Laboratory-grown human muscle shows that exercise can “almost completely” prevent chronic inflammation that causes tissue loss
- Inflammation comes from the excessive reaction of the body’s immune system
- Chronic inflammation can cause muscle tissue to lose and lose its structure
- Experts believe a molecule called “gamma interferon” is behind this waste
- Still, it wasn’t clear how it worked and why it seemed to exercise to mitigate it
- To make research easier, American researchers grew their own muscles in the lab
- This allowed them to reset the cells to focus on the relevant processes
Exercise can prevent “almost completely” the chronic inflammation that causes muscle loss, according to a study on laboratory-grown human tissue.
Inflammation occurs when our body’s immune system responds to bacterial or tissue damage, but it can sometimes overreact and end up attacking its own cells.
And some diseases, such as arthritis and sarcopenia, can cause long-term “chronic inflammation,” which causes muscle wasting.
A molecule known as “gamma interferon” is believed to be one of the culprits of various types of muscle wasting and dysfunction.
Previous studies indicated that exercise may mitigate the effects of inflammation in general, but it is not clear what role muscle cells and gamma interferon play.
To find out, researchers at Duke University in the United States developed a platform to allow them to grow their own human muscles in the lab.
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Exercise can prevent “almost completely” the chronic inflammation that causes muscle loss, according to a study on laboratory-grown human tissue. In the image: long, thin and well-defined muscle fibers (in the upper left) lose their structure after prolonged inflammation (in the upper right), but not when they are also subjected to exercise (in the upper part). lower left). The same applies to force (bottom right)
“There are many processes throughout the human body during exercise and it is difficult to separate what systems and cells are doing what is inside an active person,” said the paper’s author and biological engineer Nenad Bursac .
“Our designed muscle platform is modular, meaning we can mix and match various types of cells and tissue components if we want.”
“But in this case, we found that muscle cells were able to take anti-inflammatory actions on their own.”
For their studies, the researchers began by growing functional human skeletal muscle in a Petri dish, to which they added immune cells and stem cell deposits.
When the muscles grew fully, the team “flooded” them with high levels of gamma interferon for seven days to mimic the effects of long-lasting chronic inflammation.
As expected, the muscles in the lab shrank and lost much of their strength.
They then repeated the experiment, but this time they put the muscles into a simulated exercise regimen using electric shocks.
The researchers found that the regimen “almost completely” prevented the effects of chronic inflammation by blocking a specific molecular pathway.
“We know that chronic inflammatory diseases induce muscle atrophy, but we wanted to see if the same would happen to our human muscles created on a Petri dish,” said the author of the paper and biomedical engineer Zhaowei Chen.
“Not only did we confirm that gamma interferon works primarily through a specific signaling pathway,” he continued.
“We have shown that exercise in muscle cells can directly counteract this proinflammatory signaling regardless of the presence of other cell types or tissues.”
The researchers found that exercise had the same anti-inflammatory effect as tofacitinib and baricitinib, two drugs commonly used to treat arthritis.
“When they exercised, the muscle cells themselves were directly opposed to the proinflammatory signal induced by gamma interferon, which we did not expect to happen,” Professor Bursac said.
These results show the value that laboratory-grown human muscles can have in discovering new disease mechanisms and potential treatments.
“There are notions that optimal levels and regimens of exercise could fight chronic inflammation without stressing cells.”
“Perhaps with our muscle designed, we can help find out if these notions are true.”
The full findings of the study were published in the journal Science Advances.