Catherine Gibbons1, John E Blundell1, Phillipa Caudwell1,2, Dominic-Luc Webb2, Per M Hellström3, Erik Näslund4, Graham Finlayson1. 1. Appetite Control and Energy Balance Group, School of Psychology, University of Leeds, Leeds LS2 9JZ, United Kingdom. 2. Novo Nordisk A/S, Krogshøjvej 55, DK-2880 Bagsværd, Denmark. 3. Department of Medical Sciences, Gastroenterology and Hepatology, Uppsala University, SE 75185 Uppsala, Sweden. 4. Department of Clinical Sciences, Danderyd Hospital, Karolinska Institutet, SE 182 88 Stockholm, Sweden.
Abstract
Context: Prolonged physical activity gives rise to variable degrees of body weight and fat loss, and is associated with variability in appetite control. Whether these effects are modulated by postprandial, peptides is unclear. We examined the role of postprandial peptide response in compensatory eating during 12 weeks of aerobic exercise and in response to high-fat, low-carbohydrate (HFLC) and low-fat, high-carbohydrate (LFHC) meals. Methods: Of the 32 overweight/obese individuals, 16 completed 12 weeks of aerobic exercise and 16 nonexercising control subjects were matched for age and body mass index. Exercisers were classified as responders or nonresponders depending on net energy balance from observed compared with expected body composition changes from measured energy expenditure. Plasma samples were collected before and after meals to compare profiles of total and acylated ghrelin, insulin, cholecystokinin, glucagon-like peptide 1 (GLP-1), and total peptide YY (PYY) between HFLC and LFHC meals, pre- and postexercise, and between groups. Results: No differences between pre- and postintervention peptide release. Responders had greater suppression of acylated ghrelin (P < 0.05) than nonresponders, as well as higher postprandial levels of GLP-1 (P < 0.001) and total PYY (P < 0.001) compared with nonresponders and control subjects. Conclusion: No impact on postprandial peptide release was found after 12 weeks of aerobic exercise. Responders to exercise-induced weight loss showed greater suppression of acylated ghrelin and greater release of GLP-1 and total PYY at baseline. Therefore, episodic postprandial peptide profiles appear to form part of the pre-existing physiology of exercise responders and suggest differences in satiety potential may underlie exercise-induced compensatory eating.
Context: Prolonged physical activity gives rise to variable degrees of body weight and fat loss, and is associated with variability in appetite control. Whether these effects are modulated by postprandial, peptides is unclear. We examined the role of postprandial peptide response in compensatory eating during 12 weeks of aerobic exercise and in response to high-fat, low-carbohydrate (HFLC) and low-fat, high-carbohydrate (LFHC) meals. Methods: Of the 32 overweight/obese individuals, 16 completed 12 weeks of aerobic exercise and 16 nonexercising control subjects were matched for age and body mass index. Exercisers were classified as responders or nonresponders depending on net energy balance from observed compared with expected body composition changes from measured energy expenditure. Plasma samples were collected before and after meals to compare profiles of total and acylated ghrelin, insulin, cholecystokinin, glucagon-like peptide 1 (GLP-1), and total peptide YY (PYY) between HFLC and LFHC meals, pre- and postexercise, and between groups. Results: No differences between pre- and postintervention peptide release. Responders had greater suppression of acylated ghrelin (P < 0.05) than nonresponders, as well as higher postprandial levels of GLP-1 (P < 0.001) and total PYY (P < 0.001) compared with nonresponders and control subjects. Conclusion: No impact on postprandial peptide release was found after 12 weeks of aerobic exercise. Responders to exercise-induced weight loss showed greater suppression of acylated ghrelin and greater release of GLP-1 and total PYY at baseline. Therefore, episodic postprandial peptide profiles appear to form part of the pre-existing physiology of exercise responders and suggest differences in satiety potential may underlie exercise-induced compensatory eating.
Authors: J M Jakicic; K Clark; E Coleman; J E Donnelly; J Foreyt; E Melanson; J Volek; S L Volpe Journal: Med Sci Sports Exerc Date: 2001-12 Impact factor: 5.411
Authors: H J Leidy; J K Gardner; B R Frye; M L Snook; M K Schuchert; E L Richard; N I Williams Journal: J Clin Endocrinol Metab Date: 2004-06 Impact factor: 5.958
Authors: Ali Ataeinosrat; Marjan Mosalman Haghighi; Hossein Abednatanzi; Mohammad Soltani; Abbass Ghanbari-Niaki; Akbar Nouri-Habashi; Sadegh Amani-Shalamzari; Ali Mossayebi; Mitra Khademosharie; Kelly E Johnson; Trisha A VanDusseldorp; Ayoub Saeidi; Hassane Zouhal Journal: Front Physiol Date: 2022-02-21 Impact factor: 4.566
Authors: James Dorling; David R Broom; Stephen F Burns; David J Clayton; Kevin Deighton; Lewis J James; James A King; Masashi Miyashita; Alice E Thackray; Rachel L Batterham; David J Stensel Journal: Nutrients Date: 2018-08-22 Impact factor: 5.717