Lab-grown human muscle shows that exercising can ‘almost completely’ prevent chronic inflammation which causes tissue to waste away
- Inflammation stems from the over-reaction of the body’s immune system
- Chronic inflammation can cause muscle tissue to waste and lose its structure
- Experts believe a molecule called ‘interferon gamma’ is behind this wastage
- Yet it was unclear how this worked and why exercise appeared to mitigate it
- To investigate more simply, US researchers grew their own muscles in the lab
- This allowed them to zero in on the cells to focus on the relevant processes
Exercise can ‘almost completely’ prevent chronic inflammation that causes muscle to waste away, a study in lab-grown human tissue has revealed.
Inflammation occurs when our body’s immune system responds to bacteria or tissue damage — but it can sometimes 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 ‘interferon gamma’ is one of the culprits behind various types of muscle wasting and dysfunction.
Past studies indicated that exercise can mitigate the effects of inflammation in general — but it has been unclear what role muscle cells and interferon gamma play.
To find out, researchers from Duke University in the US developed a platform to allow them to grow their own human muscles in the laboratory.
Exercise can ‘almost completely’ prevent chronic inflammation that causes muscle to waste away, a study in lab-grown human tissue has revealed. Pictured: long, thin, well-defined muscle fibres (top left) lose their structure after prolonged inflammation (top right) but not when subjected to exercise as well (bottom left). The same applies for strength (bottom right)
‘Lots of processes are taking place throughout the human body during exercise, and it is difficult to tease apart which systems and cells are doing what inside an active person,’ said paper author and biological engineer Nenad Bursac.
‘Our engineered muscle platform is modular, meaning we can mix and match various types of cells and tissue components if we want to.’
‘But in this case, we discovered that the muscle cells were capable of taking anti-inflammatory actions all on their own.’
For their studies, the researchers began by growing functional skeletal human muscle in a Petri dish — to which they then added immune cells and reservoirs of stem cells.
When the muscles were fully grown, the team ‘inundated’ them with high levels of interferon gamma for seven days in order to mimic the effects of a long-lasting chronic inflammation.
As expected, the lab grown muscles got smaller and lost much of their strength.
They then repeated the experiment, but this time put the muscles through a simulated exercise regime using electric shocks.
The regime ‘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 thing would happen to our engineered human muscles grown in a Petri dish,’ said paper author and biomedical engineer Zhaowei Chen.
‘Not only did we confirm that interferon gamma primarily works through a specific signalling pathway,’ he continued.
‘We showed that exercising muscle cells can directly counter this pro-inflammatory signalling independent of the presence of other cell types or tissues.’
Exercising had the same anti-inflammatory effect as tofacitinib and baricitinib, two drugs commonly used to treat arthritis, the researchers found.
‘When exercising, the muscle cells themselves were directly opposing the pro-inflammatory signal induced by interferon gamma, which we did not expect to happen,’ said Professor Bursac.
‘These results show just how valuable lab-grown human muscles might be in discovering new mechanisms of disease and potential treatments.
‘There are notions out there that optimal levels and regimes of exercise could fight chronic inflammation while not over stressing the cells.’
‘Maybe with our engineered muscle, we can help find out if such notions are true.’
The full findings of the study were published in the journal Science Advances.