Exercise training and muscle–lung crosstalk: The emerging roles of Irisin and Semaphorin-3A in pulmonary diseases. A narrative review

Document Type : Review Articles


1 Chemical Injuries Research Center, Baqiyatallah University of Medical Sciences, Tehran, Iran.

2 Exercise Physiology Research Center, Life Style Institute, Baqiyatallah University of Medical Sciences, Tehran, Iran

3 Department of Physical Education and Sport Sciences, West Tehran Branch, Islamic Azad University, Tehran, Iran


COPD is an inflammatory disorder caused by prolonged inhalation of harmful substances such as cigarette smoke that leads to an irreversible respiratory disorder. Airway obstruction usually has a progressive period characterized by chronic cough, sputum production, and dyspnea, resulting in decreased physical activity. Two hypotheses have been proposed for the pathogenesis of lung diseases, especially COPD, including the oxidant-antioxidant imbalance hypothesis and the protease-antioxidant imbalance hypothesis. Oxidants can cause irreversible damage to lung cells. Oxidants activate inflammatory gene expression primarily through NFκB signaling. Increase inflammation promotes apoptosis in the epithelial cells, endothelial cells, and airways, that resulting Emphysema. This pathological period causes progress the disease. Recently, has been shown that decreased physical activity is associated with COPD injuries, and the level of physical activity is most associated with COPD mortality. Therefore, the tendency to maintain and improve the physical activity of pulmonary patients, especially COPD was increased. In lung diseases, muscle mass usually decreases and severe atrophy occurs. Most studies suggest increased mobility and exercise to enhance cardiorespiratory endurance and decrease atrophy. However, the exact biological mechanism for the recovery of patients with COPD after a physical activity has not been explained. Exercise can produce Irisin and Semaphorin-3A by stimulating muscle and nerve cell, which have positive effects on other tissues, including the lungs. Limited studies have examined the role of these factors in lung tissue. Therefore, in this mini-review, the lung muscle cross-talk is examined by evaluating the role of Irisin and Semaphorin-3A.

What is already known on this subject?

Previous studies have only examined the positive effects of increasing serum levels of Irisin on the lung parenchyma and reducing COPD-induced emphysema.


What this study adds?

The present study showed that in addition to Irisin, semaphorin-3A induced by muscle contraction, prevents inflammation and lung damage caused by COPD or other lung disease.


Main Subjects

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