Exercise, Appetite and Appetite-Regulating Hormones: Implications for Food Intake and Weight Control

Knowledge about the relationship between exercise and appetite is important both for athletes wishing to optimise performance and for those interested in maintaining a healthy body weight. A variety of hormones are involved in appetite regulation including both episodic hormones, which are responsive to episodes of feeding, and tonic hormones, which are important regulators of energy storage over the longer term (e.g. insulin and leptin). Notable among the episodic appetite-regulating hormones is ghrelin, which plays a unique role in stimulating appetite and energy intake. Many studies have demonstrated that acute bouts of moderately vigorous exercise transiently suppress appetite and this has been termed ‘exercise-induced anorexia’. The mechanisms by which acute exercise suppresses appetite are not fully understood but may involve lowered concentrations of ghrelin and increased concentrations of satiety hormones, notably peptide YY and glucagon-like peptide 1. Evidence suggests that chronic exercise training typically causes a partial but incomplete compensation in energy intake perhaps due to beneficial changes in appetite-regulating hormones. The Published online: February 22, 2011 Dr. David Stensel School of Sport, Exercise and Health Sciences Loughborough University Loughborough, LE11 3TU (UK) Tel. +44 1509 226 344, Fax +44 1509 226 301, E-Mail D.J.Stensel @ lboro.ac.uk © 2011 S. Karger AG, Basel 0250–6807/10/0576–0036$26.00/0 Accessible online at: www.karger.com/anm Exercise and Appetite Ann Nutr Metab 2010;57(suppl 2):36–42 37 how exercise influences appetite may help in facilitating weight gain in those who are underweight due to disease or malnutrition. The purpose of this article is to review recent developments in this field with particular emphasis on the role of appetite-regulating hormones in moderating the interrelationships between exercise, appetite and weight management. Appetite-Regulating Hormones Appetite regulation is a complex process involving communication between the hypothalamus within the brain, various gastrointestinal organs (including the stomach, the pancreas, and the intestines) and adipose tissue. Satiation (the process that causes one to stop eating) may be initiated by neural input from the stomach to the brain signalling gastric distension after food consumption. This is quickly followed by the release of a variety of hormones which are able to sense the digestion and absorption of nutrients and signal satiety (the feeling of fullness that persists after eating). These hormones include cholecystokinin (secreted from the duodenum and jejunum), glucagon-like peptide 1 (GLP-1), oxyntomodulin (OXM) and peptide YY (PYY) (all secreted from the small and large intestines) and pancreatic polypeptide (PP) and amylin (both secreted from the pancreas). These hormones act as short-term or episodic signals because they occur in unison with episodes of eating. They signal satiation and satiety either via the vagus nerve (which connects the gut to the brain) or via blood perfusing the hypothalamus. In addition to these episodic hormonal signals there are also tonic hormonal signals which indicate the level of energy storage in the body. Two important tonic satiety signals are insulin (released from the pancreas) and leptin (released from adipose tissue). These hormones assist in the regulation of energy balance over the long term. For detailed explanations about how the hormones introduced here regulate appetite, the reader is referred to several recent reviews [1–4] . All of the hormones mentioned so far act to a greater or lesser extent as satiety signals, i.e. high concentrations of each hormone in the blood suppress appetite. In contrast, the gut hormone ghrelin, released predominately from the gastric cells within the stomach, is known to have appetite-stimulating properties as demonstrated in experiments where either intravenous [5] or subcutaneous [6] ghrelin infusion has led to increased ad libitum energy intake during buffet meals (for a detailed review of ghrelin metabolism, see Chen et al. [7] and Stengel et al. [8] ). Recently ghrelin therapy has been found to be effective for improving appetite and food intake and limiting weight loss in patients with gastric cancer after total gastrectomy [9] confirming its function as an appetite stimulant. Ghrelin is unique as the only gut hormone known to enhance appetite and because of this there is great interest in the potential for lifestyle factors (including exercise) to modify ghrelin concentrations and assist in weight control [10] . It is important to note that the homeostatic mechanisms of appetite regulation mentioned here may be modified at times by reward pathways relating to the pleasurable qualities of food and drink. These pathways are sometimes termed hedonistic drives and in an environment characterised by an abundance of palatable foods hedonistic drives may frequently override homeostatic ones [11, 12] . Figure 1 provides an overview of the appetite-regulating hormones described here and their potential interaction with exercise. Evidence relating to exercise and appetite-regulating hormones is discussed below. Acute Effects of Exercise on Appetite and Appetite-Regulating Hormones Improved understanding of the metabolism of appetite-regulating hormones has enhanced interest about the effects of exercise on appetite and whether these effects are mediated by appetite-regulating hormones. Studies have investigated the effects of exercise on appetite (the desire for food or drink) using visual analogue scales. These scales consist of a line, usually 100 or 150 mm long, anchored by answers to a question posed above the line, e.g. ‘How hungry are you?’, ‘Not at all hungry’ vs. ‘As hungry as I have ever felt’. Scales have been devised for a variety of sensations beyond hunger including fullness, satiety, prospective food consumption (i.e. how much do you think you can eat?) and others (see Benelam [1] and Blundell et al. [13] for further details). These scales have been shown to have good reproducibility and are deemed reliable for appetite research [14] . Using visual analogue scales many studies have demonstrated that exercise does not acutely increase appetite and vigorous exercise may lead to a temporary suppression of appetite (for recent reviews of these studies, see Bilski et al. [15] and Martins et al. [16] ). This temporary suppression of appetite has been termed ‘exercise-induced anorexia’ and it leads to a short-term negative energy balance. Due to ghrelin’s unique appetite-stimulat-