There is general agreement that exercise-induced energy expenditure is not entirely compensated for at the next meal or over the following 24 h, but inter-individual variability is high. The role of ‘fatness and fitness’ in this variability has never been assessed. Therefore, eighteen non-obese male subjects aged 22·2 (sd 2·0) years were selected and separated into a ‘high-fatness and low-fitness’ (Hfat/Lfit, n 9) and a ‘low-fatness and high-fitness’ (Lfat/Hfit, n 9) group, according to three criteria: maximal oxygen uptake; weekly hours of physical activity; fat mass index. At 1 h before lunch, they were subjected to 60 min of exercise on a cycle ergometer (70 % VO2max), or stayed at rest. Then, they self-reported food intake in diaries until the next breakfast. Intake at lunch was not different between conditions, but was higher after exercise than after rest over the 24 h, leading to a significant but partial mean level of compensation of 49·8 (sem 16·5) and 37·8 (sem 24·6) % for the Hfat/Lfit and Lfat/Hfit groups, respectively. Energy compensation at lunch and over the 24 h were strongly correlated (r 0·76, P< 0·001). Both groups consumed more fat and protein after exercise than after rest over the 24 h, but the percentage of energy derived from fat increased only in the Hfat/Lfit group (2·1 (sem 0·6) %, P= 0·026). Thus, the energy cost of an aerobic exercise session was partially compensated over the next 24 h independently of the ‘fatness and fitness’ status, but ‘high-fat and low-fit’ individuals compensated more specifically on fats.

The present study assessed the relationship between breakfast frequency and measures of obesity in Hong Kong Chinese children aged 9–18 years. A total of 11 570 children (50 % boys) underwent anthropometric measurements and completed a simple self-administered dietary behaviour questionnaire. Their parents completed a questionnaire providing demographic information. Breakfast frequency was assessed by a single question, ‘How many days over the past week did you have breakfast?’ Children were categorised into three groups: skippers (ate breakfast 0–2 times/week); semi-skippers (ate breakfast 3–4 times/week); non-skippers (ate breakfast 5–7 times/week), to assess all associated characteristics. Of the 3644 primary and 7926 secondary school students, 8 % (8·7 % of boys and 6·9 % of girls) and 14 % (14 % of boys and 15 % of girls), respectively, were breakfast skippers. The prevalence of obesity among breakfast skippers, semi-skippers and non-skippers was, respectively, 9·8, 10·6 and 3·8 % (P < 0·001) for primary school students and 3·9, 3·1 and 2·4 % (P < 0·001) for secondary school students. The 12 % of Hong Kong children aged 9–18 years who skipped breakfast had higher BMI, BMI z-scores and percentage of body fat (PBF) than their counterparts. The dose effects of breakfast frequency (unstandardised regression coefficient, P < 0·001) on BMI and PBF were, respectively, − 0·125 kg/m2 and − 0·219 % for boys and − 0·165 kg/m2 and − 0·353 % for girls, adjusting for physical activity per additional breakfast meal per week. Further study is recommended to elucidate whether regular breakfast consumption may have a role in the prevention of childhood obesity.

The distribution of the four macronutrients is associated with energy intake and body fatness according to short-term interventions. The present study involves macronutrient distribution in relation to energy intake and body fatness over a period of 23 years in individuals who have ad libitum access to food. Eight follow-up measurements have been performed in 168 men and 182 women who participate in the Amsterdam Growth and Health Longitudinal Study. From the age of 13 years onwards, dietary intake, physical activity and the thickness of four skinfolds have been assessed. Body fatness was assessed using dual-energy X-ray absorptiometry at the age of 36 years. Generalised estimating equation regression analyses showed that energy percentages (En%) from protein and (in men) carbohydrates were inversely related to energy intake, while the En% from fat was positively related with energy intake. The men and women with high body fatness at the age of 36 years had a 1 En% higher protein intake, and the women with high body fatness had a 2 En% lower alcohol intake at the age of 32 and 36 years. The apparent inconsistent relationships between protein and energy intake and protein and body fatness can in women be explained by reverse causation and underreporting, as in women, low energy intake could not be explained by low physical activity. In conclusion, high intake of protein and (in men) carbohydrate, and low intake of fat are inversely related to total energy intake. High body fatness at the age of 36 years is related to a higher protein intake and, in women, to a lower alcohol intake.

Adipose tissue produces signals that can have a profound effect on many physiological functions, including energy expenditure and food intake. The hypothesis that variation in food intake of sheep resulting from differences in animal fatness can be predicted from effects of animal fatness on energetic efficiency was subjected to three tests. First, an existing food intake model was adapted to account for effects of animal fatness, as estimated by condition score, on food intake. Parameter values were derived from data obtained with two of five treatment groups of an experiment where ewe lambs were fed either chopped hay or pelleted concentrates. The model predicted the intake of the remaining three treatment groups satisfactorily. The energy intake model was subsequently extended with a protein module based upon a Gompertz curve to simulate changes in body weight and condition score. The model predicted these changes satisfactorily for most treatment groups during the experimental period of 50 weeks. In a last test, the final body weights and body lipid contents of animals fed either hay or concentrates for a period of 3 years were predicted. The predictions for final body weight (77 or 118 kg) and lipid content in the empty body (26 or 58 %) were within the range of expectations for sheep with access to hay or concentrates, respectively. The biological implications of the hypothesis that body fatness acts upon voluntary intake via its effects on energetic efficiency are discussed.

