Research revealed that the immune system fights inflammation and improves endurance during exercise. Since an early 20th-century study revealed a surge in white cells in the blood of Boston marathon participants following the race, researchers have been fascinated by the link between exercise and inflammation.
A new Harvard Medical School study published on November 3 in Science Immunology may provide a biological explanation for this century-old observation.
The study in mice implies that the immune system may play a role in the positive effects of exercise. It demonstrates that exertion-induced muscle inflammation mobilizes inflammation-fighting T cells, or Tregs, which improves the muscles’ ability to use energy as fuel and total exercise endurance.
Long known for their function in combating the abnormal inflammation associated with autoimmune illnesses, Tregs are now emerging as essential participants in the body’s immunological responses during exercise, according to the research team.
“The immune system, and particularly the T cell arm, has a broad impact on tissue health that extends beyond pathogen protection and cancer control.” “Our findings show that the immune system has powerful effects inside the muscle during exercise,” said research senior investigator Diane Mathis, Morton Grove-Rasmussen Professor of Immunology at HMS.
Mice are not humans, and the findings must be repeated in future studies, according to the researchers. The study, however, is an essential step toward elucidating the cellular and molecular changes that occur during exercise and offer health advantages.
Understanding the molecular basis of exercise
Protecting against cardiovascular disease, lowering the risk of diabetes, and protecting against dementia. Exercise has been shown to have numerous health benefits. But how precisely can exercise make us healthier? For a long time, researchers have been intrigued by the question.
The new findings come as researchers work harder to grasp the molecular basis of exercise. Untangling the immune system’s role in this process is only one component of these endeavors.
“We’ve known for a long time that physical exertion causes inflammation, but we don’t fully understand the immune processes involved,” said Kent Langston, a postdoctoral researcher in the Mathis lab and study first author. “Our study shows, at very high resolution, what T cells do at the site where exercise occurs, in the muscle.”
The majority of past exercise physiology research has been on the role of numerous hormones released during exercise and their impact on various organs such as the heart and lungs. The new research deciphers the immunological cascade that occurs within the actual site of exercise – the muscle.
T cells are both heroes and devils in the fight against inflammation
Exercise is known to induce transient muscle injury, triggering a chain reaction of inflammatory reactions. It increases the expression of genes that regulate muscle shape, metabolism, and mitochondrial activity, the small powerhouses that fuel cell function. Mitochondria play an important part in exercise adaptation by assisting cells in meeting the increased energy demand of exercise.
The team examined what happens in cells collected from the hind-leg muscles of mice that ran on a treadmill once versus animals that ran on a regular basis in the new study. The researchers then compared them to muscle cells from sedentary mice.
Muscle cells from mice that ran on treadmills, whether once or repeatedly, displayed conventional markers of inflammation, including increased activity in genes that govern several metabolic processes and higher amounts of substances that promote inflammation, such as interferon.
Treg cells were seen in abundance in both groups’ muscles. Further research revealed that Tregs reduced exercise-induced inflammation in both groups. Sedentary mice’s muscle cells showed none of these alterations.
However, the metabolic and performance benefits of exercise were only shown in frequent exercisers – mice who ran on a daily basis. The trials revealed that Tregs not only suppressed exertion-induced inflammation and muscle injury, but also affected muscle metabolism and performance. This discovery is consistent with human observations that a single bout of exercise does not result in significant gains in performance and that regular action over time is required to reap advantages.
Further research demonstrated that Tregs were really to blame for the larger benefits observed in frequent exercisers. Animals lacking Tregs experienced uncontrolled muscle inflammation, as seen by the rapid buildup of inflammation-promoting cells in their hindleg muscles. Their muscle cells also had unusually enlarged mitochondria, indicating a metabolic problem.
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