<h4>Background</h4>The magnitude of the negative energy balance induced by exercise may be reduced due to compensatory increases in energy intake.<h4>Objective</h4>TO ADDRESS THE QUESTION: Does increased exercise or physical activity alter ad-libitum daily energy intake or macronutrient composition in healthy adults?<h4>Data sources</h4>PubMed and Embase were searched (January 1990-January 2013) for studies that presented data on energy and/or macronutrient intake by level of exercise, physical activity or change in response to exercise. Ninety-nine articles (103 studies) were included.<h4>Study eligibility criteria</h4>Primary source articles published in English in peer-reviewed journals. Articles that presented data on energy and/or macronutrient intake by level of exercise or physical activity or changes in energy or macronutrient intake in response to acute exercise or exercise training in healthy (non-athlete) adults (mean age 18-64 years).<h4>Study appraisal and synthesis methods</h4>Articles were grouped by study design: cross-sectional, acute/short term, non-randomized, and randomized trials. Considerable heterogeneity existed within study groups for several important study parameters, therefore a meta-analysis was considered inappropriate. Results were synthesized and presented by study design.<h4>Results</h4>No effect of physical activity, exercise or exercise training on energy intake was shown in 59% of cross-sectional studies (n = 17), 69% of acute (n = 40), 50% of short-term (n = 10), 92% of non-randomized (n = 12) and 75% of randomized trials (n = 24). Ninety-four percent of acute, 57% of short-term, 100% of non-randomized and 74% of randomized trials found no effect of exercise on macronutrient intake. Forty-six percent of cross-sectional trials found lower fat intake with increased physical activity.<h4>Limitations</h4>The literature is limited by the lack of adequately powered trials of sufficient duration, which have prescribed and measured exerc Objective To address the question: Does increased exercise or physical activity alter ad-libitum daily energy intake or macronutrient composition in healthy adults? Data Sources PubMed and Embase were searched (January 1990–January 2013) for studies that presented data on energy and/or macronutrient intake by level of exercise, physical activity or change in response to exercise. Ninety-nine articles (103 studies) were included. Study Eligibility Criteria Primary source articles published in English in peer-reviewed journals. Results No effect of physical activity, exercise or exercise training on energy intake was shown in 59% of cross-sectional studies (n = 17), 69% of acute (n = 40), 50% of short-term (n = 10), 92% of non-randomized (n = 12) and 75% of randomized trials (n = 24). Ninety-four percent of acute, 57% of short-term, 100% of non-randomized and 74% of randomized trials found no effect of exercise on macronutrient intake. Forty-six percent of cross-sectional trials found lower fat intake with increased physical activity. Limitations The literature is limited by the lack of adequately powered trials of sufficient duration, which have prescribed and measured exercise energy expenditure, or employed adequate assessment methods for energy and macronutrient intake. Conclusions We found no consistent evidence that increased physical activity or exercise effects energy or macronutrient intake. This review was funded by the International Life Sciences Institute. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. Short-Term Studies: Results Energy intake Five of 10 short-term studies (50%) reported increased absolute energy intake (∼200–335 kcal/day) over periods of 2 to14 days when exercise was imposed compared with a non-exercise control period [87] , [88] , [93] , [95] , [96] . Three studies that reported increased absolute energy intake showed relative energy intake at a level to maintain a negative energy balance during the exercise period [87] , [88] , [93] ; however, Tremblay et al [95] showed that participants achieved a positive energy balance when presented with a high fat diet. Macronutrient intake Seven of the 10 short-term studies (70%) reported macronutrient intake [87] – [90] , [92] , [94] , [96] . Four of 7 studies (57%) showed no effect of exercise on macronutrient intake [89] , [90] , [92] , [94] . Farah et al. [96] reported increased intake of carbohydrate and protein while Stubbs et al. [87] observed increased intake of carbohydrate and fat with exercise compared to control. Whybrow et al. [88] noted increased intake of carbohydrate, fat and protein with exercise vs. control in men but not in women. Manthou et al. (2010) [21] 34 women: Age = 31.7 (8.1) years; BMI = 29.3 (4.3); VO 2 max = 2.1 (0.38) L/min. 8 wks CHO intake (g/day) increased, no change in fat or PRO intake. Whites: Reductions in EI below baseline at both wks 9 (12.7%) and wk. 16 (5.1%) were observed, statistically significant at wk. 8 only. CHO intake decreased significantly (wk. 9), no change in fat or PRO intake. Broeder et al. (1992) [108] 64 men randomized. Control, n = 20; Endurance, n = 22; Resistance, n = 22. 47 men completed the study. Control n = 19; Age = 18–35; BMI = 25.3 (1.0); VO 2 max = 49.1 (2.2) ml/kg/min. Endurance, n = 15; Age = 18–35; BMI = 25.1 (1.1); VO 2 max = 49.6 (2.2) ml/kg/min. The sample size in each of these 3 trials was <20 participants/group. Inadequate statistical power may explain the disconnect between the results of our review, which found no effect of exercise training on energy intake and other trials that have evaluated the effect of exercise on body weight. For example, studies have reported high individual variability in weight loss in response to the same level of exercise energy expenditure [18] and no significant increase in weight loss in response to increased level of exercise energy expenditure [11] , [121] .

