Physical activity protects us from heart attacks and strokes. It reduces the risk of diabetes. It keeps neurodegenerative diseases such as Alzheimer’s at bay. It lowers the risk of developing cancer. How does it manage this? Science has long been asking itself, and a new study from Harvard Medical School has recently added an important clue, revealing a molecular mechanism through which physical activity helps counteract inflammation by modulating the activity of some essential components of our immune system.
Muscles inflamed by exertion
The research, published in Science Immunology, was carried out on mice and analyzed the metabolic processes that take place in the muscles following a session of running on a treadmill, both in trained animals and in “sedentary” animals subjected to a one-off exercise session. By comparing the data collected with those of animals that did not use the treadmill, the researchers were able to better understand the effects of physical exertion and exercise on inflammation, on the molecular mechanisms that induce it, and on those that, conversely, counteract its effects.
First of all — something long known — the experiments showed that following physical exertion the muscles produce an inflammatory response, linked to the microscopic damage that muscle tissues suffer during vigorous use. The analyses revealed an increase in the activity of genes involved in regulating various metabolic processes, and a greater presence of molecules, such as interferon, that promote inflammation.
At the same time, after physical activity, a greater presence of regulatory T cells was observed in the mice’s muscles: a type of immune system cell that plays, among other things, an important role in keeping inflammatory responses under control. In trained mice, however, these immune cells seem to do even more: unlike what happened in sedentary animals, in fact, the presence of regulatory T cells in trained animals did not merely counteract inflammation, but was also linked to an improvement in muscle metabolism and performance.
After physical activity, a greater presence of regulatory T cells was observed in the mice’s muscles: a type of immune system cell that plays an important role in keeping inflammatory responses under control.
Counteracting the effects of interferon
To take their investigation further, the study’s authors then turned to mice lacking regulatory T cells. The tissues of these animals reacted worse to physical exertion, showing greater signs of inflammation and metabolic abnormalities with damage to the mitochondria (the organelles that supply energy to cells). The animals lacking regulatory T cells also proved unable to benefit from regular training as normal animals did, showing a lower aerobic capacity and, in general, fewer positive effects from physical activity.
All these negative effects linked to the lack of regulatory T cells, however, disappeared when the researchers neutralized the interferon present in their muscle tissues. “The enemy in this case is interferon,” Langston stresses. “In the absence of the regulatory T cells that combat its effects, interferon was in fact shown to cause uncontrolled damage.”
The increase in regulatory T cell activity produced by physical activity seems to counteract the effects of inflammation not only in the muscles, but more generally wherever chronic inflammatory processes are present in the body.
According to the study’s authors, the results could indicate that the increase in regulatory T cell activity produced by physical activity helps counteract the effects of inflammation not only in the muscles, but more generally wherever chronic inflammatory processes are present in the body. If so, this boost to immune system activity could explain why physical activity is so beneficial in counteracting the onset of chronic diseases such as diabetes and cardiovascular disorders. To be sure, however, further research will be needed to analyze the phenomenon outside muscle tissues and confirm these results in humans as well.
