Wednesday, June 1, 2011

Exercise and appetite: Does working out sabotage your diet? by Jerry Brainum

In his otherwise excellent, well-researched book, Good Calories, Bad Calories, author Gary Taubes suggests that exercise is overplayed as an effective technique to help shed excess body fat. His reasoning is that exercise causes an expenditure of calories, which will be sensed by the body, causing a reaction of hunger to replace the lost calories expended through exercise. At the surface, Taubes reasoning makes perfect sense. Yet, it this is so, why has exercise been recommended for years as a necessary adjunct in any effective weight-loss plan? In addition, why is that those who follow strict diets, but don't exercise, nearly always regain the lost weight, and then some? Taubes doesn't say that exercise is bad. He even admits that it offers health benefits, such as promoting cardiovascular fitness. It's just antithetical to effective weight-loss due to the resultant hunger effect stimulated by exercise, says Taubes.

    While Taubes says in interviews that he researched his book for over a decade, it seems strange that he somehow didn't find all the latest information on the relationship between exercise and appetite.He appears to overlook the extensive date showing a relationship of  exercise and certain peptides that are now known to control appetite sensations through relaying messages to the brain. These recently discovered peptides, or chains of amino acids, include leptin and ghrelin. Insulin, which is a main focus of Taube's book, is also involved in the control of appetite.In fact, insulin turns off the appetite center located in the hypothalamus in the brain.This is one reason why eating a lot of fructose stimulates appitite: it doesn't foster an insulin release.
    Ghrelin and leptin are the most interesting of the appetite control peptides.Leptin is secreted directly from adipocytes, or fat cells, and then travels to the brain with a signal that turns off appetite. Obese people actually secrete higher than normal levels of leptin, but the message to turn off appetite isn't registered in the brain. This leads to an increase in appetite that serves to perpetuate obesity.

      Ghrelin was discovered in 1999, two years after leptin was first isolated. ghrelin was found to be a ligand, or a substance that can interact with the growth hormone-secreting hormone receptor in the brain. As such, among its functions, ghrelin potently promotes GH release. Since GH release is associated with an increase in fat mobilization, you would think that ghrelin would function as a "fat burner." In actuality, however, ghrelin is perhaps the most potent appetite-stimulating substance produced in the human body. Levels of ghrelin gradually rise between meals, then rapidly decline when you eat a meal. In short, ghrelin stimulates you to eat. Besides being produced in the hypothalamus of the brain, ghrelin is also produced in the stomach and the pancreas.As noted earlier, leptin sends a signal to lower appetite, while ghrelin increases feelings of hunger. As such, they have a yin and yang effect in controlling appetite sensations. When it reaches the hypothalamus, ghrelin promotes the release of neuropeptide Y, which causes an uncontrollable urge to eat carbohydrates. But ghrelin isn't all bad. It also appears to lower depression. The happy feeling you get when eating something you like is attributable to ghrelin. Ghrelin also seems to increase learning and intelligence through stimulating memory centers in the hippocampus area of the brain.But ghrelin also tends to promote shorter sleep duration, and vice-versa: that is, not getting enough sleep boosts ghrelin and lowers leptin, leading to increased appetite and subsequent increased bodyfat levels. Perhaps worst of all, ghrelin suppresses fat utilization from adipose tissue, thus making it even harder to lose excess bodyfat.

      Ghrelin comes in two flavors: aceylated ghrelin and des-acetylated ghrelin. But only the acetylated version contains an n-octanoyl group that allows it to bind to the GHSH receptors in the brain. This means that only this form of ghrelin can enter the appetite center of the brain and promote hunger. The other form was at first thought to be inert, but later research showed that it tended to inhibit the more active form. What has all this to do with exercise and appetite?

     First, Taubes wasn't entirely wrong in his assertion that exercise promotes hunger, since some studies have indeed shown this effect. Other studies have shown a lowering of appetite following exercise, and still others have shown no effect at all. But a closer look at these studies clears up some of the confusion. It turns out that low and moderate intensity exercise doesn't induce appetite supression. Only high intensity exercise appears to promote decreased hunger. This is ironic when you consider that the usual recommendation for exercise as a means to lower bodyfat levels suggests low intensity exercise as measured by heart rate, since this is the level at which the greatest amount of fat is oxidized during exercise. But acetylated ghrelin, which promotes appetite and hunger, is only suppressed under high intensity exercise conditions. This form of ghrelin is also supressed by insulin, glucose, and leptin. Taking this information into practical use, if you follow a low-carb diet to lose bodyfat, but also do low intensity aerobics, the lack of insulin release associated with the diet will foster hunger than isn't blocked by the exercise. No wonder that Taubes thinks that exercise is ineffective for weight-loss!

      But what if you used a combination of longer duration, moderate intensity exercise, followed immediately by high intensity exercise? This was the precise scenario used in a new study. The study focused on 10 young men, average age, 20, who engaged in a crossover designed study. In the first part of the study, the subjects ran for 105 minutes at low intensity (50% of maximal oxygen intake), followed by an intense run for the last 15 minutes at a heart rate of 70% of maximal heart rate. They then rested for 2 hours. The other part of the study had the men just resting for 4 hours. During both stages of the study, the men consumed a buffet meal after either exercising or resting. When engaged in the treadmill exercise, the men burned 1,549 calories. According to Taubes, they should have been ravonously hungry with that much energy being burned. Yet, this didn't happen.Both hunger and acetylated ghrelin were suppressed after the exercise.The high intensity exercise is though to divert blood from the splanchnic (gut) area to the muscles because of heightened sympathetic nervous system activity. This decreased blood flow in the gut contributes to lower appetite sensations after exercise, and also blunts ghrelin release. Hunger did briefly increase following the exercise, but despite this, the men consumed less food after exercise compared to when they rested. Note that the meals were consumed several hours after exercise, when the hunger sensations should have peaked as the body pushed to replace the calories expended during exercise.The study authors think that the exercise may have also boosted levels of des-acyl ghelin, which blocks the hunger effect of acetylated ghrelin. The findings of this study are consistent with past studies, which showed a 19% increase in appetite after exercise; 16% showed a lowering of appetite after exercise; and 65% showed no change. The take home message is that, contrary to Taubes opinion, exercise despite incurring a caloric deficit, does not increase hunger and does not overly stimulate appetite. But the calories lost from exercise do contribute to helping you to lose bodyfat, As such, exercise should be an integral part of any effective weight-loss plan. In addition, engaging in weight-training will help preserve muscle mass under dieting conditions, which serves to help prevent the usual yo-yo weight rebound effect that is common in those who diet without exercise.

Vatansever S, et a. The effects of exercise on food intake and hunger: Relationship with acetylated ghrelin and leptin.J Sports Sci Med 2011;10:283-91.

©,2013 Jerry Brainum. Any reprinting in any type of media, including electronic and foreign is expressly prohibited.

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