Four sheep sustained by intragastric nutrition were used to study saliva secretion and the relationship between osmotic pressure in the rumen and net water transport across the rumen wall. Different concentrations of buffer were infused into the rumen to change the rumen osmotic pressure. Salivary secretion was estimated from entrance of P into the rumen. Net water transport across the rumen wall was calculated as the difference between water inflow and water outflow from the rumen. A negative linear relationship between the rumen osmotic pressure (X, mOsm/kg) and the water absorption across the rumen wall (Y, ml/h) was found: Y = (394 SE 8·3)–(l·22 SE 0·03) X, r20·83, (P < 0·001), and a positive linear relationship was found between the rumen osmotic pressure (X, mOsm /kg) and the outflow rate of rumen fluid (Y, ml/h): Y = (34·0 SE 8·0) + (0·97 SE 0·03), X, r2 0·56, (P < 0·001). The implication is that rumen osmotic pressure can be a key factor in the control of the net water transport across the rumen wall, the outflow of rumen fluid to omasum and the rumen liquid dilution rate. A method is suggested by which salivary secretion in sheep may be calculated from the water balance in the rumen.

In adults, body mass (BM) and its components fat-free mass (FFM) and fat mass (FM) are normally regulated at a constant level. Changes in FM and FFM are dependent on energy intake (EI) and energy expenditure (EE). The body defends itself against an imbalance between EI and EE by adjusting, within limits, the one to the other. When, at a given EI or EE, energy balance cannot be reached, FM and FFM will change, eventually resulting in an energy balance at a new value. A model is described which simulates changes in FM and FFM using EI and physical activity (PA) as input variables. EI can be set at a chosen value or calculated from dietary intake with a database on the net energy of foods. PA can be set at a chosen multiple of basal metabolic rate (BMR) or calculated from the activity budget with a database on the energy cost of activities in multiples of BMR. BMR is calculated from FFM and FM and, if necessary, FFM is calculated from BM, height, sex and age, using empirical equations. The model uses existing knowledge on the adaptation of energy expenditure (EE) to an imbalance between EI and EE, and to resulting changes in FM and FFM. Mobilization and storage of energy as FM and FFM are functions of the relative size of the deficit (EI/EE) and of the body composition. The model was validated with three recent studies measuring EE at a fixed EI during an interval with energy restriction, overfeeding and exercise training respectively. Discrepancies between observed and simulated changes in energy stores were within the measurement precision of EI, EE and body composition. Thus the consequences of a change in dietary intake or a change in physical activity on body weight and body composition can be simulated.

To study the importance of site of recovery and other factors related to mobile-bag (MB) digestion values, two consecutive experiments in which diets were applied in a 3 × 3 Latin square design, were carried out with cannulated growing heifers. In Expt 1, several types of experimental feed were exposed to intestinal digestion in mobile bags made of two cloth types and filled with intact or rumen-undegradable (RUD) feed material to be recovered either from the ileum (IB) or faeces (FB). In Expt 2, mean retention time (MRT) of Yb-labelled digesta particles within the intestine and in vivo digestibility of diets were measured. With vegetable concentrates, FB resulted generally in slight overestimation of small-intestinal dry matter and N digestion, while with meat-and-bone meal no difference between FB and IB was found. The respective N digestibility of RUD late-cut silage was clearly underestimated as measured from FB. The disappearance of neutral-detergent fibre (NDF) of all feeds under test was higher from FB than from IB. It was not possible to isolate the influence of the large intestine on the MB values by changing bag cloth type. Irrespective of the longer retention time of bags and longer MRT of Yb in the intestine on a low as compared with a high level of feeding, only NDF disappearance of feeds increased due to lower feeding level. Altering the diet type to increase large-intestinal fermentation, as indicated in vivo, usually had no effect on the MB values. It is concluded that the site of collection of bags does not practically affect small-intestinal digestion values of feed N, unless the feed is rich in fibre.