Although ample evidence supports the notion that an acute bout of endurance exercise performed at or greater than 70% of maximum oxygen uptake suppresses appetite partly through changes in appetite-regulating hormones, no study has directly compared the influence between the phases of the menstrual cycle in women. The present study compared the effects of an acute bout of exercise on orexigenic hormone (acylated ghrelin) and anorexigenic hormones (peptide YY and cholecystokinin) between the early follicular phase (FP) and the mid luteal phase (LP) of the menstrual cycle in physically active women. Ten healthy women (age, 20.6 ± 0.7 years) completed two 3.5-h trials in each menstrual phase. In both trials, participants performed cycling exercises at 70% of heart rate reserve (at a corresponding intensity to 70% of maximum oxygen uptake) for 60 min followed by 90 min of rest. Following 90 min of rest, participants were provided with an ad libitum meal for a fixed duration of 30 min. Blood samples and subjective appetite were collected and assessed before, during, immediately post-, 45 min post-, and 90 min post-exercise. The exercise increased estradiol (327 %) and progesterone (681 %) in the LP more than the FP respectively (P < 0.001, f = 1.33; P < 0.001,f = 1.20). There were no between-trial differences in appetite-regulating hormones, subjective appetite, or energy intake of ad libitum meal. These findings indicate that exercise-induced increases in ovarian hormones in the LP may not influence appetite-regulating hormones in physically active women.

Abstract This study examined whether supplementation with collagen peptides (CP) affects appetite and post-exercise energy intake in healthy active females. In this randomised, double-blind cross-over study, fifteen healthy females (23 (sd 3) years) consumed 15 g/d of CP or a taste matched non-energy control (CON) for 7 d. On day 7, participants cycled for 45 min at ∼55 % Wmax, before consuming the final supplement. Sixty-min post supplementation an ad libitum meal was provided, and energy intake recorded. Subjective appetite sensations were measured daily for 6 d (pre- and 30 min post-supplement) and pre (0 min) to 280 min post-exercise on day 7. Blood glucose and hormone concentrations (total ghrelin, glucagon-like peptide-1 (GLP-1), and peptide YY (PYY), cholecystokinin (CCK), dipeptidyl peptidase-4 (sDPP-4), leptin, and insulin) were measured fasted at baseline (day 0), then pre-breakfast (0 min), post-exercise (100 min), post-supplement (115, 130, 145, 160 min) and post-meal (220, 280 min) on day 7. Ad libitum energy intake was ∼10 % (∼41 kcal) lower in the CP trial (P = 0·037). There was no difference in gastrointestinal symptoms or subjective appetite sensations throughout the trial (P ≥ 0·412). Total plasma GLP-1 (AUC, CON: 6369 (sd 2330); CP: 9064 (sd 3021) pmol/l; P < 0·001) and insulin (+80 % at peak) were higher after CP (P < 0·001). Plasma ghrelin and leptin were lower in CP (condition effect; P ≤ 0·032). PYY, CCK and glucose were not different between CP and placebo (P ≥ 0·100). CP supplementation following exercise increased GLP-1 and insulin concentrations and reduced ad libitum energy intake at a subsequent meal in physically active females. There was no difference in gastrointestinal symptoms or subjective appetite sensations throughout the trial ( P ≥ 0·412). Total plasma GLP-1 (AUC, CON: 6369 ( sd 2330); CP: 9064 ( sd 3021) pmol/l; P < 0·001) and insulin (+80 % at peak) were higher after CP ( P < 0·001). Plasma ghrelin and leptin were lower in CP (condition effect; P ≤ 0·032). PYY, CCK and glucose were not different between CP and placebo ( P ≥ 0·100). CP supplementation following exercise increased GLP-1 and insulin concentrations and reduced ad libitum energy intake at a subsequent meal in physically active females. 