Weight control is a reflection of energy balance (EB) and body composition. The maintenance of EB involves adaptations in physiology and behaviour. In turn, behaviour represents approximately 20-45 % of energy expenditure (EE) but 100 % of energy intake (EI). The interaction between these components is far from fully understood. Initially, the importance of habitual diet for weight control, and the impact of physical activity on EI will be considered separately. It is widely agreed that the macronutrient composition of the diet that people habitually consume has implications for EB and therefore for weight control. A high intake of dietary fat is a potent risk factor for body weight gain, but the relationship does not constitute a biological inevitability. There is considerable individual variability in responses to similar dietary intakes. Analysis of data bases such as the DNSBA (1990) indicates the existence of both lean and obese high fat consumers. This observation led to studies on individuals with similar BMIs but quite distinctive dietary patterns. These different consumers have been referred to as behavioural phenotypes. These high- and low-fat phenotypes (young adult males) have significantly different energy and fat intakes but similar BMIs. They display differences in RMR, RQ, resting and sleeping heart rates, plasma leptin levels, DIT responses to fat and CHO, control of meal size, tendency to passively overconsume fat, and hedonic responses to food. They do not differ in sensory responsiveness to fatty substances, energy cost of exercise and daily level of physical activity (though HF show a slight increase in the amount of time in sedentary activity). Our initial assumption was that the differences in EI (foods selected and eaten) of these phenotypes was countered by metabolic adjustments (i.e. thermogenesis). At the present time it has not been possible to detect the nature of this adjustment, although sleeping metabolism is a promising component. However, these phenotypes appear to achieve energy balance through quite distinctive profiles of behaviour and metabolism. A first attempt to genotype these groups has failed to find an association with either of two polymorphisms of the galanin-1 receptor.

In contrast to the HF and LF phenotypes, other groups can be identified who have similar habitual diets (> 43 % fat, > 120 g fat day^-1) but with high or low BMIs. These are the obese susceptible or resistant individuals. These individuals have been identified within databases and in the local community. Ultimately their characterization will involve measurement of all components of EB along with body composition. This investigation is at an early stage but a preliminary finding is that one difference between these groups (susceptible and resistant) may reside in the hedonic response to food and the impact of this on satiety.

More than 25 years ago it was argued that the driving of EI by EE constituted the basis for a mechanism controlling appetite. We have investigated this by imposing no (NEX), moderate (MEX) or high (HEX) exercise loads on groups of men and women, and monitoring changes in EI and activity. Initially there is a loose coupling between activity and EI with no immediate increase in either hunger or food intake to exercise loads of up to 5-6 MJ per day. Over periods of up to 16 days partial compensation occurs so that increased EI accounts for approximately 30 % of the increase in EE. There is evidence that it takes a considerable period of time for EI to adjust to elevations in EE, and that there is substantial individual variability in the time course of this process. Indeed, individuals in our studies can be divided into compensators and non-compensators. This feature may well help to explain why exercise is effective for inducing weight loss in some people but not in others. The physiological and behavioural characterization of these types of individuals is currently ongoing. However, in addition to the direct impact of physical activity on EB, habitual exercise can enhance the signalling sensitivity of the satiety control system and therefore adjust appetite control by improving meal to meal regulation.

The interaction between diet and exercise manipulations was examined in a study in which NEX and MEX treatments were combined with enforced high and low fat dietary regimes. Adaptation was observed in opposition to the direction of the perturbation in EB. Adaptation was stronger to negative than to positive energy balances. Enforced sedentariness (experimental suppression of physical activity in a human calorimeter) is not compensated by a reduction in EI, and therefore generates an immediate positive energy balance leading to weight gain. However, changes in body weight in response to changes in physical activity and diet are complex and can only be fully understood in the light of adjustments in body composition and the cost of energy storage.