The consequences of exercise-induced weight loss on food reinforcement. A randomized controlled trial

Abstract

Background Obesity remains a primary threat to the health of most Americans, with over 66% considered overweight or obese with a body mass index (BMI) of 25 kg/m 2 or greater. A common treatment option many believe to be effective, and therefore turn to, is exercise. However, the amount of weight loss from exercise training is often disappointingly less than expected with greater amounts of exercise not always promoting greater weight loss. Increases in energy intake have been prescribed as the primary reason for this lack of weight loss success with exercise. Research has mostly focused on alterations in hormonal mediators of appetite (e.g.: ghrelin, peptide YY, GLP-1, pancreatic polypeptide, and leptin) that may increase hunger and/or reduce satiety to promote greater energy intake with exercise training. A less understood mechanism that may be working to increase energy intake with exercise is reward-driven feeding, a strong predictor of energy intake and weight status but rarely analyzed in the context of exercise. Design Sedentary men and women (BMI: 25-35 kg/m 2 , N = 52) were randomized into parallel aerobic exercise training groups partaking in either two or six exercise sessions/week, or sedentary control for 12 weeks. Methods The reinforcing value of food was measured by an operant responding progressive ratio schedule task (the behavioral choice task) to determine how much work participants were willing to perform for access to a healthy food option relative to a less healthy food option before and after the exercise intervention. Body composition and resting energy expenditure were assessed via DXA and indirect calorimetry, respectively, at baseline and post testing.

Effect of exercise training interventions on energy intake and appetite control in adults with overweight or obesity: A systematic review and meta‐analysis

“… 6 , 7 , 37 , 47 , 66 Fourth, at the time of peer‐review, the search had been over a year old and three new studies were identified. 87 , 88 , 89 The findings are briefly reported here.…”

“…In their secondary analysis of a 12‐week aerobic exercise intervention of either six sessions per week, two sessions per week, or no‐exercise control, Flack et al found no significant changes in the reinforcing value of healthy and unhealthy snack foods (i.e., food reward). 87 Mason et al found no changes in eating behavior traits relating to binge eating, uncontrolled eating, emotional eating, and restrained eating after 12 months of aerobic exercise training in postmenopausal women. 88 And Paravidino et al showed that during 2 weeks of moderate‐intensity, vigorous‐intensity, or no‐exercise control in Brazilian Naval Academy cadets with overweight, changes in self‐reported energy intake were not different among groups nor were there any changes in appetite sensations taken before and after an ad libitum cafeteria breakfast.…”

Physiology of weight regain: Lessons from the classic Minnesota Starvation Experiment on human body composition regulation

“…124,125 A nonleptin system (and so far unidentified adipostatic signals) has recently been implicated in the compensatory hypophagia that plays a critical role in the recovery from rapid weight gain induced by overfeeding. 126 On the other hand, the notion of a feedback loop between FFM deficit and compensatory hyperphagia (Figure 9), as suggested by the MSE reanalysis 63 and by recent studies of weight regain after caloric restriction in humans [98][99][100][101][102] and in mice, 127…”

“…Specifically in their reanalysis of the DiOGenes study, they showed that the fraction of weight loss as FFM in men was positively associated with weight regain and with increased appetitive factors such as hunger and desire to eat. 101 Finally, the recent report 102 that following a 12-week aerobic exercise intervention aimed at weight loss in young adults with overweight/obesity, those who lost the greatest amount of FFM showed that the highest increase in reward-driven feeding (which is a strong predictor of energy intake) provides further support for the notion that FFM deficit drives food intake. Consequently, a role for lean tissue depletion driving hyperphagia has direct repercussions for obesity management, as it suggests that various strategies (dietary, behavioral, or pharmacologic) that reduce the loss of lean tissue are also likely to reduce the drive for hunger and thus improve the efficacy of dietary weight loss interventions.…”

“…A nonleptin system (and so far unidentified adipostatic signals) has recently been implicated in the compensatory hypophagia that plays a critical role in the recovery from rapid weight gain induced by overfeeding 126 . On the other hand, the notion of a feedback loop between FFM deficit and compensatory hyperphagia (Figure 9), as suggested by the MSE reanalysis 63 and by recent studies of weight regain after caloric restriction in humans 98–102 and in mice, 127 posits that there are sensors and signals arising from FFM that link to the brain's hunger–appetite neuronal circuitry. It is, however, not known which component of FFM is being sensed and whether the signals are related to protein mass, skeletal muscle mass, organ size, or their metabolic activities.…”