Study Explains Why Brains Get Tired When Exercising

A recent study has identified that a braking mechanism in the brain, which swings into effect can make us tired when exercising.

What may be occurring is what is referred to as 'central fatigue,' said researchers.

"Our discovery is helping to shed light on the paradox which has long been the subject of discussion by researchers," said Associate Professor Jean-Francois Perrier from the Department of Neuroscience and Pharmacology, who has spearheaded the new research.

"We have always known that the neurotransmitter serotonin is released when you exercise, and indeed, it helps us to keep going. However, the answer to what role the substance plays in relation to the fact that we also feel so exhausted we have to stop has been eluding us for years. We can now see it is actually a surplus of serotonin that triggers a braking mechanism in the brain. In other words, serotonin functions as an accelerator but also as a brake when the strain becomes excessive," said Jean-Francois Perrier.

He hopes that mapping the mechanism that prompts central fatigue will be useful in several ways.

Central fatigue is a phenomenon that has been known for about 80 years; it is a sort of tiredness, which, instead of affecting the muscles, hits the brain and nervous system.

By conducting scientific experiments, it is possible to observe and measure that the brain sends insufficient signals to the muscles to keep going, which in turn means that we are unable to keep performing. This makes the mechanism behind central fatigue an interesting area in the battle against doping, and it is for this reason that Anti Doping Danmark has also helped fund the group's research.

"In combating the use of doping, it is crucial to identify which methods athletes can use to prevent central fatigue and thereby continue to perform beyond what is naturally possible. And the best way of doing so is to understand the underlying mechanism," said Jean-Francois Perrier.

The brain communicates with our muscles using so-called motoneurons. In several diseases, motoneurons are hyperactive. This is true, for example, of people suffering from spasticity and cerebral palsy, who are unable to control their movements.

Jean-Francois Perrier therefore hopes that, in the long term, this new knowledge can also be used to help develop drugs against these symptoms and to find out more about the effects of antidepressants.

Source: ANI