Exercise leads to unexpected benefits deep in your bones

Exercise can stimulate cells deep in our bones to regenerate and strengthen our immunity, suggests new research. It is a process that takes the meaning of “shaking bones” to a whole new level.

We already know that exercise can improve almost every aspect of health: sleep, mental health and risk of disease.

However, studies are increasingly reinforcing the importance of exercise as people adjust to old age. New research published in Nature adds to the pile, finding movement stimulates bone regeneration and strengthens the immune system in ways hitherto unknown.

The study, which involved placing elderly rats on exercise wheels and assessing their bone density and composition, among other tests, revealed an area specializing in bone marrow that generates the precursors of bone cells and immune response cells.

Usually, this “niche” decreases with age. However, the study team noted stimulation linked to movement, such as high-impact exercises, which increase activities that increase health.

If the idea that cells respond to movement seems new – or even strange – it is because it is.

“Our study raises the possibility that there may be much more that depends on mechanical stimulation than we imagined,” said senior author Sean Morrison, director of the Children’s Medical Center Research Institute at UT Southwestern. Inverse.

“We know that exercise is really good for you, but we are getting a more complete picture of why it is good for you.”

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How does this affect longevity – Bones are known to deteriorate as we age. Cells specializing in bone marrow, including osteolectin cells and lymphoid progenitors, also become weaker over time.

The immune system, in turn, is hit because the older bone marrow produces less lymphocytes – also known as T and B cells that fight disease.

It is established that certain types of exercise stimulate bones in a way that leads to bone formation – usually, high-impact activities such as jumping, running or climbing. This study takes that knowledge to the next level.

“The essential advance in this study is to identify a new way in which exercise strengthens our bones and immune function,” says Morrison.

It also provides a more accurate way to understand the ways in which aging bones and the immune system can weaken over time, explains Morrison. The team noted that mice that ran on a wheel experienced an expansion of bone and immune-reinforcing “niche” in the load-bearing bone marrow – as well as increased bone thickness and density.

Deep images of the bone marrow of a mouse femur show cells that express Osteolectin in red.Nature / Shen et. al

In addition, the researchers found that a subset of stem cells destined to become the precursors of bone cells known as osteocytes can be identified by their ability to produce a growth factor called osteolectin.

This growth factor, in turn, is involved in the generation of immune cells. When osteolectin was impaired, so was the ability of mice to fight a bacterial infection.

The study also revealed that a suppressor receptor (called PIEZO1) within osteolectin cells has depleted the specialized cell area in response to mechanical force. This reinforces the idea that exercise – especially exercise that physically affects bones – is crucial to keeping the cells that keep our bones and immune systems strong.

These results also bring us a step closer to understanding why and how exercise helps to combat the effects of osteoporosis, for example, which is a common disease of aging, especially in women.

Why is it a hack – Although this study looked at the bone marrow of mice and how their cells responded to exercise, the study’s findings are likely to have implications for human life.

“We can’t say for sure,” says Morrison. “But there is a remarkable degree of similarity between the blood-forming system in mice and the blood-forming system in humans.”

The study is in line with what we can already see in human life – but we may not fully understand.

“When astronauts go up into space and their bones are discharged, they become thinner and their immune system goes down,” explains Morrison. “So these observations are completely consistent with things that we know are happening in humans.”

And although the researchers understood that mechanical strength could stimulate bone cells closer to the meeting between bone and bone marrow, “people had no way of explaining how mechanical forces would actually penetrate the bone marrow itself,” he says.

The next time you are climbing a ladder, you can think about the movement of your feet reaching deep into the smallest blood vessels within your bones, stimulating the creation of new crucial cells.

Hack score out of 10 – ☠️☠️☠️☠️ (4/10)

Summary: Stromal cells in the adult bone marrow that express the leptin receptor (LEPR) are a critical source of growth factors, including stem cell factor (SCF), for the maintenance of hematopoietic stem cells and early restricted progenitors. LEPR+ the cells are heterogeneous, including skeletal stem cells and osteogenic and adipogenic progenitors, although few markers are available to distinguish these subsets or to compare their functions. Here we show that the expression of an osteogenic growth factor, osteolectin, distinguishes peri-arteriolar LEPR+ cells ready to undergo osteogenesis of peri-sinusoidal LEPR+ cells about to undergo adipogenesis (but retain osteogenic potential). Peri-arteriolar LEPR+osteolectin+ the cells are short-lived, fast-dividing osteogenic progenitors that increase in number after fracture and are depleted during aging. Exclusion of Scf of adult osteolectin+ the cells did not affect the maintenance of hematopoietic stem cells or most restricted progenitors, but eliminated common lymphoid progenitors, impairing lymphopoiesis, bacterial clearance and survival after acute bacterial infection. Peri-arteriolar osteolectin+ maintaining the cells required mechanical stimulation. Voluntary running increased, while lower limb discharge decreased, frequencies of peri-arteriolar osteolectin+ common lymphoid cells and progenitors. Deletion of the musculoskeletal ion channel PIEZO1 of osteolectin+ cell-depleted osteolectin+ common lymphoid cells and progenitors. These results show that a peri-arteriolar niche for osteogenesis and lymphopoiesis in the bone marrow is maintained by mechanical stimulation and depleted during aging.

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