Exercise as an anti-inflammatory therapy for rheumatic diseases—myokine regulation

Abstract

Persistent systemic inflammation, a typical feature of inflammatory rheumatic diseases, is associated with a high cardiovascular risk and predisposes to metabolic disorders and muscle wasting. These disorders can lead to disability and decreased physical activity, exacerbating inflammation and the development of a network of chronic diseases, thus establishing a 'vicious cycle' of chronic inflammation. During the past two decades, advances in research have shed light on the role of exercise as a therapy for rheumatic diseases. One of the most important of these advances is the discovery that skeletal muscle communicates with other organs by secreting proteins called myokines. Some myokines are thought to induce anti-inflammatory responses with each bout of exercise and mediate long-term exercise-induced improvements in cardiovascular risk factors, having an indirect anti-inflammatory effect. Therefore, contrary to fears that physical activity might aggravate inflammatory pathways, exercise is now believed to be a potential treatment for patients with rheumatic diseases. In this Review, we discuss how exercise disrupts the vicious cycle of chronic inflammation directly, after each bout of exercise, and indirectly, by improving comorbidities and cardiovascular risk factors. We also discuss the mechanisms by which some myokines have anti-inflammatory functions in inflammatory rheumatic diseases.

Physical Activity and Serum Cytokines Levels in Depressed Individuals - Gender Differences

“…On the other hand, there is a constant decrease in this cytokine concentration during the period of recovery from the exercise. These alterations provoked by physical exercise may justify our results [34,36,37]. Similar results have been found by other authors [11,38], who did not find a significant association between serum IL-6 levels and the practice of physical activity.…”

Exercise-Dependent Regulation of NK Cells in Cancer Protection

“…A large number of these myokines are cytokines, and their release during exercise is believed to direct energy substrate fluxes to working muscles, coordinating the adaptive metabolic response in muscle following exercise cessation [44]. Yet, several of the proposed exercise-induced myokines, are primarily recognized for their role in controlling immune cells, including IL-15, IL-7, and IL-6 [45]. These immune cell-modulating cytokines provide a conceptual basis for understanding how contracting muscles communicate with circulating immune cells during exercise, establishing a muscle-toimmune cell crosstalk axis that links physical activity to immune cell regulation.…”

Juvenile idiopathic arthritis and physical activity: Possible inflammatory and immune modulation and tracks for interventions in young populations

“…The small changes of these pro-inflammatory cytokines could well be mediated by antiinflammatory cytokines such as IL-1ra, IL-6 and IL-10 and cytokine inhibitors (cortisol, prostaglandin E2 and soluble receptors against TNF and IL-2), which are known to increase markedly in the circulation following endurance exercise [69]. Indeed, in response to muscle contraction, the first cytokine secreted is IL-6, followed by anti-inflammatory cytokines such as IL-1ra, IL-10 and TNF receptor (TNF-R) [64,70,71] (Fig. 1).…”