The effects of physical activity during pregnancy and lactation on the fetal outcome and the growth of pups was studied in Wistar rats (n 144). Rats were trained to swim for 2 h every day, 6 dsweek through pre-pregnancy, pregnancy and lactation. Maternal exercise during pregnancy, despite the dams having ad lib. access to food, resulted in low-birth-weight pups (5·6 (SD 0·7) g; n 178 in exercised dams v. 6·2(SD 0·8)g; n 238 in sedentary dams). Maternal exercise continued through lactation exaggerated further the growth retardation of these pups (30·0 (SD 4·7) g; n 78 in exercised dams v. 36·0 (SD 6·9) g; n 126 in sedentary dams). The effects of maternal exercise during pregnancy and lactation studied over two successive generations revealed a reduction in the growth rates of the second generation progeny of both exercised (5·3 (SD 0·9) g; n 125 at birth and 25·1 (SD 6·8) g; n 54 at weaning) and sedentary rats (6·0 (SD 0·2) g; n 110 at birth and 31·3 (SD 4·3) g at weaning) born to first-generation exercised rats. While slower growth in the former indicates a cumulative effect of exercise stress over two generations, that of the latter indicates that the generational effects are manifest even though the dams of the F1 generation were not exposed to exercise stress during pregnancy and lactation. These findings suggest that the adverse effect of maternal exercise during pregnancy and lactation on fetal outcome in one generation is transferred to the subsequent generation.

Using a first-order model to describe ruminal in situ digestion implies that the rate of digestion is affected only by the quantity of potentially digestible substrate remaining. Other factors, like the microbial efficacy for digesting substrate, are assumed to be constant. However, microbes are not only the cause but also the result of digestion, being one of the digestion end-products. Two sigmoidal models (a logistic and a Gompertz-like model) were derived from a general digestion function in which the rate of digestion equals the product of the quantity of potentially digestible substrate remaining and a non-constant fractional rate of digestion (microbial efficacy function). The models were compared with a first-order model with a discrete lag time. The logistic model specifically accounted for the conversion of substrate mass to microbial mass, but did not describe microbial migration between the substrate and the ruminal fluid. In contrast, the Gompertz-like model assumed that the change in microbial efficacy was only time-dependent. There was little difference between models in estimates of scale parameters, but the asymptotic microbial efficacy was consistently higher for the logistic model than for the other models. Estimates of discrete lag time in the first-order model were biased towards obtaining values identical to the independent variable. Scale estimators appeared to be more robust than kinetic estimators. Lack-of-fit was present for most model-data set combinations. The similar patterns of residuals between models suggested that a four-parameter model may be insufficient to describe the data. It was concluded that if a four-parameter model is to be used, the model with a discrete lag time would be the least biologically appropriate.

Dietary intakes of starch and non-starch polysaccharides (NSP) have been estimated for a rural West African community. These people eat directly from shared bowls of cooked food, and so measurement of any individual's food intake is not possible. Recently developed methodology for estimating food intake under these circumstances and the analysis of samples for dietary polysaccharides are combined to yield estimates of intakes of about 375 g starch and 25 g NSP/d for adult males, with lower intakes for women and children, related to their smaller body weights. These intakes are not direct measurements but are extremely plausible when compared with values obtained for other societies where the complication of the shared food bowl does not impinge upon the measurements.

