Journal of Exercise & Organ Cross Talk

Abstract Metabolic syndrome (MetS) elevates thrombotic risk through dysregulated coagulation factors, including plasminogen activator inhibitor-1 (PAI-1) and fibrinogen, driven by visceral adiposity and metabolic dysfunction. High-intensity interval training (HIIT) improves cardiometabolic health, but its effects on hemostatic markers in MetS remain underexplored. Twenty-four men with MetS (ATP-III criteria; age 44.4 ± 5.4 years, BMI 31.7 ± 2.3 kg·m⁻²) were randomized to HIIT (n=12) or control (n=12). HIIT comprised 3 sessions/week for 8 weeks (4 × 4-min intervals at 90% HRmax, interspersed with 3-min active recovery at 70% HRmax). Fasting plasma PAI-1, fibrinogen, insulin resistance (HOMA-IR), body composition, and lipid profiles were assessed pre/post-intervention. HIIT significantly reduced PAI-1 (−30.7%, p<0.001) and fibrinogen (−21.8%, p<0.001) versus controls. Concurrent improvements occurred in HOMA-IR (−20.6%, p<0.001), body fat (−3.8%, p<0.05), systolic/diastolic BP (−7.5%/−5.2%, p<0.05), LDL-c (−5.6%), triglycerides (−9.4%), and HDL-c (+3.0%; all p<0.05). Control group exhibited no significant changes. HIIT attenuates prothrombotic risk in MetS, evidenced by reductions in PAI-1 and fibrinogen. These hemostatic improvements are mechanistically linked to ameliorated metabolic dysfunction, highlighting HIIT’s role in modulating adipose tissue–vascular cross talk.

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.