +/- 1.8 to 21.3 +/- 1.5 mumol min-1 kg-1 body weight after 12, 36 and 72h respectively (P < 0.001). Glucose oxidation fell from 16.9 +/- 1.1 to 8.7 +/- 1.7 to 0.2 +/- 1.3 mumol min-1 kg-1 body weight over the same period (P < 0.001). Non-oxidative glucose disposal rates did not change significantly. 4. Basal plasma palmitate turnover increased with duration of fasting, being 1.16 +/- 0.08, 1.72 +/- 0.17 and 2.30 +/- 0.35 mumol min-1 kg-1 body weight. In response to the clamp, palmitate turnover fell to 0.42 +/- 0.05, 0.69 +/- 0.08 and 1.28 +/- 0.45 mumol min-1 kg-1 body weight. Plasma palmitate oxidation was 0.58 +/- 0.04, 0.75 +/- 0.06 and 1.13 +/- 0.11 mumol min-1 kg-1 body weight basally, and fell to 0.16 +/- 0.02, 0.28 +/- 0.04 and 0.43 +/- 0.13 mumol min-1 kg-1 body weight by the end of the clamp. The proportion of total lipid oxidation represented by plasma non-essential fatty acid oxidation was not affected by fasting, but fell in response to the clamp. 5. Fasting caused a progressive resistance to the effects of insulin and glucose on oxidative glucose disposal and on forearm glucose uptake. Insulin-mediated glucose storage was unaffected by fasting, but the apparent cost of this storage was reduced by fasting.