Exercise can help brain healing process

Jun 2 2004

Exercise can stimulate injured neurons to regenerate their axons, which are the primary transmission lines of the nervous system, according to a study published June 1 in the print edition of the Proceedings of the National Academy of Sciences, and the last week of May in the early online edition.

"Our experiments show that the nervous system responds to injury in the same way that it responds to activity that creates or eliminates connections needed for brain cells to communicate with one another," said Jeffery L. Twiss, head of Nemours neuroscience research lab and corresponding author of the study, titled "Voluntary Exercise Increases Axonal Regeneration From Sensory Neurons."

"In time, our further understanding of the mechanisms behind this process could aid research into new treatments for brain diseases that affect the lives of millions of Americans," Twiss said.

Neuronal activity enhances synaptic plasticity, with new connections forming between frequently used neural pathways. The term "synaptic plasticity" refers to the ability to maintain or improve synapse function. Twiss' team and a group of researchers from UCLA, under the leadership of Fernando Gómez-Pinilla, found that this plasticity can affect the ability of nerves to regenerate.

Previous research from the UCLA laboratory of Gómez-Pinilla, professor of neurosurgery and physiological science, has shown that following exercise, neurotrophin levels increase in the brain and spinal cord. Neurotrophins, growth factors that promote neuron survival, positively regulate synaptic plasticity underlying high-order neural processes such as learning and memory, and walking. This research clearly demonstrates that managed physical activity can be a realistic therapy to promote functional recovery after brain and spinal cord injury.

To investigate how exercise-induced changes in neurotrophins affect synaptic plasticity, Twiss and Gómez-Pinilla's groups examined the growth of sensory neurons from rats that had access to running wheels for zero, three or seven days.

The researchers observed that sensory neurons grew longer neurites, a type of extension, when cultured from animals that had exercised, compared to sedentary animals. Neurite length correlated directly with the distance that animals ran.

To determine whether exercise could also enhance axon regeneration within a living organism, the researchers crushed the sciatic nerve of animals that had exercised for seven days prior to the injury.  Significantly more sciatic nerve axons regenerated in the exercised animals than the sedentary animals.  Injecting an inhibitor of neurotrophin receptor activity into neurons prior to exercise blocked the activity-induced axon growth.

According to researchers, these results indicate that physical activity may alter synaptic plasticity and regenerative capacity through neurotrophin signaling mechanisms.

"There is much work to be done, but we hope to take advantage of the molecular changes seen after exercise to optimize repair or regeneration of the nervous system in the future," Twiss said.

Nemours Biomedical Research, which owns and operates the Alfred I. duPont Hospital, has a long-standing commitment to scholarly and scientific endeavors directed towards improving the health of children.  For more information, please visit the Web site at www.nemours.org.