Exercise & Appetite

The “eat less, exercise more approach” to weight loss is more complicated than it appears.  This is because human physiology works in direct opposition to this approach. When we exercise more, the natural compensatory reaction of the body is to eat more and when we exercise less, the body responds by burning less.

To achieve lasting weight loss, appetite must be managed. And to help control the compensatory eating that occurs with exercise, it is helpful to know what type of exercise to use to provide the best impact on calorie use, hormonal balance and appetite control.

Appetite signaling molecules

The two most important appetite regulating hormones are leptin and ghrelin and exercise impacts both (2-6).  Leptin is produced in the fat cell and acts like the body’s fuel gauge communicating to the brain how much fuel (fat) it has in it tanks (adipose tissue). Rising leptin levels shut off hunger and stimulate metabolism via thyroid and adrenal stimulation. Falling leptin levels induce appetite and slow metabolism.

One confusing addendum to this mechanism is that when leptin levels are very high for long periods of time, leptin resistance sets in. This means both very high and low levels of leptin can cause increased hunger and slowed metabolism. Leptin is usually thought of as a day-to-day appetite regulator.

Ghrelin is made in the stomach and controls hunger hour to hour.  When ghrelin is high we get hungry and crave highly palatable foods.  When ghrelin is low hunger dissipates. Ghrelin like leptin is impacted by exercise (2,4-5).

Glucose-dependent insulinotropic peptide (GIP), peptide YY (PYY), and glucagon like peptide-1 (GLP-1) are all gut derived signaling molecules that control appetite. These gut “hormones”, are part of the entero-endocrine system helping relay information from the digestive system to the brain. All of these “gut hormones” also seem to be impacted by exercise (1).

Another consideration is the impact of stress hormone production during exercise.  Stress hormones, in particular cortisol, may play a role in increasing not only hunger but cravings as well (10). Higher intensity, shorter duration (i.e. sprinting) exercise and longer duration moderate intensity exercise (i.e jogging) both raise cortisol levels, but short intense exercise is unique because it also suppresses ghrelin and is balanced by growth promoters (5,9).  Low intensity walking, especially in nature settings, lowers cortisol (13).

Exercise, appetite and hormones

Research hints that longer duration moderate intensity exercise, such as aerobic zone biking, swimming and running, generates increased appetite shortly after exercise and this mechanism may work through decreasing leptin and raising ghrelin (3-4,8).  While higher intensity short duration activity, like sprinting & interval training, may have a short-term appetite suppressing effect by lowering both leptin and ghrelin (2,5,8).

Low intensity walking seems to have a neutral impact on appetite and may be the only type of exercise where there is little to no hunger and craving compensations (7,11). It is important to distinguish between lower intensity “leisure-walking” and high intensity “power-walking”.  A 2004 study out of the American Journal of Clinical Nutrition showed low intensity walking (40% of Vo2max) vs. high intensity walking (70% of Vo2max) had less of an impact on appetite despite burning the same number of calories per session (350 kcal/session) (7).

Leisure-walking resulted in significantly less eating compensation following exercise compared to power walking (25% vs. 41%). The compensation in the power-walking group was almost enough to completely abolish the calories burned during exercise as stated by the researchers: “increasing exercise intensity……..leads to an increase in energy intake during the meal that follows the exercise session……sufficient to almost completely compensate for the exercise-induced energy expenditure.”

Exercise & appetite compensation

Church et. al. in the February 2009 issue of PLos ONE showed how important exercises impact on weight loss can be (12). In this study the researchers had participants exercise at the recommended calorie expenditure advocated by the NIH of roughly 18 Kcals per pound per week (136 minutes of exercise/week). They then had 2 other groups exercise to burn calories 50% below (72 Minutes exercise per week) and 50% above (194 minutes exercise per week) this level. A fourth group acted as the control and did no exercise. The study continued for 6 months.

The group exercising at the highest level (194 min/week) lost less than half the weight that would be predicted based on energy expenditure equations. The “less exercise group” (72 min/week) lost more weight than predicted. The 8 Kcal per pound per week group (136 min/week) lost about what was predicted.  The researchers, while careful in the wording of their conclusion, believed compensatory eating was the most likely culprit for the observed effect. They summed it up this way “While we cannot conclude that an increase in energy intake in response to increased energy expenditure is the source of the observed compensation, based on the work of others we conclude it is the most likely cause.”

Final thoughts

There is more research to be done on exercise and appetite, but the research is providing clues.  Duration or total amount of exercise may be the most salient issue to controlling appetite compensations induced by exercise.  Short intense exercise, as well as very low intensity exercise like walking, seem to be most beneficial in controlling eating compensations induced by exercise. Exercising too much and/or for too long may result in compensatory reactions that could sabotage weight loss efforts through increasing how much patients eat and what types of foods they choose.

 

References:

  1. Martins et al. Effects of exercise on gut peptides, energy intake and appetite. Journal of Endocrinology. 2007;193:m251-258
  2. Broom et. al, Influence of resistance and aerobic exercise on hunger, circulating levels of acylated ghrelin, and peptide YY in healthy males. 2009;296(1):R29-35.
  3. Karamouzis, et. al. The effects of marathon swimming on serum leptin and plasma neuropeptide Y levels. Clin Chem Lab Med. 2002;40(2):132-6.
  4. Plinta, et al. The effect of three-month pre-season preparatory period and short-term exercise on plasma leptin, adiponectin, visfatin and ghrelin levels in young female handball and basketball players. Journal of Endocrinological Investigation. October 2011. Epub ahead of print.
  5. Erdmann, et. al. Plasma ghrelin levels during exercise – effects of intensity and duration. Regul Pept. 2007;;143(1-3):127-35.
  6. Guerra, et al. Is sprint exercise a leptin signaling mimetic in human skeletal muscle? Journal of Applied Physiology. 2011;111(3):715-725.
  7. Pomerleau, et al. Effects of exercise intensity on food intake and appetite in women. American Journal of Clinical Nutrition. 2004;80120-1236.
  8. Bozinovski, et. al. The effect of duration of exercise at the ventilation threshold on subjective appetite and short-term food intake in 9 to 14 year old boys and girls. International Journal of Behavioral Nutrition and Physical Activity. 2009;6:
  9. McMurray, et. al. Interactions of Metabolic Hormones, Adipose Tissue and Exercise. Sports Med. 2005;35(5):393-412.
  10. Epel, et. al. Stress may add bite to appetite in women: a laboratory study of stress-induced cortisol and eating behavior. Psychoneuroendocrinology. 2001;26(1):37-49
  11. Unick, et al. Acute effect of walking on energy intake in overweight/obese women. Appetite. 2010;55(3):413-9.
  12. Church, et al. Changes in weight, waist circumference and compensatory responses with different doses of exercise among sedentary, overweight postmenopausal women. PLoS ONE. 2009;4(2):e4515
  13. Park, et al. The physiological effects of Shinrin-yoku (taking in the forest atmosphere or forest bathing): evidence from field experiments in 24 forests across Japan. Environmental Health and Preventive Medicine. 2010;15(1):18-26.

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