15–70 g) or over several days, may reduce appetite, as measured by decreased energy intake ( 1 – 4 ) , increased subjective feelings of fullness and reduced hunger ( 4 – 6 ) and/or increased levels of satiety hormones such as glucagon peptide-1 (GLP-1) ( 7 , 8 ) . This has sparked an interest in the effects of different protein sources and supplements (e.g. whey, soy) on appetite suppression and weight management, particularly in combination with exercise to manage obesity-related disease ( 4 , 9 , 10 ) . Collagen peptides (CP) are low in branched chain amino acids, but rich in hydroxyproline, glycine and proline ( 21 ) . In animals, gelatin hydrolysates were shown to stimulate secretion of insulin and GLP-1 ( 22 ) , and in humans, circulating glycine is strongly associated with reduced hunger and energy intake ( 23 ) , suggesting CP supplements also have the potential to affect appetite. Recently, Duarte et al. Energy intake (kcal; (a)) and eating rate (kcal/min; (b)) from the ad libitum meal on day 7, for control (CON) and collagen peptides (CP) trials. Bars represent means and lines individual responses. * denotes P < 0·05. Data presented for n 15. Subjective appetite ratings There were time ( P < 0·001) effects, but no condition ( P ≥ 0·376) or time × condition interaction effects ( P ≥ 0·279) for hunger ( Figure 4 (a)), fullness ( Figure 4 (c)), desire to eat ( Figure 4 (e)), The moderate and strong correlations ( r ≥ –0·477) between the difference in GLP-1 and insulin post-supplement on day 7, with the difference in energy intake between conditions, lend some support to this (online Supplementary Material). As ghrelin stimulates hunger ( 61 ) , suppression of this hormone could have contributed to the reduced energy intake in the ad libitum meal with CP. However, there was no interaction effect, and a weak correlation with the difference in energy intake (online Supplementary Material) and the effect size was markedly lower than that for GLP-1. Interestingly, GLP-1, which stimulates insulin secretion and delays gastric emptying ( 62 ) , remained significantly higher than the control in the 2 h after the ad libitum meal, suggesting the initial increase following CP intake cannot be attributed to energy intake. We are unaware of any previous studies examining CP on these hormones in humans, but in vitro studies suggest that CP ( 63 ) or collagen hydrolysates ( 64 ) increase GLP-1 partly though inhibiting DPP-4. However, in our study, sDPP-4 was slightly elevated in the CP trial (condition effect; d z = 0·566) suggesting other mechanisms likely explain the increased GLP-1. The increase could be partly attributed to the insulinotropic effects of specific peptides, or glycine, which has previously been shown to stimulate GLP-1 ( 64 – 66 ) . Notwithstanding, our findings are in line with human studies involving gelatin supplementation whereby a single 20 g dose of gelatin (in both individuals with obesity and lean individuals) was shown to increase GLP-1 and insulin concentrations but not total PYY or total ghrelin ( 67 ) . In another study, diets rich in gelatin (10 % or 25 % of energy intake) increased GLP-1 and decreased ghrelin after meals and to a greater extent than after an energy matched casein protein diet ( 6 ) . The discrepancy in findings with our study could be due to differences in dose and/or the comparator. Although leptin is thought to suppress food intake, ad libitum energy intake in our study was reduced by CP, suggesting leptin did not significantly influence appetite. This could be because the increase was small and not physiologically meaningful, or because leptin has a limited effect on acute hunger and satiety.