As we all know, one of the best ways to stay healthy is to do aerobic exercise. But why? Recently, research published in the journal Nature Communications found that exercise can promote mitophagy and remove damaged mitochondria to maintain muscle health. Researchers from the University of Virginia have elucidated the signaling pathways involved in this process in mice.

Whether you are running, cycling or swimming, we all know that the best way to stay healthy is Just do aerobic exercise. The benefits you get from it are not just weight loss, but also improving sleep, relieving stress, improving mood, fighting high blood pressure, strengthening bones and muscles...

"The health of muscles really determines the health of the entire body. ," said Zhen Yan of the University of Virginia (UVA) School of Medicine. "Exercise capacity, primarily determined by muscle size and function, is the best predictor of mortality in the general population."

But why does exercise make us more What about health? Yan may be able to provide some answers. He and his colleagues at UVA turned their attention to cells, trying 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 powerhouses: mitochondria. This research was published in the recent journal Nature Communications.

Exercise induces mitochondrial oxidative stress

Yan and colleagues conducted this study in mice and found that moderate to vigorous exercise can induce mitochondrial oxidative stress. Mitochondrial stress induced by aerobic exercise promotes the process of mitophagy, in which muscles deal with damaged or dysfunctional mitochondria to maintain muscle health.

Autophagy, as the name suggests, means "eating yourself." Autophagy is an important process of intracellular material turnover that is evolutionarily conserved in eukaryotes. In autophagy, some damaged proteins or organelles are wrapped in autophagy vesicles and sent to lysosomes for degradation and recycling, thereby realizing the metabolic needs of the cell itself and the renewal of certain organelles.  “Aerobic exercise can remove damaged mitochondria from skeletal muscle,” Yan said. “If you exercise regularly, you will continue to remove damaged mitochondria. Have healthy muscles with better mitochondrial quality.”

Image source: Nature Communications

Motion How to remove damaged mitochondria?

In this study, Yan colleagues evaluated the skeletal muscles of mouse models in which they expressed a protein called Mitochondrial reporter gene of “pMitoTimer”. "Mitochondria fluoresce green when healthy and turn red when damaged or degraded by lysosomes, the cell's waste disposal system."

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

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

Ulk1 plays an important role in exercise-induced mitophagy

Next, the researchers deleted the Ulk1 gene in mouse skeletal muscle and found that without the gene, the clearance of damaged or dysfunctional mitochondria was significantly inhibited, suggesting that Ulk1 plays a role in exercise and mitophagy. plays an important role.

“Those mice that are unable to engage in mitophagy do not receive the benefits of exercise,” explained study co-author Joshua Drake, a postdoctoral researcher in Yan’s lab, although they are able to exercise just as well as normal mice. , but they don’t get the metabolic benefits from training. "

Drake noted that some patients with type 2 diabetes do not respond to exercise, which is a growing clinical problem. He hopes that follow-up research from Yan's lab will lead to new discoveries to help these people. .

References:

Ampk phosphorylation of Ulk1 is required for targeting of mitochondria to lysosomes in exercise-induced mitophagy