The relationship between total body water (TBW) and extracellular water (ECW), measured by deuterium oxide dilution and bromide dilution respectively, and impedance and impedance index (height2/impedance) at 1, 5, 50 and 100 kHz was studied. After correction for TBW, ECW was correlated only with the impedance index at 1 and 5 kHz. After correction for ECW, TBW was best correlated with the impedance index at 100 kHz. The correlation of body-water compartments with impedance values obtained with modelling programs was lower than with measured impedance values. Prediction formulas for ECW (at 1 and 5 kHz) and TBW (at 50 and 100 kHz) were developed. The prediction errors for ECW and TBW were 1·0 and 1·7 kg respectively (coefficient of variation 5%). The residuals of both ECW and TBW were related to the ECW/TBW value. Application of the prediction formulas in a population, independently measured, revealed a slight overestimation of TBW and ECW, which could be largely explained by differences in the validation group in body-water distribution and in body builds. The ratio of impedance at 1 kHz to impedance at 100 kHz was correlated with body-water distribution (ECW/TBW). The relation is however not strong enough to be useful as a predictor. It is concluded that an independent prediction of ECW and TBW, using impedance at low and high frequency respectively, is possible, but that the bias depends on the body-water distribution and body build of the measured subject.

The relationship between body fat and stature-adjusted weight indices was explored. Assuming the term height2 is a valid indicator of a subject's lean body mass, height2/weight was shown to be an accurate measure of percentage lean body mass and, as such, a better predictor of percentage body fat than the traditional body mass index (BMI; weight/height2). The name, lean body mass index (LBMI), is proposed for the index height2/weight. These assumptions were confirmed empirically using the results from the Allied Dunbar National Fitness Survey (ADNFS). Using simple allometric modelling, the term heightp explained 74% of the variance in lean body mass compared with less than 40% in body weight. For the majority of ADNFS subjects the fitted exponent from both analyses was approximately p = 2, the only exception being the female subjects aged 55 years and over, where the exponent was found to be significantly less than 2. Using estimates of percentage body fat as the dependent variable, regression analysis was able to confirm that LBMI was empirically, as well as theoretically, superior to the traditional BMI. Finally, when the distributional properties of the two indices were compared, BMI was positively skewed and hence deviated considerably from a normal distribution. In contrast, LBMI was found to be both symmetric and normally distributed. When height and weight are recorded in centimetres and kilograms respectively, the suggested working normal range for LBMI is 300–500 with the median at 400.

The β-agonist ractopamine (RAC) promotes protein deposition with little effect on fat deposition in the pig. To assess whether the lack of effect on fat deposition was due to changes in response to homeostatic signals, eight crossbred gilts (73 kg body weight (BW)) with venous catheters were used to examine plasma metabolite and hormone concentrations before and after intravenous injections of insulin and the β2-agonist fenoterol during dietary RAC (0 or 20 mg/kg) treatment. Pigs received intravenous challenges of insulin (1μg/kg BW) on days 3, 9 and 23 and fenoterol (2 μg/kg BW) on days 4, 10 and 24 of treatment. RAC was then withdrawn from the diet and insulin and fenoterol challenges were repeated 6 and 7 d later respectively. Blood samples for the determination of metabolite and hormone concentrations were taken at -30, -20, -10, -1, 2·5, 5, 10, 20, 30, 45, 60 and 120 min relative to the challenges. Dietary RAC decreased basal plasma insulin concentrations but had no effect on plasma glucose or non-esterified fatty acids (NEFA). Hypoglycaemic responses to insulin were not affected by RAC while the anti-lipolytic effects of insulin tended to be augmented. Dietary RAC decreased the lipolytic response to fenoterol, this being evident after 4 d treatment. Hypoglycaemic response to fenoterol was not changed whereas the hyperinsulinaemic response to fenterol was attenuated by dietary RAC. Previous treatment with RAC did not influence basal hormone and metabolite concentrations or responses to homeostatic signals during the withdrawal period. While these results suggest little change in glucose metabolism, the de-sensitization of adipose tissue β-adrenergic receptors is consistent with the observations that dietary RAC has little effect on the rate of fat deposition in the growing pig.

To assess the effect of an antenatal nutrition programme designed specifically for the local population, questionnaires on nutrition knowledge, attitudes to healthier eating and 4 d diet diaries were completed by women attending routine antenatal clinics. Women who received the nutrition education programme were allocated into an Intervention Education Group whilst those women who did not were allocated into a Routine Education Group. The results showed that knowledge about nutrition was significantly higher in the intervention group. However, no significant differences were detected between the two groups for attitude variables or nutrient intake. It is concluded, therefore, that the most-widely-read form of nutrition advice for pregnant women may have some impact on nutrition knowledge but has little effect on nutrient intake during pregnancy.

