Increases in ghrelin and decreases in leptin without altering adiponectin during extreme weight loss in male competitive bodybuilders Jarek Mäestu a, , Jaak Jürimäe b , Ivo Valter c , Toivo Jürimäe b a Department of Psychology, Centre of Behavioral and Health Sciences, University of Tartu, 50104 Tartu, Estonia b Institute of Sport Pedagogy and Coaching Sciences, Centre of Behavioral and Health Sciences, Faculty of Exercise and Sport Sciences, University of Tartu, 50104 Tartu, Estonia c Centre for Clinical and Basic Research, J. Pärna 4, 10128 Tallinn, Estonia Received 12 July 2007; accepted 25 September 2007 Abstract The aim of this study was to investigate responses of ghrelin, leptin, and adiponectin to a weight reduction period of 10 weeks in male subjects with high lean body mass and low body fat values. Fourteen male bodybuilders (7 competitors: 28.3 ± 10.3 years, 175.3 ± 5.4 cm, 82.2 ± 9.3 kg; 7 controls: 22.4 ± 3.0 years, 182.4 ± 6.9 cm, 85.3 ± 10.5 kg) participated in this study. The subjects were tested 3 times: 11 weeks (TEST1), 5 weeks (TEST2), and 3 days (TEST3) before the national championships. Testing procedure included dual-energy x-ray absorptiometry scan; calculation of daily energy intake and expenditure; and venous blood sampling for fasting ghrelin, leptin, and adiponectin. In the competitors' group, a significant (P b .05) 4.1-kg loss of body fat was observed that resulted in 6.5% ± 1.5% of the body fat at the end of the study. Ghrelin increased significantly by 20.4% by TEST2. By TEST3, ghrelin was further increased by 6% (P N .05). The pattern of leptin was opposite, with a significant 27.7% decrease at TEST2 and no further decrease at TEST3 (P N .05). No significant change was observed in adiponectin concentration during the study. In the control group, no significant changes in biochemical parameters were observed. In conclusion, ghrelin concentration significantly increases, but is suppressed in conditions of limited energy availability that is accompanied by significant body mass loss in male subjects with initial low body fat values. © 2008 Elsevier Inc. All rights reserved. 1. Introduction Body mass is regulated by a powerful homeostatic system that, in response to weight loss, triggers compensatory changes in appetite and energy expenditure to promote weight regain [1]. There have been several efforts in describing the regulation in the energy homeostasis. Implicit in this regulatory system is the existence of several peripheral factors that communicate the status of body energy stores to the brain including ghrelin, leptin, and adiponectin hormones that affect energy homeostasis. The research objective is to identify the behavior of these hormones in various energy restriction/abundance situations, as they represent pathways for obvious anti-obesity therapeutics [2]. Leptin is a hormone primarily secreted by the adipose tissue and represents several physiological functions. Probably the most important function is the role of influen- cing energy balance. Furthermore, leptin is closely correlated with body fat content in sedentary people, but not always in competitive sportsmen [3]. Adiponectin is probably the most abundant adipose tissuespecific factor [4]. Serum concen- trations of adiponectin are low in obese people and increase after weight loss. Adiponectin has also been found to affect postprandial fatty acid levels and hepatic glucose output [5]. Ghrelin is a recently described peptide hormone that is secreted by endocrine cells in the gastrointestinal tract. It has been found to regulate feeding behavior by modulating expression levels of orexigenic peptides in the hypothalamus [6] and in the coordination of energy balance and weight regulation [7]. Ghrelin administration increases hunger and stimulates food intake and might work as a hormone signaling the need to conserve energy and is one of the few known circulating orexigens [1]. Recent studies describing ghrelin action after weight loss or exercise treatment have used female subjects with relatively high amount of body fat [8-11]. Hansen et al [9] found that plasma ghrelin concentration increases with Available online at www.sciencedirect.com Metabolism Clinical and Experimental 57 (2008) 221 225 www.elsevier.com/locate/metabol Corresponding author. Tel.: +372 564 772 36; fax: +372 737 6152. E-mail address: jarek.maestu@ut.ee (J. Mäestu). 0026-0495/$ see front matter © 2008 Elsevier Inc. All rights reserved. doi:10.1016/j.metabol.2007.09.004