Cross talk between physical activity and appetite control: does physical activity stimulate appetite?

Abstract

Abbreviations: EB, energy balance; EE, energy expenditure; EI, energy intake; Hex, high exercise level; Mex, medium exercise level; Nex, no exercise. 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 ≤ 4 MJ 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.Energy balance: Physical activity: Appetite EB, energy balance; EE, energy expenditure; EI, energy intake; Hex, high exercise level; Mex, medium exercise level; Nex, no exercise.

Interaction between Disinhibition and restraint: Implications for body weight and eating disturbance

“…It is known that there is an uncoupling between energy expenditure and energy intake (53,54), where the low level of energy expenditure does not lead to a corresponding down regulation in energy intake. The classic study by Mayer, Roy and Mitra (55) demonstrated that appetite is poorly regulated at low activity levels.…”

Exercise in rats does not alter hypothalamic AMP-activated protein kinase activity

“…We were interested to investigate whether exercise could affect AMPK activity in the hypothalamus, thereby providing a potential mechanism for the coordination of energy expenditure and energy intake during or following exercise. For instance, exercise leads to changes in appetite such that appetite is suppressed during strenuous exercise and a short while after exercise [18; 19] whereas increases in appetite after a single bout of exercise are not always found [19]). These changes in appetite could therefore be expected to stem from changes in hypothalamic AMPK activity.…”

“…Exercise leads to changes in appetite such that appetite is suppressed during strenuous exercise [18; 19] and a short while after exercise whereas increases in appetite after a single bout of exercise are inconsistent (For review see [19]). The mechanism behind this exercise-induced change in appetite is not known [19] but could involve changes in hypothalamic AMPK activity which may serve the function of coordinating energy expenditure during exercise with energy intake during or after exercise.…”

Effects of physical activity on food intake

“…50 The adipocytokines, under normal weight conditions, guarantee homeostasis of glucose and lipid metabolism, but their dysregulated production in the obese state is associated with 52 and that compensatory responses in intake to altered levels of exercise may not begin to act until the excess energy stores become depleted and the energy homeostasis is at risk. 3 …”