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.

Background: Postprandial dysmetabolism, an important cardiovascular disease risk factor, can be improved by exercise. Further systematic review and meta-analysis is needed to compare the effects of accumulated exercise with a single session of energy-matched continuous exercise on postprandial glucose (PPG), insulin, and triglycerides in adults with or without diabetes. Methods: Eight electronic databases were searched on August 28, 2020, and updated on April 27, 2021. Eligible studies were randomized, quasi-randomized, or non-randomized controlled or crossover trials that evaluated the acute or longitudinal effects of accumulated exercise compared with a single session of energy-matched continuous exercise on PPG, postprandial insulin, and triglycerides in diabetic and non-diabetic adults. Same-day and second-morning effects were assessed separately for acute intervention studies. Subgroup analyses were conducted based on the number of exercise bouts (2–3 bouts or frequent brief bouts (e.g., 1–6 min) throughout the day at 20–60-min intervals (known as physical activity [PA] breaks, ≥ 5 bouts)), exercise intensity, and populations. Risk of bias was assessed using the revised Cochrane risk-of-bias tool for randomized trials. Pooled effects were reported as standardized mean differences (SMD) and 95% CI using a random effects model. Results: Twenty-seven studies (635 participants) were included. A significant difference was found for same-day PPG control, which favored accumulated exercise over one bout of energy-matched continuous exercise (SMD − 0.36 [95%CI: (− 0.56, − 0.17)], P = 0.0002, I² = 1%), specifically in accumulated exercise with PA breaks (SMD − 0.36 [95%CI: (− 0.64, − 0.08)], P = 0.01, I² = 30%), low-moderate intensity exercise (SMD − 0.38 [(95%CI: (− 0.59, − 0.17)], P = 0.0005, I² = 0%), and in non-diabetic populations (SMD − 0.36 [95%CI: (− 0.62, − 0.10)], P = 0.007, I² = 16%). No differences were found for same-day postprandial insulin and triglycerides, and second-morning effects (postprandial or fasting glucose, insulin, and triglycerides) between different exercise patterns. Conclusion: Compared with one session of continuous exercise, accumulated exercise—specifically in subgroups of PA breaks, low-moderate intensity exercises—produced greater acute effects on same-day PPG control for non-diabetic adults. There were no differences between continuous and accumulated patterns of exercise in terms of same-day postprandial insulin and triglycerides, and second-morning effects on all previously mentioned markers. The findings provide additional PA options for PPG control for individuals with limited time or exercise capacity to engage in PA in one session. Registration: PROSPERO (identification code: CRD42021251325).

Although a single bout of continuous exercise (≥30 min) reduces postprandial triglyceride (TG), little evidence is available regarding the effect of multiple short (≤10 min) bouts of exercise on postprandial TG in individuals at increased risk for cardiovascular diseases. This study compared the effects of different patterns of walking on postprandial TG in postmenopausal, older women with hypertriglyceridemia. Twelve inactive women (mean age ± SD, 71 ± 5 yr) with hypertriglyceridemia (fasting TG ≥1.70 mmol·L−1) completed three, 1-d laboratory-based trials in a random order: 1) control, 2) continuous walking, and 3) multiple short bouts of walking. On the control trial, participants sat in a chair for 8 h. For the walking trials, participants walked briskly in either one 30-min bout in the morning (0900–0930 h) or twenty 90-s bouts over 8 h. Except for walking, both exercise trials mimicked the control trial. In each trial, participants consumed a standardized breakfast (0800 h) and lunch (1100 h). Venous blood samples were collected in the fasted state and at 2, 4, 6, and 8 h after breakfast. The serum TG incremental area under the curve was 35% and 33% lower on the continuous and multiple short bouts of walking trials than that on the control trial (8.2 ± 3.1 vs 8.5 ± 5.4 vs 12.7 ± 5.8 mmol per 8 h·L−1, respectively; main effect of trial: effect size = 0.459, P = 0.001). Accumulating walking in short bouts limits postprandial TG in at-risk, inactive older women with fasting hypertriglyceridemia.

