Why can exercise “strengthen the bones”?

Why can exercise “strengthen the bones”? Nature paper discovers the mechanism behind it!

If you want to ask, why is exercise good for health? It is estimated that everyone can give at least no less than five reasons, such as promoting metabolism, enhancing immunity, promoting blood circulation, increasing cardiopulmonary function, reducing fat and increasing muscle, and so on.

Speaking of muscle gain, in a study published in “Science Advances” not long ago, researchers from Duke University in the United States proved this mechanism by using engineered muscles cultivated in the laboratory: human muscles can exercise Resist the destructive effects of chronic inflammation.

Therefore, the mechanism by which exercised muscles can resist inflammation and strengthen “muscles” has been revealed, so what is the role of the bones wrapped by muscles? As we all know, exercise can improve bone strength and immune function, but what is the mechanism behind this phenomenon?

Recently, in a new study published in “Nature”, an international research team led by the Southwestern Medical Center of the University of Texas (UT) clarified this mechanism. They found a special ecological niche called “niche” in the bone marrow, and this “niche” is a place where new bone cells and immune cells are produced. Exercise-induced stimulation is necessary to maintain the niche and the production of bones and immune cells in it. In other words, exercise strengthens the immune system and increases bone density to prevent osteoporosis.

Bone marrow has hematopoietic, immune and defensive functions. The bone marrow of an adult is one of the largest organs in the human body, 2.8 kg per capita, accounting for 3.5-5.9% of body weight. In bone marrow, there are two kinds of stem cells, one is hematopoietic stem cells; the other is bone stem cells. Hematopoietic stem cells can differentiate into blood cells such as lymphocytes (B cells and T cells that the immune system resists infection); while skeletal stem cells can differentiate into mesenchymal cells such as osteoblasts. As we age, the “niche” in the bone marrow changes, and the cells responsible for maintaining bone quality and immune function are gradually depleted. However, scientists know little about how this niche changes and why bone cells decrease with age.

In this new study, the researchers found through experiments in mice that the mechanical force generated by walking or running is transmitted from the surface of the bone to the bone marrow along the small arteries and blood vessels. Bone-forming cells that line the outside of arterioles can sense these forces and be induced to proliferate. Not only can this form new bone cells, which helps thicken the bones, but the bone-forming cells secrete a growth factor that increases the frequency of lymphocytes forming around the small arteries.

When the ability of bone-forming cells to sense mechanical forces (generated by exercise) is inactivated, the production of new bone cells and lymphocytes is reduced, resulting in thinning of the bones and reducing the ability of mice to clear bacterial infections.

Previous research in the laboratory of Sean Morrison, director of the UT Southwestern Medical Center and a researcher at the Howard Hughes Medical Institute, found that bone stem cells can produce most of the new bone cells in the adult bone marrow. These cells are leptin receptor + (LEPR +) cells, which are arranged on the outside of the bone marrow blood vessels to form the key growth factor that maintains hematopoietic cells. The team also discovered that a subset of LEPR+ cells synthesizes Osteolectin (Oln), a previously undiscovered osteogenic growth factor. Oln is a secreted protein that can activate skeletal stem cells, osteoblastic progenitor cells and other related signals on the cell surface, and promote the maintenance of adult bones by allowing LEPR+ to form new bone cells.

In this new study, the researchers studied a subset of LEPR+ cells that produce Osteolectin and found that these cells only exist around small arteries in the bone marrow and maintain nearby lymphoid progenitor cells by synthesizing stem cell factor (SCF). SCF is a growth factor on which these cells depend. Deleting SCF from Oln+ cells depletes lymphoid progenitor cells and destroys the mice’s immune response to bacterial infections.

Bo Shen, the first author of the study and a postdoctoral researcher in Morrison’s lab, said: “Combined with our previous research, this new study shows that Oln+ cells create a special niche for bone formation and lymphoid progenitor cells around arterioles.” In the elderly. Therapeutic intervention to increase the number of Oln+ cells can enhance bone formation and immune response.”

Shen found that the number of Oln+ cells and lymphoid progenitor cells decreases with age. Out of curiosity about whether this trend could be reversed, Shen put the mice in a cage with running wheels to allow them to exercise. He found that the bones of these mice became stronger with exercise, and the number of Oln-containing cells and lymphoid progenitor cells around the arterioles was also increasing. For the first time, he discovered that mechanical stimulation can regulate the “niche” in the bone marrow. . This discovery may have a broad impact on stem cell biology.

Shen found that Oln cells express a receptor called PIEZO1 on their surface, which signals when the cell responds to mechanical forces. When PIEZO1 is deleted from Oln cells in mice, these cells and the lymphoid progenitor cells they support are depleted, weakening the bones and impairing the immune response.

Morrison said: “We have discovered another important mechanism through which exercise improves immunity and strengthens bones.”

(source:internet, reference only)

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