ALS, Amyotrophic Lateral Sclerosis.

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In A Nutshell

  • Tongue exercise lifted weak nerve signals close to healthy levels in rats with ALS-like damage.
  • It did not save the roughly half of motor neurons that were lost.
  • Immune cells called microglia rose in damaged, exercised rats, but exercise was not proven the cause.
  • Results come from nine days of rat testing, so benefits for people remain unproven.

Exercise did not bring dead nerve cells back to life, yet a new rat study found that working the tongue still pushed a damaged nerve to send much stronger signals. In rats whose tongue nerves had been deliberately injured, overnight tongue exercise lifted nerve output close to the level of healthy animals, even though about half of the tongue’s motor neurons, the cells that carry movement commands, were already gone.

Published in the Journal of Neurophysiology, the work comes from University of Missouri researchers who study the hypoglossal nerve, which controls the tongue. In ALS and related diseases, that nerve gradually fails. The tongue does more than help with talking and tasting; it keeps the airway open and moves food toward the throat, so a weakened tongue makes swallowing harder and, during sleep, can let the airway collapse. Earlier research cited in the paper links lower tongue strength to shorter survival in people with ALS.

ALS has no cure, and few treatments protect swallowing and breathing. A simple behavior that improves nerve output without requiring new nerve cells would be worth a close look. The authors don’t oversell it, calling tongue exercise a possible option for some patients, not a proven one.

Tongue Exercise Did Not Save Motor Neurons in Damaged Rats

Researchers divided 3-to-4-month-old male rats into four groups. Two groups got a tongue injection of a toxin designed to mimic some of the nerve cell loss seen in ALS. The toxin travels from the tongue muscle back to the brainstem, where it kills motor neurons. The other two groups got a harmless control injection. In each pair, one group exercised and the other did not.

Working out meant drinking sugar water. On days 4 and 6 after the injection, exercising rats found a spout in their cage that released a 30% sugar solution only when they licked hard. Each spout demanded 50% more force than that rat’s own maximum lick strength, measured before the injections, and rats used it overnight, when rodents are most active. Non-exercising rats got a spout that took almost no effort.

Nine days after the injection, a stopping point chosen because later time points caused severe swallowing trouble in the rats, the researchers counted what was left. Among 42 rats counted, those given the toxin had about half as many tongue motor neurons as healthy rats, whether or not they exercised. Under the microscope, the tongue nerves of 26 rats also told the same story: fewer fibers, and the ones that remained were more misshapen. Exercise did not significantly change either result. Neurons in the brain that send commands to those motor neurons showed no measurable loss.

Tongue Exercise and Nerve Output in Rats
Rats with ALS-like nerve damage sent near-normal signals to the tongue after exercise, but benefits for people are unproven. (Image by StudyFinds)

Tongue Exercise Brought Nerve Signals Back Near Normal in Damaged Rats

Next came the real test. In 29 anesthetized rats, researchers placed electrodes on the tongue nerve and measured its electrical output, first at rest and then during a stress test that raised carbon dioxide and lowered oxygen to push the nerve as hard as possible, a rough stand-in for a breathing emergency.

Damaged rats that skipped exercise produced weak signals, about one-seventh as strong as healthy rats at rest and one-third as strong under stress. Damaged rats that exercised looked like healthy ones at rest, and their output under stress was not statistically different from healthy animals either. The nerve fired just as often in every group, so exercise changed how strong the signals were, not how frequent. In plain terms, the damaged nerve was speaking up again, even with fewer cells carrying the message.

One surprise showed up in the tissue. Microglia, immune cells that live in the brain and spinal cord, covered more area and were more densely packed in the brainstem area that controls the tongue in damaged, exercised rats than in healthy, exercised ones. But damaged rats that exercised and those that did not were not significantly different, so the study cannot say exercise caused the rise. Microglia help rewire nerve circuits and respond to injury, so the rise is a lead worth chasing, but what these cells are doing here remains a mystery.

Tongue Exercise for ALS Still Needs Testing in People

Big caveats apply. The experiment lasted just nine days, which left no room for more exercise sessions, and the toxin imitates only parts of motor neuron disease, not the slow march of ALS itself. Because the recordings captured electrical activity in the nerve rather than actual swallowing or breathing, the results cannot show that tongue exercise protects those functions in people.

Still, the finding fits with earlier work from the same group, where exercise improved tongue strength, airflow and swallowing-related licking in this rat model. Together, those results hint that a weakened tongue nerve can be coaxed into working harder even after many of its cells are gone.

Gone cells stay gone, but the wiring left behind may still be pushed to do more. With so few options for ALS, that is reason enough to test tongue exercise in longer-running disease models first, then in people.


Disclaimer: This article summarizes an animal study and is not medical advice. A physician should be consulted about ALS or swallowing concerns.


Paper Notes

Limitations

The authors note that the brain region examined for upper motor neuron survival holds millions of cells, with only about 6,000 belonging to the pathway that reaches tongue nerves, so a small loss could have been hidden by surrounding healthy cells. They also acknowledge that exercise may not have been rigorous enough to produce benefits in nerve structure, and that the nine-day timeline left no room for extra sessions because the rats needed recovery time. A longer exercise period, they suggest, might bring greater functional benefits, and they call for testing in models with a longer disease timeline, such as genetic models of ALS. The mechanism behind the improved signals remains unknown. Beyond the authors’ own caveats, only male rats were studied, group sizes were small for several measures (as few as 4 to 5 rats), the microglia difference appeared only against exercised healthy rats, not against unexercised damaged rats, and nerve activity was recorded in anesthetized animals instead of measuring swallowing or breathing directly.

Funding and Disclosures

The work was supported by a multi-investigator R01 grant (HL153612) from the National Institutes of Health, the University of Missouri Research Board, the University of Missouri College of Veterinary Medicine Committee on Research, and an Excellence in Electron Microscopy grant. One author, Amy N. Keilholz, received salary support from a National Institutes of Health T32 grant (OD011126). The authors declared no conflicts of interest, financial or otherwise.

Publication Details

Title: Impact of tongue exercise on hypoglossal axis survival, structure, and output in a rodent model of hypoglossal motor neuron degeneration Authors: Amy N. Keilholz, Stephanie Lopez, Minasadat Attari, Nguyen P. Nguyen, Jay Henry, Catherine L. Smith, Ashley Feldberg, Kate L. Osman, Mojgan Golzy, Filiz Bunyak, Teresa E. Lever, and Nicole L. Nichols Correspondence: Nicole L. Nichols, University of Missouri ([email protected]) Journal: Journal of Neurophysiology, Vol. 135, pages 1421 to 1436, American Physiological Society; first published April 21, 2026 (submitted December 30, 2024; accepted April 1, 2026) DOI: 10.1152/jn.00631.2024 (https://doi.org/10.1152/jn.00631.2024) License: Creative Commons Attribution CC-BY-NC-ND 4.0

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