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Effect of Chronic Exercise on Appetite Control in Overweight and Obese Individuals

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Effect of Chronic Exercise on Appetite Control in Overweight and Obese Individuals This may be the author’s version of a work that was submitted/accepted for publication in the following source: Martins, Catia, Kulseng, Bard, Rehfeld, Jens, King, Neil, & Blundell, John (2013) Effect of chronic exercise on appetite control in overweight and obese in- dividuals. Medicine and Science in Sports and Exercise, 45(5), pp. 805-812. This file was downloaded from: https://eprints.qut.edu.au/57926/ c Consult author(s) regarding copyright matters This work is covered by copyright. Unless the document is being made available under a Creative Commons Licence, you must assume that re-use is limited to personal use and that permission from the copyright owner must be obtained for all other uses. If the docu- ment is available under a Creative Commons License (or other specified license) then refer to the Licence for details of permitted re-use. It is a condition of access that users recog- nise and abide by the legal requirements associated with these rights. If you believe that this work infringes copyright please provide details by email to [email protected] Notice: Please note that this document may not be the Version of Record (i.e. published version) of the work. Author manuscript versions (as Sub- mitted for peer review or as Accepted for publication after peer review) can be identified by an absence of publisher branding and/or typeset appear- ance. If there is any doubt, please refer to the published source. https://doi.org/10.1249/MSS.0b013e31827d1618 . Published ahead of Print Impact of Chronic Exercise on Appetite Control in Overweight and Obese Individuals Catia Martins1,2, Bard Kulseng1,2, Jens F Rehfeld3, Neil A King4, and John E Blundell5 1Obesity Research Group, Department of Cancer Research and Molecular Medicine, Faculty of Medicine, Norwegian University of Science and Technology, Trondheim, Norway; 2Center for Obesity, Department of Surgery, St. Olav Hospital – Trondheim University Hospital, Trondheim, Norway; 3Department of Clinical Biochemistry, Rigshospitalet, University of Copenhagen, Denmark; 4Institute of Health and Biomedical Innovation, Queensland University of Technology, Brisbane, Australia; 5BioPsychology Group, Institute of Psychological Sciences, University of Leeds, Leeds, United Kingdom Accepted for Publication: 7 November 2012 ACCEPTED Medicine & Science in Sports & Exercise® Published ahead of Print contains articles in unedited manuscript form that have been peer reviewed and accepted for publication. This manuscript will undergo copyediting, page composition, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered that could affect the content. Copyright © 2012 American College of Sports Medicine Medicine & Science in Sports & Exercise, Publish Ahead of Print DOI: 10.1249/MSS.0b013e31827d1618 Impact of Chronic Exercise on Appetite Control in Overweight and Obese Individuals Catia Martins1,2, Bard Kulseng1,2, Jens F Rehfeld3, Neil A King4 and John E Blundell5 1Obesity Research Group, Department of Cancer Research and Molecular Medicine, Faculty of Medicine, Norwegian University of Science and Technology, Trondheim, Norway; 2Center for Obesity, Department of Surgery, St. Olav Hospital – Trondheim University Hospital, Trondheim, Norway 3Department of Clinical Biochemistry, Rigshospitalet, University of Copenhagen, Denmark 4Institute of Health and Biomedical Innovation, Queensland University of Technology, Brisbane, Australia 5BioPsychology Group, Institute of Psychological Sciences, University of Leeds, Leeds, United Kingdom Funding: Catia Martins was supported by a PostDoctoral grant (SFRH/BPD/36940/2007) from Fundação para a Ciência e Tecnologia (Portugal) under the 3rd European Union community support programme. Running costs were covered by a grant from the Liaison Committee between Central Norway Regional Health Authority and the Norwegian University of Science and ACCEPTEDTechnology in partnership with St. Olav Hospital (Trondheim, Norway). Copyright © 2012 by the American College of Sports Medicine. Unauthorized reproduction of this article is prohibited. Conflict of interest The authors declare that there is no conflict of interest that would prejudice the impartiality of this scientific work. Moreover, the results of the present study do not constitute endorsement by ACSM. Corresponding author: Catia Martins Obesity Research Group, Department of Cancer Research and Molecular Medicine, Faculty of Medicine, Norwegian University of Science and Technology, Trondheim, Norway email: [email protected] phone: 0047 72825358 fax: 0047 72 57 14 63 Running title: Exercise and appetite control ACCEPTED Copyright © 2012 by