Why can sports live longer? The answer lies in - mitochondrial autophagy

As everyone knows, one of the best ways to stay healthy is to do aerobic exercise. But why? Recently, a study published in the journal Nature Communications found that exercise can promote mitochondrial autophagy and clear damaged mitochondria to maintain muscle health. Researchers from the University of Virginia elaborated on the signaling pathways in this process in mice.

Why can sports live longer? The answer lies in - mitochondrial autophagy

Whether it's running, cycling or swimming, one of the best ways to stay healthy is to do aerobics. The benefits you get from it are not just to lose weight, but also to improve sleep, relieve stress, improve mood, fight high blood pressure, strengthen bones and muscles...

“The health of the muscles really determines the health of the entire body,” said Zhen Yan of the University of Virginia (UVA) School of Medicine. “Sports ability, determined primarily by muscle size and function, is the best predictor of total population mortality.”

But why does exercise make us healthier? Yan may be able to provide some answers. He and his colleagues at UVA turned their attention to the cell and tried to understand at the molecular level why exercise is so important to the body. They found that one of the key benefits was related to the cellular power plant, the mitochondria. The study was published in the recent issue of Nature Communications.

Exercise-induced mitochondrial oxidative stress

Yan and colleagues completed the study in mice and found that moderate to severe exercise can lead to mitochondrial oxidative stress. The aerobic exercise-induced mitochondrial stress promotes the process of mitochondrial autophagy (mitophagy), in which muscles treat damaged or dysfunctional mitochondria and maintain muscle health.

Self-discipline, as the name suggests, is "to eat yourself." Autophagy is an evolutionarily conserved process in eukaryotes that processes the turnover of intracellular substances. In autophagy, some damaged proteins or organelles are encapsulated by autophagic vesicles, sent to lysosomes for degradation and recycled, thereby realizing the metabolic needs of the cells themselves and the renewal of certain organelles. “Aerobic exercise removes damaged mitochondria from skeletal muscle,” says Yan. “If you exercise regularly, you will continue to remove damaged mitochondria. Have healthy muscles with better mitochondria quality.”

Why can sports live longer? The answer lies in - mitochondrial autophagy

How does exercise remove damaged mitochondria?

In this study, Yan colleagues evaluated the skeletal muscles of a mouse model in which they expressed a mitochondrial reporter gene called “pMitoTimer”. "The mitochondria glow green when they are healthy, and turn red when they are damaged or destroyed by the cell's waste treatment system, the lysosome."

The mice ran for 90 minutes on a small treadmill and the team observed mitochondrial stress and some mitochondrial autophagy 6 hours after exercise. Yan explained that the movement in these mice stimulated a kinase called AMPK in the body, and AMPK activated another kinase, Ulk1. These chemical reactions appear to be important for the regulation of dysfunctional mitochondrial clearance.

"When Ulk1 is turned on, it activates other components in the cell to clear dysfunctional mitochondria," Yan said. "However, we still don't know how these activities are coordinated."

Ulk1 plays an important role in exercise-induced mitochondrial autophagy

Next, the researchers deleted the Ulk1 gene in mouse skeletal muscle and found that if this gene is absent, mitochondrial clearance of injury or dysfunction is significantly inhibited, suggesting that the Ulk1 gene plays an important role in exercise and mitochondrial autophagy. Character.

Joshua Drake, a co-author of the study and a postdoctoral fellow at Yan Labs, explained: "Those mice that are unable to perform mitochondrial autophagy are unable to benefit from exercise." Although they can move like normal mice, they are unable to train. Get the benefits of metabolism. ”

Drake pointed out that some patients with type 2 diabetes do not respond to exercise, which is a growing clinical problem. He hopes that the follow-up study of Yan's lab will bring new discoveries to help these people.

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