Health: Laboratory-grown human muscles show that exercise can prevent chronic inflammation

Laboratory-grown human muscle shows exercise can ‘almost completely’ prevent chronic inflammation that causes tissue to wither

  • Inflammation stems from the overreaction of the body’s immune system
  • Chronic inflammation can cause muscle tissue to waste and lose its structure
  • Experts believe that a molecule called ‘interferon gamma’ is behind this waste
  • Still, it was unclear how this worked and why exercise seemed to mitigate it
  • To make the research easier, American researchers grew their own muscles in the lab
  • This allowed them to focus on the cells to focus on the relevant processes

Exercise can “almost completely” prevent chronic inflammation that causes muscles to wither away, according to a study in laboratory-grown human tissue.

Inflammation occurs when our body’s immune system reacts to bacteria or tissue damage, but it can sometimes overreact and eventually attack its own cells.

And some illnesses – such as arthritis and sarcopenia – can lead to long-lasting, “chronic inflammation,” which causes muscle loss.

A molecule known as ‘interferon gamma’ is believed to be one of the culprits behind various types of muscle wasting and dysfunction.

Previous studies indicated that exercise can mitigate the effects of inflammation in general, but it was unclear what role muscle cells and interferon gamma play.

To find out, researchers at Duke University in the US developed a platform that allowed them to grow their own human muscles in the lab.

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Exercise can “almost completely” prevent chronic inflammation that causes muscles to wither, according to a study in laboratory-grown human tissue.  Pictured: Long, thin, well-defined muscle fibers (top left) lose their structure after prolonged inflammation (top right) but not during exercise (bottom left).  The same goes for strength (bottom right)

Exercise can ‘almost completely’ prevent chronic inflammation that causes muscles to wither, according to a study in laboratory-grown human tissue. Pictured: Long, thin, well-defined muscle fibers (top left) lose their structure after prolonged inflammation (top right) but not during exercise (bottom left). The same goes for strength (bottom right)

“Many processes take place throughout the human body during exercise, and it is difficult to tell apart which systems and cells are doing what in an active person,” said paper author and biological engineer Nenad Bursac.

“Our developed muscle platform is modular, which means that we can mix and match different types of cells and tissue components if we want to.”

“But in this case we discovered that the muscle cells could take anti-inflammatory actions on their own.”

For their studies, the researchers started by growing functional human skeletal muscle in a petri dish, to which they then added immune cells and reservoirs of stem cells.

When the muscles matured, the team “ flooded ” them with high levels of interferon-gamma for seven days to mimic the effects of long-term chronic inflammation.

As expected, the muscles grown in the lab got smaller and lost much of their strength.

They repeated the experiment, but this time the muscles underwent a simulated exercise regimen using electric shocks.

The regimen ‘almost completely’ prevented the effects of chronic inflammation by blocking a specific molecular pathway, the researchers found.

“We know that chronic inflammatory diseases cause muscle atrophy, but we wanted to see if the same thing would happen to our engineered human muscles grown in a petri dish,” said paper author and biomedical engineer Zhaowei Chen.

“We have not only confirmed that interferon-gamma works primarily through a specific signaling pathway,” he continued.

“We have shown that training muscle cells can directly counteract this pro-inflammatory signaling, independent of the presence of other cell types or tissues.”

Exercise had 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 were directly against the pro-inflammatory signal from interferon-gamma, which we did not expect,” said Professor Bursac.

These results show just how valuable laboratory-grown human muscles can be in discovering new disease mechanisms and potential treatments.

“There are ideas that optimal levels and exercise regimens can fight chronic inflammation without putting too much stress on the cells.”

“Maybe we can use our developed muscle to help find out if such concepts are true.”

The full findings of the study are published in the journal Science Advances.

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