The hormone ghrelin is the only known hormone to directly cause appetite. Acute bouts of exercise suppress it, but long-term exercise programs have no effect on ghrelin levels.
Ghrelin is sometimes called the “hunger hormone” because the peptide hormone is a powerful appetite stimulant. Ghrelin is 28 amino acids in length and assembled primarily in the stomach fundus. The hormone was discovered in 1999 and the subsequent decade saw a flurry of research on the influence of exercise and food intake on ghrelin. A comprehensive review published in the September 2013 issue of Appetite provides a nice summary of this research (Exercise and Ghrelin. A narrative overview of research, 2013. King, et al.).
Ghrelin exists as an acylated and unacylated hormone. The acylated form binds to a Growth Hormone activating receptor, which generates appetite and subsequent feeding. The unacylated form produces a variety of metabolic effects, but its relationship to exercise is not as well understood and, thus, will not be discussed further here. Ghrelin administration promotes weight gain by reducing fat oxidation (the break down of stored fat), limiting energy expenditure and increasing fat storage. Interestingly, ghrelin administration causes individuals to seek energy dense, high-fat foods. In agreement with its role in maintaining weight balance, ghrelin levels in the body vary inversely with BMI. Therefore, obese individuals have low levels of ghrelin and vice versa.
Appetite is suppressed after an intense workout or race. This seems counterintuitive: appetite is suppressed at the time the body is most starved of energy. Regardless of the reason, ghrelin provides the signal for appetite suppression following intense exercise. Ghrelin levels are reduced in the 30 minutes following intense exercise. One study found that treadmill running at 75% of VO2 max significantly suppressed ghrelin, but treadmill running at 50% of VO2 max had no effect on ghrelin levels. Thus, acute exercise suppresses ghrelin post-bout at an exercise intensity threshold. Whether this is a graded suppression response above the threshold has not been studied.
Although an acute bout of exercise produces a transient response, it appears to produce no long-term effect on ghrelin levels. Ghrelin levels in study participants the morning following an intense exercise bout showed no difference from non-exercised controls. This is surprising because it suggests that the body does not recover the energy expended during the intense exercise bout. In fact, a study done on a cyclist in the Tour de France found that energy consumption did not compensate for energy expended on tough climb days. In other words, the cyclist had a negative energy balance. In contrast, ghrelin levels are responsive to energy deficits induced by food restriction. One study found that creating a negative energy balance by restricting calories in meals generated a strong increase in ghrelin levels 9 hours into the calorie restriction. However, creating an identical negative energy balance with a 90 minute run produced no perturbation of ghrelin levels 7.5 hours later. Thus, it appears that a food intake disturbance to energy balance, but not an acute exercise disturbance, continues to influence ghrelin levels more than 2 hours post-disturbance. The figure below illustrates the results of the discussed study.
What about long-term exercise programs? Long-term exercise programs do not influence ghrelin levels directly. Instead, exercise acts through changes in body mass to modify ghrelin levels. Total ghrelin levels measured during a fast increase with the amount of weight lost during the exercise program. This may be one reason why participants in weight loss programs find the initial pounds the easiest to shed. However, one study found that females did increase acylated ghrelin levels in response to an exercise intervention program, regardless of whether or not a steady energy balance was maintained with increased food intake. Yet, no changes were observed in males.
Obese individuals generally have reduced ghrelin sensitivity. That is, ghrelin levels are abnormally low during a fast and then remain low following a meal, showing little fluctuation. However, researchers have found that a long-term exercise intervention reduced ghrelin suppression during a fast and lowered ghrelin following a meal in obese subjects. Thus, exercise produces greater ghrelin fluctuation in obese individuals, which causes increased appetite and hunger during a fast and higher satiety following a meal.
It is important to remember that appetite and the amount of food we eat is influenced by many factors. Recall from a previous post on exercise’s influence on brain activity that the hormone leptin plays a critical role as well. Research on exercise’s effect on appetite is still in its infancy; the studies presented here provide many more questions to be answered.