Athletic exertion triggers a beneficial inflammatory response
Last reviewed: 07.06.2024
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The immune system improves the adaptation of those muscle groups that are regularly exposed to vigorous exercise.
The inflammatory response is an ambiguous and interesting process. It is the immune system's first response to infection and tissue damage, which can be acute or chronic, go unnoticed, or be complicated by a variety of pathologies, from diabetes to oncology. Researchers at Harvard University and the Dana-Farber Cancer Institute say that the inflammatory process can also be beneficial - for example, if it is associated with regular athletic muscular exercise.
The term "sports muscle inflammation" has been around in medicine for many years. It refers to a reaction caused by minor damage to muscle fibers by physical activity. These micro-damages activate the immune system's inflammatory response, which consists of clearing tissues and stimulating their repair. Regulatory T-lymphocytes participate in the inflammation, restraining the immune response, which significantly reduces the danger of this process for the whole body.
Scientists set up an experiment on rodents. One group of rodents led a passive lifestyle, another group was subjected to regular exercise on a treadmill, and the third group exercised on the wheel, but not regularly. It was found that in the "athlete" mice, regardless of the regularity of exercise, many pro-inflammatory particles and regulatory T lymphocytes appeared in the limb muscles. However, in rodents that exercised regularly, T-lymphocytes not only inhibited the inflammatory response, but also influenced metabolic processes in the musculature, which ultimately led to an increase in their adaptation. Thus, repeated physical activity decreased the likelihood of new inflammatory processes as systematic training strengthened muscle structures.
When attempting to eliminate regulatory T-lymphocytes, the inflammatory response was not only aggravated: the benefit of regular training was completely leveled, endurance did not increase, and there was no adaptation of metabolic processes. In muscles without T-lymphocytes, γ-interferon, one of the mediators of general inflammation, was significantly increased. In this situation, interferon had a negative effect on muscle fibers, disrupted the functioning of mitochondrial energy organelles. Muscle fibers under conditions of increasing energy deficit lost the ability to adapt to overload.
Based on all of the above, we can conclude that sports training strengthens the body, triggers anti-inflammatory reactions that improve muscle adaptation to high loads. Knowing this, it is possible to trace how physical activity can help prevent the development of diabetes, atherosclerosis, etc.
The full article can be accessed at SCIENSE.ORG