This is an excerpt from Physiology of Sport and Exercise 6th Edition With Web Study Guide by W. Larry Kenney,Jack Wilmore & David Costill.
Hormonal Regulation of Caloric Intake
The regulation of appetite, the sensations of hunger and satiety, and the feeling of fullness are part of a complex system that involves hormonal signaling from all over the body including the gastrointestinal system and fat cells. Food intake is primarily under the control of the hypothalamus with some input from higher brain centers. The satiety area of the brain is located in the ventromedial nucleus, while the hunger center is located in the lateral hypothalamus. The hypothalamus, as it does for many aspects of homeostasis, integrates neural and hormonal signals for both the short- and long-term regulation of eating behavior and calorie intake.
Hormones that influence these brain centers are synthesized in, and released from, peripheral tissues including the gut and fat cells (adipocytes). These hormones can be categorically split into those that are anorexigenic, meaning that they suppress appetite, and those that are orexigenic, meaning that they stimulate appetite. The main hormones that regulate appetite and satiety are cholecystokinin, leptin, peptide YY, GLP-1, insulin, and ghrelin.
Gastrointestinal Tract Hormones
Short-term control of food intake is regulated by plasma concentrations of nutrients including amino acids, glucose, and lipids. However, another significant influence on short-term regulation of food intake involves hormones released in the gastrointestinal (GI) tract. Gastrointestinal distention caused by a full stomach triggers the release of the hormone cholecystokinin (CCK), which stimulates afferent fibers of the vagus nerve to send signals to the brain to suppress hunger. In addition, other hormones including GLP-1 and peptide YY (PYY) are secreted from the large and small intestines during and after eating. These hormones travel through the blood to the brain where they suppress hunger. Peptide YY also acts on the hypothalamus to inhibit gastric motility. Insulin released from the pancreas in response to eating also acts as a satiety hormone.
Conversely, the hormone ghrelin is secreted from the stomach and pancreas when the stomach is empty; it can be thought of as a hunger hormone. Ghrelin is transmitted through the blood to the brain where it crosses the blood - brain barrier to act on the hunger areas in the lateral hypothalamus. After eating, ghrelin concentrations decrease.
Adipose Tissue as an Endocrine Organ
In addition to hormones secreted by the stomach and intestines to signal hunger or fullness, additional hormones are secreted by adipocytes (fat cells) that likewise act on the hunger and satiety centers in the hypothalamus. Because the level of these hormones depends on the amount of adipose tissue in the body, which changes slowly, these hormones are more involved in the long-term regulation of food intake. The hormone leptin is primarily secreted by fat cells and acts on receptors in the hypothalamus to decrease hunger. Leptin is also an indicator of energy balance, as its circulating concentrations are proportional to body fat. A simple schematic of how leptin and ghrelin interact to modify appetite and satiety is presented in figure 4.9.
Hormonal regulation of appetite and satiety by ghrelin and leptin. Acting through specific hypothalamic receptors (GH secretagogue receptor or GHS-r for ghrelin and obesity receptor or Ob-r for leptin), ghrelin increases, and leptin decreases, appetite.
A great deal has been discovered about what leptin does in terms of energy balance from a mouse model using mice that lack the ability to make leptin in their fat cells. These mice have a voracious appetite and are massively obese. In obese humans, circulating concentrations of leptin are elevated, but many obese humans are leptin resistant. This suggests that despite an elevated signal they are in an overfed state; the signal is not being transmitted through the hypothalamus to initiate the sensations of satiety. Interestingly, obese humans also appear to have a dampened ghrelin signal. Researchers are only beginning to understand how hormonal appetite signaling changes with weight gain and obesity. This is critical in order to determine how best to treat obesity, as well as how exercise may influence appetite and satiety hormones.
Effects of Acute and Chronic Exercise on Satiety Hormones
Acute bouts of moderate- to vigorous-intensity exercise temporarily suppress appetite, likely by decreasing ghrelin and increasing GLP-1 and PYY released from the GI tract.12 These hormonal changes are most pronounced with aerobic exercise and are not observed after resistance exercise training.3
With chronic exercise training comes a shift in energy balance due to the calorie deficit induced by exercise. This is accompanied by a partial compensation to increase hunger and therefore caloric intake through changes in the appetite-regulating hormones. Several studies have observed an increase in plasma PYY concentrations after exercise training, which would be consistent with improved satiety. Counterintuitively, the hunger hormone ghrelin does not change in people who do not lose weight during exercise training but increases significantly in those who do lose weight.9 In general, appetite and satiety hormones are sensitive to the total energy balance that is modulated by regular exercise. It has been suggested that for elite athletes who need to monitor their energy balance, measures of circulating leptin and ghrelin may help to determine when the athlete is overtraining and may help predict states of energy deficit.5