Context Prolonged sitting elevates postprandial metabolic markers, resulting in increased risks of cardiovascular diseases and type 2 diabetes. Interrupting prolonged sitting may reduce these risks. However, more information is needed to understand the patterns of interrupting prolonged sitting to obtain metabolic health benefits. Objective This study examined the effects of interrupting prolonged sitting with different intensities and durations of walking with an equivalent energy expenditure on postprandial metabolic responses in young Chinese men with central obesity. Design A randomized crossover experimental trial was conducted. Setting Participants underwent three 6-hour experiments with a 7-day washout period between each experiment: prolonged sitting, 3 min of light-intensity walking every 30 minutes, and 1.5 minutes of moderate-intensity walking every 30 minutes. Participants and Samples Baseline (fasting) and 6-hour postprandial metabolic glucose and lipid levels were analyzed among 18 young Chinese men with central obesity. Main Outcome Measures Generalized estimating equations (adjusted for the potential confounders explaining residual outcome variance (body mass index) and age), trial order, preprandial values, and lead-in activity) were used, and the incremental areas under the curve (iAUC) of each outcome were compared between prolonged sitting and interrupted prolonged sitting conditions. Results Compared with prolonged sitting, both interrupting prolonged sitting conditions reduced the iAUCs for glucose (P < .05) but not insulin, C-peptide, triglycerides, or nonesterified fatty acids. Conclusions Both conditions of interrupted prolonged sitting reduced postprandial glucose concentrations in young Chinese men with central obesity when the energy expenditure was equivalent.

We examined the effects of the timing of acute and consecutive epigallocatechin gallate (EGCG) and catechin-rich green tea ingestion on postprandial glucose in mice and human adults. In mouse experiments, we compared the effects of EGCG administration early (morning) and late (evening) in the active period on postprandial glucose. In human experiments, participants were randomly assigned to the morning-placebo (MP, n = 10), morning-green tea (MGT, n = 10), evening-placebo (EP, n = 9), and evening-green tea (EGT, n = 9) groups, and consumed either catechin-rich green tea or a placebo beverage for 1 week. At baseline and after 1 week, participants consumed their designated beverages with breakfast (MP and MGT) or supper (EP and EGT). Venous blood samples were collected in the fasted state and 30, 60, 120, and 180 min after each meal. Consecutive administration of EGCG in the evening, but not in the morning, reduced postprandial glucose at 30 (p = 0.006) and 60 (p = 0.037) min in the evening trials in mice. In humans, ingestion of catechin-rich green tea in the evening decreased postprandial glucose (three-factor analysis of variance, p < 0.05). Thus, catechin intake in the evening more effectively suppressed elevation of postprandial glucose.

Purpose Although immediate pre-meal water ingestion has been shown to reduce energy intake in healthy young men, no studies are available regarding potential mechanisms underlying the effect of energy intake in response to different temperatures of pre-meal water ingestion. This study examined the effects of consuming different temperatures of water on gastric motility and energy intake in healthy young men. Methods Eleven young men were completed three, 1-day trials in a random order. Subjects visited the laboratory after a 10-h overnight fast and consumed 500 mL of water at 2 °C, 37 °C, or 60 °C in 5 min. Then, subjects sat on a chair over 1 h to measure the cross-sectional gastric antral area and gastric contractions using the ultrasound imaging systems. Thereafter, subjects consumed a test meal until they felt completely full. Energy intake was calculated from the amount of food consumed. Results Energy intake in the 2 °C (6.7 ± 1.8 MJ) trial was 19% and 26% lower than the 37 °C (7.9 ± 2.3 MJ, p = 0.039) and 60 °C (8.5 ± 3.2 MJ, p = 0.025) trials, respectively. The frequency of the gastric contractions after 1-h consuming water was lowered in the 2 °C trial than the 60 °C trial (trial-time interaction, p = 0.020). The frequency of gastric contractions was positively related to energy intake (r = 0.365, p = 0.037). Conclusions These findings demonstrate that consuming water at 2 °C reduces energy intake and this reduction may be related to the modulation of the gastric motility.