Exercise may prompt cells deep within our bones to regenerate and strengthen our immunity, suggests new research. It’s a process that takes the meaning of “bone-rattling” to a whole new level.
However, studies are increasingly reinforcing the importance of exercise as people settle into old age. New research published in Nature adds to the pile, finding movement stimulates bone regeneration and strengthens the immune system in previously unknown ways.
The study, which involved putting elderly mice on exercise wheels and evaluating their bone density and composition among other tests, revealed a specialized area in bone marrow that generates the precursors to bone cells and immune response cells.
Typically, this “niche” diminishes with age. However, the study team observed stimulation linked to movement, such as high-impact exercise, ramps up health-boosting activity.
If the idea that cells respond to movement sounds novel — or even weird — that’s because it is.
“Our study raises the possibility that there might be a lot more that depends on mechanical stimulation than we imagined,” senior author Sean Morrison, the director of the Children’s Medical Center Research Institute at UT Southwestern, tells Inverse.
“We know that exercise is really good for you, but we're getting a more complete picture of why it's good for you.”
How this affects longevity — It’s known bones deteriorate as we age. Specialized cells in bone marrow, including osteolectin cells and lymphoid progenitors, also become weaker with time.
Immune systems, in turn, take a hit because older bone marrow produces fewer lymphocytes — also known as the T and B cells that fight off illness.
It’s established that certain kinds of exercise stimulate bones in a way that leads to bone formation — generally, high-impact activities like 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,” Morrison says.
It also gives a more precise way to understand the ways in which aging bones and immune systems can weaken over time operate, Morrison explains. The team observed that mice who ran on a wheel experienced an expansion of the bone and immune-cell boosting “niche” in the marrow of load-bearing bones — as well as increased bone thickness and density.
Additionally, researchers discovered a subset of stem cells poised to become the precursors to 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 mice’s ability to fight off a bacterial infection.
The study also revealed a suppressing receptor (called PIEZO1) within the osteolectin cells depleted the specialized cell area in response to mechanical force. This reinforces the idea that exercise — especially exercise that physically impacts bones — is crucial for maintaining the cells that keep our bones and immune system strong.
These results also bring us one step closer to understanding why and how exercise helps in countering the effects of osteoporosis, for example, which is a common disease of aging, especially in women.
Why it’s a hack — Although this study looked at the bone marrow of mice and how its cells responded to exercise, it’s likely that the study findings have implications for human life.
“We can't say it for sure,” Morrison says. “But there's a remarkable degree of similarity between the blood-forming system in mice and the blood-forming system in humans.”
The study jibes with what we can already see in human life — but may not fully understand.
“When astronauts go up into space, and their bones become unloaded, their bones become thinner, and their immune system goes down,” Morrison explains. “So these observations are completely consistent with things that we know happen in humans.”
And though researchers understood that mechanical force could stimulate bone cells closer to the meeting of bone and marrow, “people didn't have a way of explaining how the mechanical forces would really penetrate into the bone marrow itself,” he says.
Next time you’re climbing a set of stairs, you can think of the movement of your feet reaching deep within the smallest blood vessels inside your bones, spurring on the creation of crucial new cells.
Hack score out of 10 — ☠️☠️☠️☠️ (4/10)
Abstract: Stromal cells in adult bone marrow that express leptin receptor (LEPR) are a critical source of growth factors, including stem cell factor (SCF), for the maintenance of haematopoietic stem cells and early restricted progenitors. LEPR+ cells are heterogeneous, including skeletal stem cells and osteogenic and adipogenic progenitors, although few markers have been available to distinguish these subsets or to compare their functions. Here we show that expression of an osteogenic growth factor, osteolectin, distinguishes peri-arteriolar LEPR+ cells poised to undergo osteogenesis from peri-sinusoidal LEPR+ cells poised to undergo adipogenesis (but retaining osteogenic potential). Peri-arteriolar LEPR+osteolectin+ cells are rapidly dividing, short-lived osteogenic progenitors that increase in number after fracture and are depleted during ageing. Deletion of Scf from adult osteolectin+ cells did not affect the maintenance of haematopoietic stem cells or most restricted progenitors but depleted common lymphoid progenitors, impairing lymphopoiesis, bacterial clearance, and survival after acute bacterial infection. Peri-arteriolar osteolectin+ cell maintenance required mechanical stimulation. Voluntary running increased, whereas hindlimb unloading decreased, the frequencies of peri-arteriolar osteolectin+ cells and common lymphoid progenitors. Deletion of the mechanosensitive ion channel PIEZO1 from osteolectin+ cells depleted osteolectin+ cells and common lymphoid progenitors. These results show that a peri-arteriolar niche for osteogenesis and lymphopoiesis in bone marrow is maintained by mechanical stimulation and depleted during ageing.