Here’s Why This is the Best Way ‘to Boost the Body’s Immune Responses’ Against Inflammation, According to a New Study
The fascination of researchers with the link between exercise and inflammation dates back to the early 20th century when a study on Boston marathon runners revealed an increase in white blood cells in their blood after the race.
A recent study conducted by Harvard Medical School and published in Science Immunology sheds light on the molecular basis of this century-old observation.
This study, conducted on mice, proposes a potential molecular explanation for the positive effects of exercise, indicating that the immune system, particularly inflammation-countering T cells (Tregs), plays a role.
It demonstrates that muscle inflammation resulting from physical exertion triggers the activation of Tregs, enhancing the muscles’ capacity to utilize energy as fuel and improving overall exercise endurance.
Tregs, traditionally associated with countering abnormal inflammation in autoimmune diseases, now emerge as critical players in the body’s immune responses during exercise, as highlighted by the research team.
Diane Mathis, the senior investigator of the study and the Morton Grove-Rasmussen Professor of Immunology at the Blavatnik Institute at HMS, emphasized the broader impact of the immune system on tissue health, extending beyond pathogen defense and cancer control.
Mathis stated, “Our study demonstrates that the immune system exerts powerful effects inside the muscle during exercise.”
While the study was conducted in mice and further research is needed to validate these findings in humans, it represents a significant step toward understanding the cellular and molecular changes that occur during exercise and contribute to its health benefits.
Exercise has long been known to protect against cardiovascular disease, reduce the risk of diabetes, and shield against dementia. However, the precise mechanisms by which exercise promotes health have puzzled researchers for a considerable time.
This new research comes at a time when there is a growing focus on unraveling the molecular foundations of exercise. Understanding the role of the immune system in this process is just one facet of these research efforts.
The study’s first author, Kent Langston, a postdoctoral researcher in the Mathis lab, highlighted the persistent mystery surrounding the immune processes triggered by physical exertion and how this research provides detailed insights into the actions of T cells within the muscle during exercise.
Previous research in exercise physiology mainly focused on the impact of hormones released during exercise and their effects on various organs such as the heart and lungs. In contrast, this study delves into the immunological reactions that take place within the muscles during exertion.
Exercise is recognized to induce temporary muscle damage, initiating a series of inflammatory responses. It upregulates genes that regulate muscle structure, metabolism, and the function of mitochondria, the cellular powerhouses responsible for energy production. Mitochondria are essential for adapting to the increased energy demands of exercise.
The study examined muscle cells from mice that engaged in single or regular treadmill running and compared them to sedentary mice. Both groups of exercising mice exhibited signs of inflammation, with increased activity in genes regulating various metabolic processes and higher levels of inflammation-promoting chemicals, including interferon. Tregs were elevated in both groups, and they mitigated exercise-induced inflammation, while sedentary mice displayed none of these changes.
The benefits in terms of metabolism and performance were evident only in the regularly exercising mice. Tregs not only suppressed exertion-induced inflammation and muscle damage but also influenced muscle metabolism and performance. This finding aligns with the well-established observation that single bouts of exercise do not lead to significant performance improvements, emphasizing the importance of regular physical activity over time.
Additional analyses confirmed that Tregs were the key drivers of the broader benefits observed in regularly exercising mice. Mice without Tregs displayed uncontrolled muscle inflammation, swollen mitochondria indicating metabolic issues, and failed to adapt to increasing exercise demands over time. They did not experience the same systemic benefits of exercise and exhibited reduced aerobic fitness.
The study also revealed that interferon, a known inflammation promoter, acted directly on muscle fibers to alter mitochondrial function and limit energy production in the absence of Tregs. Blocking interferon prevented metabolic abnormalities and improved aerobic fitness in mice lacking Tregs.
The study’s findings emphasize the role of interferon in promoting chronic inflammation, which underlies many chronic diseases and age-related conditions. This opens possibilities for therapeutic interventions targeting interferon to reduce inflammation. Tregs, on the other hand, have garnered attention in both scientific and industrial circles as potential treatments for immune-mediated conditions characterized by abnormal inflammation.
The research provides insights into the cellular processes responsible for exercise’s anti-inflammatory effects and underscores the importance of harnessing the body’s immune defenses. While specific interventions targeting Tregs in the context of immune-related diseases require careful consideration, exercise represents a natural means of enhancing the body’s immune responses to combat inflammation.
Diane Mathis concluded by suggesting that exercise may boost Treg activity not only in the muscle but also elsewhere in the body, potentially offering ” a natural way to boost the body’s immune responses to reduce inflammation.”
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