Research report Influence of prolonged treadmill running on appetite, energy intake and circulating concentrations of acylated ghrelin § James A. King a , Masashi Miyashita b , Lucy K. Wasse a , David J. Stensel a, * a Exercise and Health Research Group, School of Sport, Exercise and Health Sciences, Loughborough University, Ashby Road, Leicestershire, LE11 3TU, UK b Division of Sports Medicine, Graduate School of Comprehensive Human Science, University of Tsukuba, Japan Introduction The global prevalence of overweight and obesity continues to rise and provokes a need to find efficacious interventions to combat this problem (Kelly, Yang, Chen, Reynolds, & He, 2008). Exercise is effective at preventing weight gain and maintaining a reduced body weight following weight loss however in the absence of a calorie restricted diet the ability of exercise to induce weight loss is less certain (Catenacci & Wyatt, 2007; Donnelly et al., 2009; Seagle, Strain, Makris, Reeves, & American Dietetic Association, 2009). A possible explanation for this is that exercise may elicit compensatory increases in appetite and energy intake, responses that would negate the ability to induce a sustained energy deficit (King et al., 2007). Findings regarding the acute influence of exercise on appetite are mixed with reports of no change in appetite along with both increases and decreases (Blundell, Stubbs, Hughes, Whybrow, & King, 2003; Martins, Morgan, & Truby, 2008). Such diversity has also been described with regards to the acute influence of exercise on energy intake (Blundell & King, 1999; Maraki et al., 2005). The inconsistency in findings likely reflects dissimilarity in study protocols and participant characteristics. Within this area of enquiry recent efforts have sought to find the mechanisms responsible for alterations in appetite during and after exercise. Peptides secreted from the gastrointestinal tract such as cholecystokinin, peptide YY, glucagon like peptide 1 and ghrelin mediate short-term feelings of hunger and satiety, therefore recent interest has focused on the response of these hormones to exercise (Broom, Batterham, King, & Stensel, 2009; Broom, Stensel, Bishop, Burns, & Miyashita, 2007; Martins, Morgan, Bloom, & Robertson, 2007; Ueda et al., 2009). Of the peptides regulating energy balance ghrelin is conspicuous as the only known peptide that stimulates appetite and food intake– all others act as satiety signals reducing appetite and promoting meal termination (Murphy & Bloom, 2006). A well defined role of ghrelin in the regulation of energy homeostasis exists with circulating values being sensitive to both acute (Callahan et al., 2004; Leidy & Williams, 2006; Liu et al., 2008) and chronic (Cummings, 2006; Leidy, Dougherty, Frye, Duke, & Williams, 2007) perturbations in energy balance. Exercise influences energy balance therefore it is possible that exercise may influence ghrelin. Appetite 54 (2010) 492–498 ARTICLE INFO Article history: Received 15 September 2009 Received in revised form 14 December 2009 Accepted 3 February 2010 Keywords: Exercise Acylated ghrelin Appetite Energy intake Energy balance Compensation ABSTRACT The effects of prolonged treadmill running on appetite, energy intake and acylated ghrelin (an appetite stimulating hormone) were examined in 9 healthy males over the course of 24 h. Participants completed 2 experimental trials (exercise and control) in a randomised-crossover fashion. In the exercise trial participants ran for 90 min at 68.8  0.8% of maximum oxygen uptake followed by 8.5 h of rest. Participants returned to the laboratory on the following morning to provide a fasting blood sample and ratings of appetite (24 h measurement). No exercise was performed on the control trial. Appetite was measured within the laboratory using visual analogue scales and energy intake was assessed from ad libitum buffet meals. Acylated ghrelin was determined from plasma using an ELISA assay. Exercise transiently suppressed appetite and acylated ghrelin but each remained no different from control values in the hours afterwards. Furthermore, despite participants expending 5324 kJ during exercise there was no compensatory increase in energy intake (24 h energy intake; control 17,191 kJ, exercise 17,606 kJ). These findings suggest that large energy deficits induced by exercise do not lead to acute compensatory responses in appetite, energy intake or acylated ghrelin. ß 2010 Elsevier Ltd. All rights reserved. § We would like to thank the Great Britain Sasakawa Foundation for funding Dr. Miyashita’s travel and living expenses during the conduct of this study. We also wish to thank Miss Rosalind West, Miss Vicky Blair and Miss Swee-Lee Liew for their help with data collection and all of the volunteers for their participation in this study. JAK recruited the participants, supervised the data collection, assisted with all aspects of the biochemistry and performed the data analysis. MM and LKW assisted with data collection and the biochemical analysis. DJS performed the venous cannulations. DJS and JAK conceived the study and wrote the manuscript. None of the authors had any conflict of interest regarding any aspect of this study. * Corresponding author. E-mail address: D.J.Stensel@lboro.ac.uk (D.J. Stensel). Contents lists available at ScienceDirect Appetite journal homepage: www.elsevier.com/locate/appet 0195-6663/$ – see front matter ß 2010 Elsevier Ltd. All rights reserved. doi:10.1016/j.appet.2010.02.002