Your exercising muscle can combat chronic inflammation on its own

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In a new study, researchers found that human muscle has an innate ability to ward off the damaging effects of chronic inflammation when exercised.

The discovery was made possible through the use of lab-grown, engineered human muscle.

The research was conducted by a team at Duke University.

Inflammation is not inherently good or bad. When the body is injured, an initial low-level inflammation response clears away debris and helps tissue rebuild.

Other times, the immune system overreacts and creates an inflammatory response that causes damage, like the often deadly cytokine storms brought on by some cases of COVID-19.

And then, there are diseases that lead to chronic inflammation, such as rheumatoid arthritis and sarcopenia, which can cause the muscle to waste away and weaken its ability to contract.

Among many molecules that can cause inflammation, one pro-inflammatory molecule, in particular, interferon-gamma, has been linked to various types of muscle wasting and dysfunction.

While previous research has shown that exercise can help mitigate the effects of inflammation in general, it has been difficult to distinguish what role the muscle cells themselves might play.

To prove that muscle alone is capable of blocking chronic inflammation, the team turned to an engineered muscle platform that the laboratory has been developing for nearly a decade.

They looked at fully functional, lab-grown muscles and inundated them with relatively high levels of interferon-gamma for seven days to mimic the effects of a long-lasting chronic inflammation.

As expected, the muscle got smaller and lost much of its strength.

The researchers then applied interferon-gamma again, but this time also put the muscle through a simulated exercise regime by stimulating it with a pair of electrodes.

They were surprised to discover that it almost completely prevented the effects of chronic inflammation.

They then showed that simulated exercise inhibited a specific molecular pathway in muscle cells, and that two drugs used to treat rheumatoid arthritis, tofacitinib and baricitinib, which block the same pathway, had the same anti-inflammatory effect.

The team says when exercising, the muscle cells themselves were directly opposing the pro-inflammatory signal.

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

One author of the study is Nenad Bursac, a professor of biomedical engineering at Duke.

The study is published in Science Advances.

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