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Human muscle grown in the lab shows exercise can ‘almost completely’ prevent chronic inflammation that leads to wasted tissue
- Inflammation is caused by the overreaction of the body’s immune system
- Chronic inflammation can lead to wasting muscle tissue and losing its structure
- Experts believe a molecule called ‘gamma interferon’ is the source of this waste
- Still, it was not clear how it worked and why exercise seemed to ease it.
- To investigate more simply, American researchers have developed their own muscles in the laboratory
- This allowed them to focus on the cells to focus on the relevant processes.
Exercise can “ almost completely ” prevent chronic inflammation that leads to muscle wasting, a study in human tissue grown in the lab has found.
Inflammation occurs when our body’s immune system reacts to bacteria or tissue damage, but sometimes it can overreact and end up attacking its own cells.
And some diseases, such as arthritis and sarcopenia, can lead to long-lasting “chronic inflammation”, which causes muscle wasting.
It is believed that a molecule known as “gamma interferon” is one of the culprits of various types of muscle wasting and dysfunction.
Previous studies have indicated that exercise may lessen the effects of inflammation in general – but it is not known what role muscle cells and gamma interferon play.
To find out, researchers at Duke University in the United States have developed a platform allowing them to develop their own human muscles in the laboratory.
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Exercise can “ almost completely ” prevent chronic inflammation that leads to muscle wasting, a study in human tissue grown in the lab has found. Pictured: Long, thin, well-defined muscle fibers (top left) lose their structure after prolonged inflammation (top right) but not when subjected to exercise as well (bottom left). The same goes for strength (bottom right)
“Many processes take place throughout the human body during exercise, and it is difficult to determine which systems and cells are doing what inside an active person,” said author and biological engineer Nenad Bursac.
“Our designed muscle platform is modular, which means we can mix and match different types of cells and tissue components if we want to.
“But in this case, we found that the muscle cells were able to take anti-inflammatory actions on their own.”
For their studies, the researchers started by growing functioning human skeletal muscle in a Petri dish – to which they then added immune cells and stem cell reservoirs.
Once the muscles were fully developed, 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 developed in the lab got smaller and lost much of their strength.
They then repeated the experiment, but this time subjected the muscles to a simulated exercise regimen using electric shocks.
The diet “ almost completely ” prevented the effects of chronic inflammation by blocking a specific molecular pathway, the researchers found.
“We know that chronic inflammatory diseases induce muscle atrophy, but we wanted to see if the same would happen to our artificial human muscles grown in a petri dish,” said author and biomedical engineer Zhaowei Chen.
“Not only have we confirmed that gamma interferon works primarily through a specific signaling pathway,” he continued.
“We have shown that exercise in muscle cells can directly counter this pro-inflammatory signaling regardless of the presence of other types of cells or tissues.
Exercise has the same anti-inflammatory effect as tofacitinib and baricitinib, two drugs commonly used to treat arthritis, the researchers found.
“During exercise, the muscle cells themselves directly opposed the pro-inflammatory signal induced by gamma interferon, which we did not expect,” said Professor Bursac.
“These results show just how valuable human muscles grown in the laboratory can be in discovering new disease mechanisms and potential treatments.
“There are notions that optimal exercise levels and regimens could fight chronic inflammation without putting too much stress on cells.
“Maybe with our artificial muscles we can help find out if such notions are true.
The full results of the study were published in the journal Science Advances.
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