With the increasing prevalence of childhood obesity, there is an urgent need to identify risk factors that are amenable to preventative action. However, there is a remarkable lack of consistency between studies that have investigated the relationships between measurements of physical activity and energy expenditure and body fatness in children. This disparity could be because energy intake is a more important determinant in preventing obesity. Alternatively, some of the conflicting results could be related to methodological limitations in assessing activity and body composition. Erroneous conclusions may be drawn if physical activity energy expenditure is not adjusted for differences in body composition, or body fat is not appropriately adjusted for body size. For public health purposes it may be more informative to evaluate the amount and intensity of physical activity required to prevent fat-mass gain than to assess energy expended in physical activity. The lack of consensus in the cut-off points applied to define intensity levels is severely hindering comparisons between studies using accelerometers that have examined relationships between activity intensity and body fatness. Thus, it is not currently possible to develop a firm evidence base on which to establish physical activity recommendations until the limitations are addressed and more prospective studies undertaken. In order to turn research into effective prevention strategies a clearer understanding of the psycho-social, behavioural and environmental factors that influence activity is needed, including the interactions between physical activity and other behaviours such as time spent sedentary, sleeping and eating.

It is widely believed that body fatness (and hence total body mass) is regulated by a lipostatic feedback system. This system is suggested to involve at least one peripheral signalling compound, which signals to the brain the current size of body fat stores. In the brain the level of the signal is compared with a desirable target level, and food intake and energy expenditure are then regulated to effect changes in the size of body fat stores. There is considerable support for this theory at several different levels of investigation. Patterns of body-mass change in subjects forced into energy imbalance seem to demonstrate homeostasis, and long-term changes in body mass are minor compared with the potential changes that might result from energy imbalance. Molecular studies of signalling compounds have suggested a putative lipostatic signal (leptin) and a complex network of downstream processing events in the brain, polymorphisms of which lead to disruption of body-mass regulation. This network of neuropeptides provides a rich seam of potential pharmaceutical targets for the control of obesity. Despite this consistent explanation for the observed phenomena at several different levels of enquiry, there are alternative explanations. In the present paper we explore the possibility that the existence of lipostatic regulation of body fatness is an illusion generated by the links between body mass and energy expenditure and responses to energy imbalance that are independent of body mass. Using computer-based models of temporal patterns in energy balance we show that common patterns of change in body mass following perturbation can be adequately explained by this ‘non-lipostatic’ model. This model has some important implications for the interpretations that we place on the molecular events in the brain, and ultimately in the search for pharmaceutical agents for alleviation of obesity.

According to the report of the World Health Organization (1985), total energy expenditure (TEE) in human subjects can be calculated as BMR×physical activity level (PAL). However, other reports have pointed out limitations in the suggested procedure related to the % body fat of the subjects. The purpose of the present study was to evaluate the World Health Organization (1985) procedure in thirty-four healthy women with BMI 18–39kg/m2. BMR and TEE were measured using indirect calorimetry (BMRmeas) and the doubly-labelled water method (TEEref) respectively. When assessed using the doubly-labelled water and skinfold-thickness methods, the women had 34 (sd 8) and 33 (sd 6) % body fat respectively. On the basis of guidelines provided by the World Health Organization (1985), 1·64 was selected to represent the average PAL of the women. Furthermore, PAL was also assessed by means of an accelerometer (PALacc), heart-rate recordings (PALHR) and a questionnaire (PALq). These estimates were: PALacc 1·71 (sd 0·17), PALHR 1·76 (sd 0·24), PALq 1·86 (sd 0·27). These values were lower than TEEref/BMRref, which was 1·98 (sd 0·21). BMR assessed using equations recommended by the World Health Organization (1985) (BMRpredicted) overestimated BMR by 594 (sd 431) kJ/24h. However, when TEE was calculated as BMRpredicted×PALacc, BMRpredicted×PALHR and BMRpredicted×PALq respectively, average results were in agreement with TEEref. Furthermore, TEE values based on BMRpredicted and PALacc, PALHR, PALq as well as on PAL=1·64, minus TEEref, were significantly correlated with body fatness. When the same PAL value (1·64) was used for all subjects, this correlation was particularly strong. Thus, the World Health Organization (1985) procedure may give TEE results that are biased with respect to the body fatness of subjects.

In order to study the influence of heredity on resting metabolic rate (RMR), 20 monozygotic and 19 dizygotic male twin pairs aged 20.6 (SD 2.9) and 21.4 (SD 3.1) years, gave their consent to participate in the experiment. Fat free weight (FFW) was estimated from underwater weighing. RMR was measured by indirect calorimetry using an open circuit system. RMR was expressed as kJ · min−1, kJ/m2 · h−1, kJ/kg · h−1 and kJ/kgFFW · h−1. Significant intraclass coefficients were observed in MZ twins for the different expressions of RMR. The values ranged from r = 0.45 (P < 0.05) to r = 0.81 (P < 0.01). However, DZ twins demonstrated lower intraclass coefficients for RMR, with a range from r = 0.21 to r = 0.44. Significant (P < 0.05) DZ resemblance was revealed only when RMR was expressed as kJ · min−1 and kJ/kg · h−1. Results of the present study suggest that variations in RMR may have a genetic component. Implications for human energy balance and body fat are discussed.