Exercise can do so much more than simply burn off body fat and increase the metabolic rate of the body. According to scientific research, medium to high intensity exercise changes the way critical hormones operate in the body and regulates appetite, reduces cravings and helps you eat less, without effort! This is indeed great news because you get “three birds with one shot”. We know that timing your meals and optimal meal composition can make a big difference in long-term weight loss, but exercise takes the whole thing to another level.
If you thought that exercise is all about muscles, think again. A study published in the journal “Diabetes” in 2006 provides direct evidence that exercise regulates appetite by changing the way the brain, and more specifically the hypothalamus, interacts with the two most important hormones for hunger satisfaction: leptin and insulin. Hypothalamus is a tiny part of the brain dedicated to connect the hormone signals with neurological functions. It regulates many different functions, especially those related to metabolism; as expected hunger is one of them.
So, based on the available research, exercise acts on the brain (hypothalamus) to reduce appetite. This is done by increasing its sensitivity to insulin and leptin, the major hormones involved in hunger and satiety. It is not that more or less of the hormones are produced, rather than the brain is way more sensitive to them after working out and sends signals of satiety to your body. The incredible thing with exercise is that it causes extensive molecular changes in the brain cells, affecting a whole biochemical pathway, resulting in the observed increased sensitivity for these vital hormones. You don’t want to have leptin or insulin unregulated if you want to lose weight; they are well- known to act as adiposity signals, meaning that they can give the signal for the body to store fat and therefore promote obesity. If you want to lose weight, it is critical to have leptin and insulin on your side because you cannot go against your brain and body for too long.
Leptin and Insulin demystified
Leptin signals the brain that the body has had enough to eat, producing a feeling of satiety. It regulates food intake, energy expenditure and body fat. With leptin, the rule is simple: too little leptin leads to obesity; if your brain does not get the signal that you are full, then you will keep on eating. Insulin is produced as a response to carbohydrate intake and triggers the absorption of glucose from the blood. When cells do not respond to insulin anymore and refuse to take in glucose (called insulin resistance), then diabetes has developed. This is caused by chronic overabundance of glucose in the blood and respective release of insulin. The rule with insulin is the opposite than leptin: too much insulin for too long, leads to obesity.
A study published in the journal “PNAS” in 2000 proved that exercise changes the genetic expression of several proteins in muscle cells and makes the absorption of glucose far more efficient. In other words, exercise makes cells more eager to take in glucose and therefore less insulin is necessary for this vital effect. Now we know that this is not just about improving the glucose uptake in the cells, but also making the brain (hypothalamus) more sensitive to insulin (and leptin). This also results in less insulin being necessary for the brain to get the message of being full and therefore a natural regulation of the appetite on the neurological level.
Disclaimer: The information on this article is not intended to provide medical advice, diagnosis or treatment and it cannot replace a one-on-one relationship with a qualified health care professional.
Ropelle ER, et al., 2010. IL-6 and IL-10 anti-inflammatory activity links exercise to hypothalamic insulin and leptin sensitivity through IKKbeta and ER stress inhibition. PLoS Biol. 8(8). pii: e1000465.
Chibalin AV, et al., 2000. Exercise-induced changes in expression and activity of proteins involved in insulin signal transduction in skeletal muscle: differential effects on insulin-receptor substrates 1 and 2. Proc Natl Acad Sci U S A. 97(1):38-43.