Objective: To identify and characterize the individual variability in compensation for exercise-induced changes in energy expenditure (EE). Design: Twelve-week exercise intervention. Subjects: Thirty-five overweight and obese sedentary men and women (body mass index, 31.874.1 kg m À2 ; age, 39.6711.0 years) were prescribed exercise five times per week for 12 weeks under supervised conditions. Measurements: Body weight, body composition, resting metabolic rate (RMR), total daily energy intake (EI) and subjective appetite sensations were measured at weeks 0 and 12. Results: When all subjects' data were pooled, the mean reduction in body weight (3.773.6 kg) was significant (Po0.0001) and as predicted, which suggested no compensation for the increase in EE. However, further examination revealed a large individual variability in weight change (À14.7 to þ 1.7 kg). Subjects were identified as compensators (C) or noncompensators (NC) based on their actual weight loss (mean NC ¼ 6.373.2 kg and C ¼ 1.57 2.5 kg) relative to their predicted weight loss. C and NC were characterized by their different metabolic and behavioural compensatory responses. Moderate changes in RMR occurred in C (À69.27268.7 kcal day À1 ) and NC (14.27242.7 kcal day À1 ). EI and average daily subjective hunger increased by 268.27455.4 kcal day À1 and 6.9711.4 mm day À1 in C, whereas EI decreased by 1307485 kcal day À1 and there was no change in subjective appetite (0.479.6 mm day À1 ) in NC. Conclusion: These results demonstrate that expressing the exercise-induced change in body weight as a group mean conceals the large inter-individual variability in body weight and compensatory responses. Individuals who experience a lower than predicted weight loss are compensating for the increase in EE.

An activity-induced increase in energy expenditure theoretically disturbs energy balance (EB) by creating an acute energy deficit. Compensatory responses could influence the weight loss associated with the energy deficit. Individual variability in compensation for perturbations in EB could partly explain why some individuals fail to lose weight with exercise. It is accepted that the regulatory system will readily defend impositions that promote a negative EB. Therefore, a criticism of exercise interventions is that they will be ineffective and futile methods of weight control because the acute energy deficit is counteracted. Compensation for exercise-induced energy deficits can be categorized into behavioral or metabolic responses and automatic or volitional. An automatic compensatory response is a biological inevitability and considered to be obligatory. An automatic compensatory response is typically a metabolic consequence (e.g., reduced resting metabolic rate) of a negative EB. In contrast, a volitional compensatory response tends to be deliberate and behavioral, which the individual intentionally performs (e.g., increased snack intake). The purpose of this review is to highlight the various metabolic and behavioral compensatory responses that could reduce the effectiveness of exercise and explain why some individuals experience a lower than expected weight loss. We propose that the extent and degree of compensation will vary between individuals. That is, some individuals will be predisposed to compensatory responses that render them resistant to the weight loss benefits theoretically associated with an exercise-induced increase in energy expenditure. Therefore, given the inter-individual variability in behavioral and metabolic compensatory responses, exercise prescriptions might be more effective if tailored to suit individuals.

2Exercise is widely regarded as one of the most valuable components of behaviour that can influence body weight and therefore help in the prevention and management of obesity. Indeed long term controlled trials show a clear dose related effect of exercise on body weight. However, there is a suspicion, particularly fuelled by media reports, that exercise serves to increase hunger and drive up food intake thereby nullifying the energy expended through activity. Not everyone performing regular exercise will lose weight, and several investigations have demonstrated a huge individual variability in the response to exercise regimes. What accounts for this heterogeneous response? First, exercise (or physical activity) through the expenditure of energy will influence the energy balance equation with the potential to generate an energy deficit. However, energy expenditure also influences the control of appetite (i.e. the physiological and psychological regulatory processes underpinning feeding) and energy intake. This dynamic interaction means that the prediction of a resultant shift in energy balance, and therefore weight change, will be complicated. In changing EI, exercise will impact on the biological mechanisms controlling appetite. It is becoming recognized that the major influences on the expression of appetite arise from fat-free mass and fat mass, Resting Metabolic Rate, gastric adjustment to ingested food, changes in episodic peptides including insulin, ghrelin, CCK, GLP-1 and PYY, as well as tonic peptides such as leptin. Moreover there is evidence that exercise will influence all of these components which, in turn, influence the drive to eat through the modulation of hunger (a conscious sensation reflecting a mental urge to eat) and adjustments in post-prandial satiety via an interaction with food composition. The specific actions of exercise on each physiological component will vary in strength from person to person (according to individual physiological characteristics) and with the intensity and duration of exercise. Therefore, individual responses to exercise will be highly variable and difficult to predict. Background Issues

These data show that the effect of exercise on appetite regulation involves at least 2 processes: an increase in the overall (orexigenic) drive to eat and a concomitant increase in the satiating efficiency of a fixed meal.