Exercise suppresses appetite temporarily, and now researchers have found a new possible explanation. The discovery provides new insight into how exercise affects appetite and potentially opens up the possibility of using drugs to exploit a signalling pathway in the body to treat people who have obesity.
Most people who exercise regularly know that right after an especially hard workout you are rarely hungry and some time may elapse before the body starts to recognise the need for food.
Researchers in an international collaboration initiated and led by Jonathan Long at Stanford Medical School in the United States have now identified a molecular signalling pathway that suppresses hunger even though the body may need to be refuelled soon after a hard workout.
The research has been published in Nature.
“The discovery supports the hypothesis that exercise can lead to weight loss – not only because you burn calories but also because the craving for food declines – at least for some time. The realisation also opens the door to the possibility that this mechanism can be exploited through drugs to suppress the appetite of people with obesity. This is an interesting discovery with some interesting perspectives,” explains one of the Danish researchers involved in the study, Erik A. Richter, Professor, August Krogh Section of Molecular Physiology, Department of Nutrition, Exercise and Sports, University of Copenhagen.
The starting-point for this research result is what happens in the body when you exercise. The concentration of lactic acid in the blood increases, and the harder you exercise, the more this increases. The reason is that part of the muscles’ energy is supplied anaerobically (without oxygen). The muscles form lactic acid as a byproduct, and then they start to “burn”.
The new study shows that an enzyme links lactate with the amino acid phenylalanine to produce N-lactoyl-phenylalanine (Lac-Phe).
The researchers examined blood plasma samples from horses, mice and humans, all of which either exercised or did not exercise before the samples were taken. The experiments showed that the more strenuous the exercise, the more lactate and Lac-Phe are formed in the body.
“Further, it is well known that people are not very hungry immediately after exercising, and it was hypothesised that Lac-Phe could play a role in regulating appetite,” says Erik A. Richter.
Lac-Phe induces mice to eat less
In the second part of the research, the researchers investigated how Lac-Phe affects appetite by injecting it into mice.
This confirmed that Lac-Phe plays a central role in the link between exercise and appetite regulation, since mice injected with Lac-Phe ate less than mice that had not been injected.
“This new discovery can add knowledge on the association between exercise and suppressed appetite. In addition, the results also show that the harder you exercise, the more Lac-Phe you produce, and the more appetite is probably suppressed for a time after exercise,” explains Erik A. Richter.
Mice without the enzyme that produces Lac-Phe become fat
The researchers then took the next step and developed mice that had the gene that codes for the enzyme that links lactate and phenylalanine knocked out.
These mice were given a high-fat diet but had access to a treadwheel, and the researchers compared the trend in their weight with mice that had the enzyme.
The mice that lacked the enzyme became fatter than mice with the enzyme, and the Lac-Phe produced by the mice while running in the treadwheel affected their weight.
This discovery is probably also relevant for humans, but there are still no results that directly show whether Lac-Phe also suppresses appetite.
May become relevant for treating people with obesity
An important question is how exercise-induced levels of Lac-Phe affect appetite.
The researchers have not yet identified this mechanism, but it is in the cards.
The researchers found that the cells that contain the enzyme linking lactate and phenylalanine are not located in the muscle cells but are spread throughout the body, including in the intestinal wall, blood vessels and some cells in the brain.
The aim of the future research is therefore to determine which cells contain a receptor for and are affected by Lac-Phe.
“We need to map the full signalling pathway from exercise to the effect on appetite before the discovery can become relevant within stimulation of the relevant cells through drugs with the aim of getting people to eat less and lose weight,” says Erik A. Richter.
Prehistoric people could delay eating
One can rightly ask why nature has designed us such that we are not hungry immediately after exercise?
The prehistoric people who had just hunted and killed an antelope on the savannah would probably need to replace some of the energy resources used in a hurry.
However, the opposite seems to be the case: nature enables us to wait before eating.
“This is very speculative, but if you envision a human, mouse or horse having just escaped a tiger, hiding rather than succumbing to the need to find food might make more sense. This may explain the existence of this mechanism,” explains Erik A. Richter.
May influence the outcome of exercise
For people who want to lose weight, having reduced appetite after exercising may be an advantage.
“The appetite-suppressing effect of exercise seems to be related to the intensity of the physical activity. This discovery may therefore mean that you can benefit from a Lac-Phe-producing sprint after relatively low-intensity work such as jogging if the purpose is weight loss, because the exercise both burns calories and suppresses appetite,” says Erik A. Richter.
However, Erik A. Richter explains that there is another side to the story.
For active athletes who do not want to lose weight, suppression of appetite after exercising can be a disadvantage.
“This can result in people not being able to replace the calories used after exercise and thereby ending up with a negative energy balance for a time after the exercise. This can reduce the full benefit of your training,” concludes Erik A. Richter.