Exercise facilitates weight control, partly through effects on appetite regulation. Single bouts of exercise induce a short-term energy deficit without stimulating compensatory effects on appetite, whilst limited evidence suggests that exercise training may modify subjective and homeostatic mediators of appetite in directions associated with enhanced meal-induced satiety. However, a large variability in responses exists between individuals. This article reviews the evidence relating to how adiposity, sex, and habitual physical activity modulate exercise-induced appetite, energy intake, and appetite-related hormone responses. The balance of evidence suggests that adiposity and sex do not modify appetite or energy intake responses to acute or chronic exercise interventions, but individuals with higher habitual physical activity levels may better adjust energy intake in response to energy balance perturbations. The effect of these individual characteristics and behaviours on appetite-related hormone responses to exercise remains equivocal. These findings support the continued promotion of exercise as a strategy for inducing short-term energy deficits irrespective of adiposity and sex, as well as the ability of exercise to positively influence energy balance over the longer term. Future well-controlled studies are required to further ascertain the potential mediators of appetite responses to exercise.

Intermittent fasting may impart metabolic benefits independent of energy balance by initiating fasting-mediated mechanisms. This randomized controlled trial examined 24-hour fasting with 150% energy intake on alternate days for 3 weeks in lean, healthy individuals (0:150; n = 12). Control groups involved a matched degree of energy restriction applied continuously without fasting (75% energy intake daily; 75:75; n = 12) or a matched pattern of fasting without net energy restriction (200% energy intake on alternate days; 0:200; n = 12). Primary outcomes were body composition, components of energy balance, and postprandial metabolism. Daily energy restriction (75:75) reduced body mass (−1.91 ± 0.99 kilograms) almost entirely due to fat loss (−1.75 ± 0.79 kilograms). Restricting energy intake via fasting (0:150) also decreased body mass (−1.60 ± 1.06 kilograms; P = 0.46 versus 75:75) but with attenuated reductions in body fat (−0.74 ± 1.32 kilograms; P = 0.01 versus 75:75), whereas fasting without energy restriction (0:200) did not significantly reduce either body mass (−0.52 ± 1.09 kilograms; P ≤ 0.04 versus 75:75 and 0:150) or fat mass (−0.12 ± 0.68 kilograms; P ≤ 0.05 versus 75:75 and 0:150). Postprandial indices of cardiometabolic health and gut hormones, along with the expression of key genes in subcutaneous adipose tissue, were not statistically different between groups (P > 0.05). Alternate-day fasting less effectively reduces body fat mass than a matched degree of daily energy restriction and without evidence of fasting-specific effects on metabolic regulation or cardiovascular health.

Acute exercise does not elicit compensatory changes in appetite parameters in lean individuals; however, less is known about responses in overweight individuals. This study compared the acute effects of moderate-intensity exercise on appetite, energy intake and appetite-regulatory hormones in lean and overweight/obese individuals. Forty-seven healthy lean (n=22, 11 females; mean (s.d.) 37.5 (15.2) years; 22.4 (1.5) kg m⁻²) and overweight/obese (n=25, 11 females; 45.0 (12.4) years, 29.2 (2.9) kg m⁻²) individuals completed two, 8 h trials (exercise and control). In the exercise trial, participants completed 60 min treadmill exercise (59 (4)% peak oxygen uptake) at 0–1 h and rested thereafter while participants rested throughout the control trial. Appetite ratings and concentrations of acylated ghrelin, peptide YY (PYY) and glucagon-like peptide-1 (GLP-1) were measured at predetermined intervals. Standardised meals were consumed at 1.5 and 4 h and an ad libitum buffet meal was provided at 7 h. Exercise suppressed appetite (95% confidence interval (CI) −3.1 to −0.5 mm, P=0.01), and elevated delta PYY (95% CI 10 to 17 pg ml⁻¹, P<0.001) and GLP-1 (95% CI 7 to 10 pmol l⁻¹, P<0.001) concentrations. Delta acylated ghrelin concentrations (95% CI −5 to 3 pg ml⁻¹, P=0.76) and ad libitum energy intake (95% CI −391 to 346 kJ, P=0.90) were similar between trials. Subjective and hormonal appetite parameters and ad libitum energy intake were similar between lean and overweight/obese individuals (P ⩾ 0.27). The exercise-induced elevation in delta GLP-1 was greater in overweight/obese individuals (trial-by-group interaction P=0.01), whereas lean individuals exhibited a greater exercise-induced increase in delta PYY (trial-by-group interaction P<0.001). Acute moderate-intensity exercise transiently suppressed appetite and increased PYY and GLP-1 in the hours after exercise without stimulating compensatory changes in appetite in lean or overweight/obese individuals. These findings underscore the ability of exercise to induce a short-term energy deficit without any compensatory effects on appetite regardless of weight status.

Breakfast omission may reduce daily energy intake. Exercising fasted impairs performance compared with exercising after breakfast, but the effect breakfast omission has on evening exercise performance is unknown. This study assessed the effect of omitting breakfast on evening exercise performance and within-day energy intake. Ten male, habitual breakfast eaters completed two trials in a randomized, counterbalanced order. Subjects arrived at the laboratory in an overnight-fasted state and either consumed or omitted a 733 ± 46 kcal (3095 ± 195 kJ) breakfast. Ad libitum energy intake was assessed at 4.5 h (lunch) and 11 h (dinner). At 9 h, subjects completed a 30-min cycling exercise at approximately 60% VO2peak, followed by a 30-min maximal cycling performance test. Food was not permitted for subjects once they left the laboratory after dinner until 0800 h the following morning. Acylated ghrelin, GLP-1(7-36), glucose, and insulin were assessed at 0, 4.5, and 9 h. Subjective appetite sensations were recorded throughout. Energy intake was 199 ± 151 kcal greater at lunch (P < 0.01) after breakfast omission compared with that after breakfast consumption and tended to be greater at dinner after consuming breakfast (P = 0.052). Consequently, total ad libitum energy intake was similar between trials (P = 0.196), with 24-h energy intake 19% ± 5% greater after consuming breakfast (P < 0.001). Total work completed during the exercise performance test was 4.5% greater after breakfast (314 ± 53 vs 300 ± 56 kJ; P < 0.05). Insulin was greater during breakfast consumption at 4.5 h (P < 0.05), with no other interaction effect for hormone concentrations. Breakfast omission might be an effective means of reducing daily energy intake but may impair performance later that day, even after consuming lunch.

The belief that breakfast is the most important meal of day has been derived from cross-sectional studies that have associated breakfast consumption with a lower BMI. This suggests that breakfast omission either leads to an increase in energy intake or a reduction in energy expenditure over the remainder of the day, resulting in a state of positive energy balance. However, observational studies do not imply causality. A number of intervention studies have been conducted, enabling more precise determination of breakfast manipulation on indices of energy balance. This review will examine the results from these studies in adults, attempting to identify causal links between breakfast and energy balance, as well as determining whether consumption of breakfast influences exercise performance. Despite the associations in the literature, intervention studies have generally found a reduction in total daily energy intake when breakfast is omitted from the daily meal pattern. Moreover, whilst consumption of breakfast supresses appetite during the morning, this effect appears to be transient as the first meal consumed after breakfast seems to offset appetite to a similar extent, independent of breakfast. Whether breakfast affects energy expenditure is less clear. Whilst breakfast does not seem to affect basal metabolism, breakfast omission may reduce free-living physical activity and endurance exercise performance throughout the day. In conclusion, the available research suggests breakfast omission may influence energy expenditure more strongly than energy intake. Longer term intervention studies are required to confirm this relationship, and determine the impact of these variables on weight management.