the American College of Sports Medicine. Unauthorized reproduction of this article is prohibited. Abstract Purpose: The impact of exercise on body mass is likely to be partially mediated through changes in appetite control. However, no studies have examined the impact of chronic exercise on obestatin and cholecystokinin (CCK) plasma concentrations or the sensitivity to detect differences in preload energy, in obese individuals. The objective of this study was to investigate the effects of chronic exercise on: 1) fasting and postprandial plasma concentrations of obestatin, CCK, leptin and glucose insulinotropic peptide (GIP) and 2) the accuracy of energy compensation in response to covert preload manipulation. Methods: 12-week supervised exercise programme in twenty-two sedentary overweight/obese individuals. Fasting/postprandial plasma concentrations of obestatin, CCK, leptin and GIP were assessed before and after the intervention. Energy compensation at a test-meal 30 minutes after a high-energy (607 kcal) or a low-energy (246 kcal) preload, and for the rest of the day (cumulative EI) was also measured. Results: There was a significant reduction in the plasma concentration of fasting plasma GIP, and both fasting and postprandial leptin concentrations after the exercise intervention (P<0.05 for all). No significant changes were observed for CCK or obestatin. A significant preload*exercise interaction (P=0.011) was observed on cumulative EI and energy compensation over the same period (-87±196 vs 68±165%, P=0.011). Weight loss (3.5±1.4 kg, P<0.0001) was not correlated with changes in energy compensation. Conclusion: This study suggests that exercise improves the accuracy of compensation for previous EI, independently of weight loss. Unexpectedly, and in contrasts to GIP and leptin, exercise-inducedACCEPTED weight loss had no impact on obestatin or CCK concentrations. Keywords: cholecystokinin; obestatin; leptin; glucose insulinotropic peptide; energy compensation Copyright © 2012 by the American College of Sports Medicine. Unauthorized reproduction of this article is prohibited. INTRODUCTION The impact of exercise on body mass is likely to be mediated not only directly, by increasing energy expenditure, but also indirectly by modulating appetite, and subsequently energy intake (22). A large body of evidence has accumulated over the last two decades suggesting first, a link between inactivity and disrupted homeostatic mechanisms involved in appetite control (16, 19, 24, 26, 32), which could contribute to positive energy balance (EB) and obesity, and second, that exercise has the ability to ‘fine-tune’ these physiological mechanisms (19, 23, 35). Exercise has been shown to improve energy compensation by leading to a more sensitive eating behaviour in response to previous energy intake (EI) (21). However, the majority of the evidence is cross-sectional (19, 35) or derived from normal- weight individuals (231). The mechanisms whereby this occurs have yet to be clarified, but exercise has been shown to induce changes in appetite-regulating hormones which may contribute to a better appetite control (22). Appetite-regulating hormones can be grouped, in a simplistic way, in two categories: episodic signals, which are periodically released, mainly from the gastrointestinal (GI) tract, in response to feeding or fasting, signalling acute nutritional state, and tonic signals, which are more uniformly released, mainly by the adipose tissue, in proportion to the amount of stored lipids, signalling chronic nutritional state (2). To the first category of peripheral GI signals belongs ghrelin, an orexigenic hormone released in response to fasting, and several hormones involved in satiation and/or satiety such as cholecystokinin (CCK), glucagon-like peptide-1 (GLP-1) and polypeptide YY (PYY), which are released in response to feeding. The second category of peripheral signals includes leptin, released mainly by the adipose tissue, and insulin,ACCEPTED released by the pancreas, whose secretion is directly proportional to the amount of fat stores. However, insulin also shows episodic characteristics since it is released periodically in response to food consumption. Copyright © 2012 by the American College of Sports Medicine. Unauthorized reproduction of this article is prohibited. Obestatin and glucose insulinotropic peptide (GIP) may also be involved in appetite control. Obestatin, a peptide encoded by the ghrelin gene, was initially shown to have anorexigenic properties (36), however, more recent research has questioned these findings and, at present, the real impact of obestatin on food intake and body mass regulation remains unknown (8). GIP, is best known for its incretin action, however, accumulating evidence over the last decade seems to suggest that GIP may also play a role in appetite
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