A new model for describing forage degradation kinetics during incubation in the rumen using polyester bags is presented. Attention is given to dealing with the problem of deviations from exponential behaviour in the early stages of degradation by devising a function capable of representing exponential or sigmoidal trends. This is achieved by allowing part of the fractional degradation rate to vary with time of incubation, thus enabling responses other than those expected under simple first-order kinetics to be described. Seven sets of data consisting of 620 curves were analysed to study the performance of the new model compared with a commonly used exponential model. The proportion of significantly better fits varied from set to set. The new model deals successfully with sigmoidal behaviour and, thus, provides a means of analysing the degradation profiles of low-quality

Feeding trials have been done with rats to assess the effects of long-term (700 d) consumption of diets based on raw cowpeas (Vigna unguiculata; moderate Bowman–Birk inhibitor content, low lectin content), lupin seeds (Lupinus angustifolius; low lectin and protease inhibitor content) or soya beans (Glycine max; high Kunitz inhibitor content, moderate Bowman–Birk inhibitor content, moderate lectin content) or diets containing low levels of raw kidney bean (Phaseolus vulgaris; high lectin content, low Bowman–Birk inhibitor content) on body weight and composition and organ weights. All the legume-based diets reduced feed conversion efficiency and growth rates during the initial 250 d. However, after 250 d the weight gains by rats given legume-based diets were similar to those of controls given the same daily feed intake. Long-term consumption of diets containing low levels of kidney bean significantly altered body composition of rats. The levels of lipid in the body were significantly reduced. As a result, carcasses of these rats contained a higher proportion of muscle/protein than did controls. Small-intestine relative weight was increased by short- and long-term consumption of the kidney-bean-based diet. However, the increase in relative pancreatic weight observed at 30d did not persist long term. None of the other legume-based diets caused any significant changes in body composition. However, long-term exposure to a soya-bean- or cowpea-based diet induced an extensive increase in the relative and absolute weights of the pancreas and caused an increase in the incidence of macroscopic pancreatic nodules and possibly pancreatic neoplasia. Long-term consumption of the cowpea-, kidney-bean-, lupin-seed- or soya-bean-based diets by rats resulted in a significant increase in the relative weight of the caecum and colon.

Twelve male subjects took part in a study to investigate the effects of overfeeding a high-fat diet (19·17 MJ/d; 58% energy from fat) for 2 weeks on plasma cholecystokinin (CCK) levels, food intake, and subjective feelings of hunger and fullness. Before and after the diet, subjects completed a 2-week weighed dietary inventory, formal measurements of food intake from a pre-selected appetizing evening meal were carried out, and blood samples were taken after a standard breakfast for measurement of CCK. Hunger and fullness were rated on visual analogue scales before and after each of these meals and at evening meals during the diet period. Following the high-fat diet there was a small non-significant increase in food intake from the pre-selected meal (6919 (SE 615) kJ ν 6405 (SE 540) kJ; P = 0·1) and a significant increase in the average daily food consumption measured from the diaries (10·25 (SE 0·49) MJ/d ν. 9·59 (SE 0·62) MJ/d; P = 0·05). Corresponding trends of increasing feelings of hunger and declining fullness also occurred over the study period. Plasma CCK responses to the standard breakfast were raised following the diet (1285 (SE 153) ν. 897 (SE 78) pM min; 3h integrated CCK production post ν. pre diet; P < ·01) with the major differences observed at 90 and 120 min following the meal. These results suggest that the increase in food intake may be related to a down-regulation in putative CCK receptors responsible for food intake. Elevated CCK levels might suggest a corresponding down-regulation in CCK receptors responsible for feedback inhibition of CCK release.