Ghrelin is an orexigenic hormone secreted from endocrine cells in the stomach and other tissues. Acylation of ghrelin is essential for appetite regulation. Vigorous exercise induces appetite suppression, but this does not appear to be related to suppressed concentrations of total ghrelin. This study examined the effect of exercise and feeding on plasma acylated ghrelin and appetite. Nine male subjects aged 19–25 yr participated in two, 9-h trials (exercise and control) in a random crossover design. Trials began at 0800 in the morning after an overnight fast. In the exercise trial, subjects ran for 60 min at 72% of maximum oxygen uptake between 0800 and 0900. After this, they rested for 8 h and consumed a test meal at 1100. In the control trial, subjects rested for 9 h and consumed a test meal at 1100. Area under the curve values for plasma acylated ghrelin concentration (assessed from venous blood samples) were lower over the first 3 h and the full 9 h of the exercise trial compared with the control trial: 317 ± 135 vs. 510 ± 186 pg·ml⁻¹·3 h and 917 ± 342 vs. 1,401 ± 521 pg·ml⁻¹·9 h (means ± SE) respectively ( P <0.05). Area under the curve values for hunger (assessed using a visual scale) were lower over the first 3 h of the exercise trial compared with the control trial ( P = 0.013). These findings demonstrate that plasma acylated ghrelin concentration and hunger are suppressed during running.

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.

Physical activity recommendations promote the accumulation of aerobic activity in bouts of >or=10 min. It is important to determine whether shorter bouts of activity can influence health. We compared the effects of accumulating ten 3-min bouts of brisk walking with those of one 30-min bout of brisk walking on postprandial plasma triacylglycerol concentrations and resting blood pressure. Fifteen healthy young men completed three 2-d trials >or=1 wk apart in a randomized, repeated-measures design. On day 1, subjects rested (no exercise) or walked briskly in either ten 3-min bouts (30 min rest between each) or one 30-min bout (gross energy expenditure: 1.10 MJ/30 min). On day 2, subjects rested and consumed high-fat test meals for breakfast and lunch. On day 2 area under the plasma triacylglycerol concentration over time curve was 16% lower on the accumulated and continuous brisk walking trials than on the control trial (x +/- SEM: 9.98 +/- 0.67 compared with 9.99 +/- 0.76 compared with 11.90 +/- 1.02 mmol x 7h/L, respectively; P = 0.005, one-factor ANOVA). Resting systolic blood pressure was 6-7% lower throughout day 2 on the accumulated and continuous trials than on the control trial (109 +/- 1 compared with 110 +/- 1 compared with 117 +/- 2 mm Hg, respectively; P < 0.0005). Accumulating 30 min of brisk walking in short (3-min) bouts is equally effective in reducing postprandial lipemia and systolic blood pressure as is one continuous 30-min bout.

Background: A sustained mismatch between energy intake and exercise energy expenditure (EEE) can lead to Low Energy Availability (LEA), health and performance impairments characteristic of Relative Energy Deficiency in Sport (RED-S). Questionnaires can conveniently identify symptoms and/or LEA/ RED-S risk factors. This study aimed to systematically identify, and critique questionnaires used or developed to measure LEA/ RED-S risk in athletic populations.Methods: A systematic search was conducted using PubMed database. Full text articles were included if: (i) the questionnaire(s) in the study identified LEA and/or RED-S risk; (ii) studies developed questionnaires to identify LEA and/or RED-S risk; (iii) participants belonged to athletic population(s); and (iv) in English.Results: Thirty-three articles met the inclusion criteria and were reviewed, 13 questionnaires were identified. Eight questionnaires had undergone validation procedures, and three questionnaires included questions related to EEE. The most widely used validated questionnaires were Low Energy Availability in Females Questionnaire (LEAF-Q) (48% articles) and Eating Disorder Examination Questionnaire (EDE-Q) (12% articles). The LEAF-Q determines LEA risk from symptoms but cannot be used in males as nearly half of the items (n = 12) relate to menstrual function. The EDE-Q serves as a surrogate marker of LEA risk in both sexes, as it measures a major risk factor of LEA, disordered eating. Better validation is needed for many questionnaires and more are needed to address LEA/RED-S risk in male athletes.Conclusion: These questionnaires may be effective in identifying intentional energy restriction but less valuable in identifying inadvertently failure to increase energy intake with increased EEE.

OBJECTIVE: Overweight in youth is associated with the risk of developing type 2 diabetes. We hypothesized that β-cell function relative to insulin sensitivity decreases with increasing 2-h glucose levels based on an oral glucose tolerance test (OGTT) in overweight youth. RESEARCH DESIGN AND METHODS: A total of 147 overweight (BMI ≥85th percentile for age and sex) youth, aged 8 to <20 years, undertook three tests: 1) a 3-h hyperinsulinemic-euglycemic clamp; 2) a 2-h hyperglycemic clamp; and 3) a 2-h OGTT. Participants were categorically assigned to five groups according to their OGTT 2-h plasma glucose level, ranging from <120 to ≥200 mg/dL. β-Cell function relative to insulin sensitivity, assessed by clamp disposition index (DI) and oral disposition index (DIO), were compared among groups. RESULTS: Insulin sensitivity, first-phase insulin, and DI declined significantly as 2-h glucose concentrations increased. The highest DI was found in youth with 2-h plasma glucose concentrations <120 mg/dL, with a significant decline of ~40% in those with glucose concentrations between 120 and 30% decline in β-cell function relative to insulin sensitivity. Against this back drop of metabolically heightened risk for type 2 diabetes, preventive measures should target the β-cell alongside insulin sensitization.