Physical activity has the potential to modulate appetite control by improving the sensitivity of the physiological satiety signalling system, by adjusting macronutrient preferences or food choices and by altering the hedonic response to food. There is evidence for all these actions. Concerning the impact of physical activity on energy balance, there exists a belief that physical activity drives up hunger and increases food intake, thereby rendering it futile as a method of weight control. There is, however, no evidence for such an immediate or automatic effect. Short (1–2 d)-term and medium (7–16 d)-term studies demonstrate that men and women can tolerate substantial negative energy balances of ≤4MJ energy cost/d when performing physical activity programmes. Consequently, the immediate effect of taking up exercise is weight loss (although this outcome is sometimes difficult to assess due to changes in body composition or fluid compartmentalization). However, subsequently food intake begins to increase in order to provide compensation for about 30% of the energy expended in activity. This compensation (up to 16 d) is partial and incomplete. Moreover, subjects separate into compensators and non-compensators. The exact nature of these differences in compensation and whether it is actually reflective of non-compliance with protocols is yet to be determined. Some subjects (men and women) performing activity with a cost of ≤4 MJ/d for 14 d, show no change in daily energy intake. Conversely, it can be demonstrated that when active individuals are forced into a sedentary routine food intake does not decrease to a lower level to match the reduced energy expenditure. Consequently, this situation creates a substantial positive energy balance accompanied by weight gain. The next stage is to further characterize the compensators and non-compensators, and to identify the mechanisms (physiological or behavioural) that are responsible for the rate of compensation and its limits.

The effects of incremental exercise on appetite, energy intake (EI), expenditure (EE) and balance (EB) in lean men and women were examined. Six men (age 29·7 (sd5·9) years, weight 75·2 (sd15·3) kg, height 1·75 (sd0·11) m) and six women (age 24·7 (sd5·9) years, weight 66·7 (sd9·10) kg, height 1·70 (sd0·09) m) were each studied three times during a 16 d protocol, corresponding to no additional exercise (Nex), moderate-intensity exercise (Mex; 1·5–2·0 MJ/d) and high-intensity exercise (Hex; 3·0–4·0 MJ/d) regimens. Subjects were fed to EB during days 1–2, and during days 3–16 they fedad libitumfrom a medium-fat diet of constant composition. Daily EE, assessed using the doubly labelled water method, was 9·2, 11·6 and 13·7 MJ/d (P < 0·001;sed0·45) for the women and 12·2, 14·0 and 16·7 MJ/d (P = 0·007;sed1·11) for the men on the Nex, Mex and Hex treatments, respectively. EI was 8·3, 8·6 and 9·9 MJ/d (P = 0·118;sed0·72) for the women and 10·6, 11·6 and 12·0 MJ/d (P = 0·031;sed0·47) for the men, respectively. On average, subjects compensated for about 30 % of the exercise-induced energy deficit. However, the degree of compensation varied considerably among individuals. The present study captured the initial compensation in EI for exercise-induced energy deficits. Total compensation would take a matter of weeks.

We assessed the effect of no exercise (Nex; control) and high exercise level (Hex; ∼4 MJ/day) and two dietary manipulations [a high-fat diet (HF; 50% of energy, 700 kJ/100 g) and low-fat diet (LF; 20% of energy, 300 kJ/100 g)] on compensatory changes in energy intake (EI) and energy expenditure (EE) over 7-day periods. Eight lean men were each studied four times in a 2 × 2 randomized design. EI was directly quantified by weight of food consumed. EE was assessed by heart rate (HR) monitoring. Body weight was measured daily. Mean daily EE was 17.6 and 11.5 MJ/day ( P < 0.001) on the pooled Hex and Nex treatments, respectively. EI was higher on HF diets (13.4 MJ/day pooled) compared with the LF diets (9.0 MJ/day). Regression analysis showed that these energy imbalances induced significant compensatory changes in EB over time of ∼0.3-0.4 MJ/day ( P < 0.05). These were due to changes in both EI and EE in the opposite direction to the perturbation in energy balance. These changes were significant, small but persistent, amounting to ∼0.2 and ∼0.35 MJ/day for EI and EE, respectively.