Objective: To develop new equations for the estimation of basal metabolic rate in children aged 10 ± 15 years, and to evaluate the impact of including pubertal stage into the equations. Design: Mixed longitudinal. Setting: The children were recruited from schools in Oxford, and the measurements were made in the schools. Subjects: 195 school children, aged 10 ± 15 years, were recruited in three cohorts. The gender distribution of the subjects was 40% boys and 60% girls. Methods: Basal metabolic rate (BMR) was measured, by indirect calorimetry, at 6-monthly intervals for 3 years. Anthropometric data, height, weight, body breadths and skinfold measurements (biceps, triceps, subscapular, suprailiac and medial calf) were collected on each occasion. Fat and fat-free mass was calculated from the skinfold measurements. Pubertal development was also assessed on annually by paediatricians. Pubic hair (PH) and gonad (G) development was assessed in boys and breast (B) development in girls. The girls were questioned about menarche. Stepwise multiple regression analysis was used to develop and assess new formulae for BMR that also incorporate pubertal development. 554). Weight was the most important factor in developing the regression equations for the calculation of BMR in both sexes (R 2 0.61 and 0.52 for boys and girls, respectively). Stepwise multiple regression analyses, with independent variables such as gender, weight, height, puberty stage and skinfolds, allowed several BMR regression equations to be developed. The inclusion of the menarche status in the regression equations signi®cantly (P`0.05) improved BMR estimation in the pre-menarche girls. Boys, pubertal stage as assessed by Pubic Hair (PH) and Gonadal Stage (G) did not contribute to a signi®cant improvement in BMR estimation, except for 11-year-olds. Conclusions: The inclusion of pubertal stage afforded only minor improvements in the derivation of regression equations for the estimation of BMR of children aged between 10 and 15 years.

The rate of protein synthesis in skeletal muscle was measured in vivo in rats at various times during the first 2 days after abdominal surgery. Protein synthesis in abdominal muscle at the site of the wound was slightly reduced 2 h after operation, had returned to normal by 24 h and was massively increased by 48 h after surgery. In contrast, there was no change at any time in the rate of protein synthesis in either the gastrocnemius muscle or abdominal muscle distant from the wound site. Surgery had no effect on the weight or protein content of the gastrocnemius muscle, although urinary nitrogen excretion was increased relative to food intake, indicating the presence of a net catabolic response. Changes in whole-body protein turnover in response to uncomplicated abdominal surgery are thus likely to reflect the anabolic processes of wound healing and repair as well as any catabolic response in uninjured tissues.

The amount of energy mobilized or stored as protein, expressed as a proportion of the total energy stored or mobilized (defined as the P ratio, Payne & Dugdale, 1977), was investigated in the young male (rapid growth) and adult female (slow growth) rat. Energy mobilization was induced by a 3 d fast and the changes in body content of fat and lean tissues were used to estimate the fasting P ratio (Pfast). Tissue storage was subsequently effected by 17 d of refeeding and the corresponding ratio (Prefed) was calculated from the amounts of lean and fat tissue regained. The same experimental protocol was used for measuring Pfast and Prefed in weanling (30d) and adult (130d) rats. Weightmatched individuals were assigned to three groups. All animals in group 1 were killed at the beginning of the experiment. Animals in group 2 were fasted for 3 d and then killed. Group 3 animals were first fasted for 3 d, then had free access to a stock diet for a further 17 d before being killed. During fasting, a close linear relationship was found between weight change and body energy changes (r 0.985, and r 0.92, P

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The relationship between essential fatty acids (EFA) deficiency and the utilization of dietary protein, growth rate and survival of offspring was investigated in rats during development and reproduction. EFA deficiency was induced by feeding a 200 g casein/kg-based diet containing 70 g hydrogenated coconut oil (HCO)/kg as the only source of fat. The conversion efficiency of dietary protein was assessed as net protein utilization (NPU), using a 10 d comparative carcass technique. Consumption of the deficient diet during the 10 d assay period induced biochemical changes characteristic of mild EFA deficiency in humans (triene:tetraene 0.27 (SD 0.04) compared with 0.026 (SD 0.004) for wn-deficient controls), but there were no significant changes in growth rate or protein utilization. These variables were also unchanged when the deficient diet was fed for an additional 7 d before the assay, although triene: tetraene increased to 0.8 (SD 0.02). Feeding the deficient diet for 63 d before assay produced severe EFA deficiency (triene:tetraene 1.4 (SD 0.3) u. 0.036 (SD 0.005) for controls), a fall in growth rate (25% during assay period), and NPU (31.5 (SD 0.63) v. 39-0 (SD 0.93) for controls). These severely-EFA-deficient animals had a 30% higher fasting-resting rate of energy metabolism than that of age-matched controls. However, there was no change in the rate of endogenous N loss. Voluntary energy consumption was increased in animals fed on deficient diets, either with 200 g protein/kg, or protein free. The reduced efficiency of protein utilization could be entirely accounted for by the restricted amount of energy available for growth and protein deposition. Consumption of an EFA-deficient diet during pregnancy and lactation resulted in high mortality (11 % survival rate at weaning compared with 79% for controls) and retarded growth in the preweaning offspring. It is concluded that animals are particularly sensitive to EFA deficiency during reproduction and pre-and post-natal stages of development. However, after weaning only severe EFA deficiency retarded growth, primarily through changes in energy balance.