A new study shows that exercise increases levels of a chemical that contributes to brain cell growth, which boosts the release of the “feel-good” hormone dopamine. Dopamine is known to play a key role in movement, motivation, and learning.
Experts have long known that regular running raises dopamine activity in the brain and may protect neurons from damage. Additionally, previous research has linked exercise-driven reinforcements in a dopamine-stimulating chemical called brain-derived neurotrophic factor (BDNF) and dopamine levels to improvements in learning and memory. However, the exact way of interaction of these three factors is still unclear so far.
Led by researchers at New York University’s Grossman School of Medicine, the investigation showed that mice that ran at a wheel for 30 days had a 40% increase in dopamine release in the dorsal cortex, the part of the brain involved in movement, compared to levels found in mice. not exercised. The runners also showed a nearly 60% increase in BDNF levels compared to their non-working counterparts. Notably, the increase in dopamine secretion remained elevated even after a week of rest. Additionally, when BDNF levels were artificially reduced, running did not trigger the release of additional dopamine.
“Our findings suggest that BDNF plays a key role in the long-term changes that occur in the brain as a result of running,” says lead author of the study and neurobiologist Guendalina Bastioli, Ph.D. Adds Bastoli, a postdoctoral fellow in the Department of Neuroscience at NYU Langone Health.
While researchers have previously measured dopamine activity during running, the new investigation provides insight into the hormone’s long-term behavior and its effects on the brain after exercise has stopped, according to Estoli. The report is published online on May 16 at Neuroscience Journal.
In order to investigate, the researchers gave dozens of male mice unlimited access to a freely spinning wheel or a locked wheel that cannot move. One month later, the team measured dopamine release and BDNF levels in brain slices. They repeated this same process on a new group of rodents, some of which had been genetically modified to produce half as much BDNF as normal mice.
The study authors note that patients with Parkinson’s disease and other movement disorders are often treated with drugs that mimic dopamine’s effects on motor neurons. However, the mechanism underlying the role of dopamine in this protective benefit of exercise has not been thoroughly explored.
Our findings help us understand why exercise relieves symptoms of Parkinson’s disease, as well as symptoms of neuropsychiatric disorders such as depression. Now that we know why physical activity helps, we can explore it as a way to increase or even replace the use of dopamine-boosting medications in these patients.”
Margaret Rice, PhD, first author of the study and a neuroscientist
Rice, a professor in the Departments of Neurosurgery, Neuroscience, and Physiology at NYU Langone, cautions that while initial results in rodents have been promising, future studies in humans will be required to fully understand the role of BDNF and dopamine in Parkinson’s disease.
She adds that the study team then plans to investigate the relationship between exercise and these chemicals in female mice, which work out more frequently than males. In addition, the researchers plan to conduct a direct examination of whether the active mice actually improved motor skills compared to those with limited physical activity.
Funding for the study was provided by National Institute on Drug Abuse grant DA0510165. Further funding support has been provided by the Marilyn and Paolo Fresco Institute for Parkinson’s Disease and Movement Disorders.
NYU Langone Health / NYU Grossman School of Medicine