Researchers at the University of Virginia School of Medicine have identified an important new benefit of exercise: It increases the ability of skeletal muscle cells to remove damaged components and other cellular debris. The discovery should prove important in the battle against the effects of aging and diseases such as diabetes – and could help explain why some people see little benefit from exercise.
That cellular cleaning process, known as autophagy, appears vital for the muscle to adapt to exercise – and for the body to receive the health benefits of the exercise. “If I can use an analogy to describe this [cellular clean-up process], it’s like a janitor. A team of janitors comes to clean up the working environment every day, to maintain the homeostasis of the cell,” explained UVA’s Zhen Yan, PhD. “Exercise training seems to increase the number of janitors and make the process more efficient. So we have a more active cleaning process of the cell.”
The effect on muscle adaptation
If there’s a problem with the cellular cleaning process, however, there will also be a problem when the skeletal muscle attempts to adapt to the exercise, the UVA researchers believe. “This impact on adaptation could mean losing the ability to improve physical performance,” Yan said, “and can also impact the effect of exercise in dealing with metabolic diseases, such as diabetes.”
Vitor A. Lira, PhD, a former postdoctoral fellow at the School of Medicine and the lead author of the paper outlining the findings, noted that a small portion of the population seems to suffer from “low trainability,” meaning that they don’t respond effectively to exercise. It’s possible, he said, that limitations in autophagy play some role in the variability in response to training. “We don’t know at this point,” he said, “but these findings suggest this could be one possibility.”
A new therapeutic?
The UVA findings could eventually lead to ways to simulate the benefits of exercise on the cellular cleansing process, such as with a drug. This would benefit people who do not respond to exercise and those who cannot exercise. It could also battle the slowing of the cellular cleansing process that comes with age, a slowing that causes loss of muscle mass and strength (sarcopenia) and impaired metabolism (aging-related diabetes).
For now Yan and his team are focusing on better understanding the effect of exercise on the skeletal muscle. “There are so many players in the autophagy process that could be altered, regulated, by exercise. We want to know which player is playing which role,” Yan said. “We would love to know which player is the most important, and we will try to mimic the effects of exercise. Hopefully one day we can identify drug targets to have that benefit for individuals who cannot exercise.”
The findings have been published online by The FASEB Journal and will appear in a forthcoming print edition. The article was authored by Lira, Mitsuharu Okutsu, Mei Zhang, Nicholas P. Greene, Rhianna C. Laker, David S. Breen, Kyle L. Hoehn and Yan, all of the UVA School of Medicine. Yan is director of the Center for Skeletal Muscle Research at the Robert M. Berne Cardiovascular Research Center at the School of Medicine.