Neurological health depends as much on signals sent by the body’s leg muscles to the brain as it does on those sent from the brain to the muscles, according to a recent study.
These results offer new clues as to why patients with neurological diseases such as spinal muscular atrophy (SMA) often rapidly decline when their movement becomes limited.
The study, “Reduction of Movement in Neurological Diseases: Effects on Neural Stem Cells Characteristics,” was published in the journal Frontiers in Neuroscience.
“Our study supports the notion that people who are unable to do load-bearing exercises — such as patients who are bed-ridden, or even astronauts on extended travel — not only lose muscle mass, but their body chemistry is altered at the cellular level and even their nervous system is adversely impacted,” Raffaella Adami, the study’s first author from the Università degli Studi di Milano in Italy, said in a press release.
The team used a mouse model with severe hind limb movement deprivation. These mice were restricted from using their hind legs, but not their front legs, over a period of 28 days.
This model is used to simulate the movement limitations experienced by people with motor diseases, those on extended bed rest, or astronauts who spend long periods in space.
Researchers looked at the impact of reduced exercise in an area of the brain responsible for maintaining nerve cell health and producing neural stem cells — brain cells that can give rise to new neurons.
Animals with restricted movement had a 70% reduction in the number of neural stem cells compared with control mice allowed to move freely.
When they looked at these cells under the microscope, researchers saw that neurons and oligodendrocytes — specialized cells that support and insulate neurons — could not fully mature when exercise was severely reduced.
Neural stem cells of the animals with restricted movements also had a lower metabolic activity and altered expression of two specific genes, one of which is very important for the health of mitochondria, which produce the energy used by cells.
These results suggest that movement, particularly load-bearing exercise, sends signals to the brain that are important in maintaining a healthy nervous system and producing new neurons when needed — such as to handle stress or environmental changes.
“It is no accident that we are meant to be active: to walk, run, crouch to sit, and use our leg muscles to lift things,” Adami said. “Neurological health is not a one-way street with the brain telling the muscles ‘lift,’ ‘walk,’ and so on.”
According to the authors, this study provides “the first evidence of a correlation between changes in NSCs [neural stem cells] attributes after movement restraint, metabolism modification, and gene expression changes.”
While the relationship between exercise and cognitive capacity has been known for centuries, recent studies have only now begun to uncover the link between physical activity and the performance of nerve cells.
Prior mouse studies showed that limiting movement decreases memory and learning capacity, as well as levels of certain neural messengers. Long-term exercise (swimming and running) has also been shown to benefit mouse models of SMA.
“The question I asked myself was: is the outcome of these diseases due exclusively to the lesions that form on the spinal cord in the case of spinal cord injury and genetic mutation in the case of SMA, or is the lower capacity for movement the critical factor that exacerbates the disease?” said Daniele Bottai, the study’s senior author also from the Università degli Studi di Milano.
Knowing the players involved in this relationship is pivotal “to develop new strategies to reduce the negative central and peripheral impact of motor deprivation in immobile patients and in astronauts,” the researchers concluded in the study.