Journal of Exercise & Organ Cross Talk

Abstract Intense exercise training is associated with Lung inflammation. Fasl protein on the cell surface is responsible for the initiation of the inflammatory response that finally leads to cell death at the site of inflammation, and can be interpreted as Fasl induced apoptosis. Therefore, the aim of this study was to investigate the effects of increasing and intense interval exercise training on Fasl levels of mature rat lungs. 30 rats within three weeks of birth with mean weight 68±9 g were randomly divided into three basic, control, and exercise groups. Increasing interval training for 6 sessions per week, each session 30 minutes at a speed of 15 to 70 meters per min was employed and Fasl levels were measured using the kitby Elisa method. The data were analyzed with two-way ANOVA and LSD test was done at p≤0.05 significant level. The results showed that Fasl protein levels in the interval training group compared to baseline group increased by 23.75 % and was significant (p≤0/05). However, although the amount of this protein in the interval training group compared to the control group was high, this value was not significant. In addition, Fasl protein levels in the control group compared to the baseline group increased by13.58 % and was significant (p≤0.05). The findings indicated that intense and prolonged exercise training causes damage of the respiratory tract, and in turn, leads to the increased levels of Fasl.

Abstract 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.