Scientists at the National Cancer Research Centre (CNIO) have discovered, in groundbreaking new research, that a “switch” in our muscles turns up one’s desire to exercise. In work led by Guadalupe Sabio, they have found how proteins activated during physical activity can significantly stimulate our wish to go on working out. The work, published in Science Advances, could eventually lead to new treatments for obesity and other metabolic disorders.
“It’s discovered that muscles themselves can control our interest in exercise, through a signaling pathway between muscles and the brain,” said the lead investigator of CNIO’s group on the interaction of organs in metabolic diseases Sabio. He suspects this pathway “might be one of probably many” that make us feel the urge to exercise more as we go along.
Experiments revealed that the exercise-induced proteins act to control one another, thus preventing the imperative to exercise from leading to bad outcomes. Studies included animal models and human volunteers: from healthy subjects who were exposed to controlled exercise to patients with obesity. These experimental findings implicate that the proclaimed pathway is centrally involved in the exercise control of both mice and human subjects.
Leticia Herrera and Cintia Folgueira of the National Center for Cardiovascular Research (CNIC) found that if muscle contraction in the body is repetitive and intense during exercise, then two proteins named p38α and p38γ are activated, which act as sensors for the exercise load. How much such proteins get activated determines our will to perform physical activity.
Yet another important player in this concert is Interleukin 15. If p38γ is activated in some way while exercising, then the synthesis of the intermediary protein interleukin 15 takes place. This immuno-modulator acts on the cortex of the brain responsible for movement and induces the owner of that brain to increase physical activity. The induction of high levels of IL-15 in the blood led to increased voluntary activity in animal experiments.
Their findings also indicated that normal exercise activates the p38γ significantly more than p38α, which could contribute toward explaining why training results in continued exercise. Humans activated both p38 proteins within the exercise muscles and increased the related IL-15 in the blood. However, it was noticed that obese subjects had much lower IL-15, an important clue to how regular exercise so effectively both prevent and treat obesity.
“Going forward, Sabio and her team will seek to understand how IL-15 functions as a biomarker, to measure the response of an individual’s urge to exercise. This means it holds the promise of formulating better exercise plans by coaches and trainers. Perhaps further in the future, we’d be able to gain an IL-15-based drug for the many struggling to be active out there, like, for instance, people with obesity.”.
Sabio also plans to use this research model to delve into understanding exercise not only with longevity and cancer but also the discoveries that would guide this aid.
This newly discovered mechanism will provide guidance not only to the biological mechanisms responsible for our need to exercise but also open to the development of new therapeutic interventions aimed to combat obesity and alleviate overall health.