Exercise-induced changes in inflammatory processes: Implications for thrombogenesis in cardiovascular disease

Sedentary lifestyle is a risk factor and a strong predictor for chronic disease and premature death. Low-grade inflammation has been proved a key player in the pathogenesis of cardiovascular disease. Inflammatory processes have been also involved in maintaining the balance between coagulation and fibrinolysis. In addition, an inverse linear dose-response relation between physical activity and mortality risks has also been reported. However, the favorable effects of structured exercise programs and the independent contribution of physical activity to cardiovascular risk are still under investigation. In response to heavy exercise, interleukin-6 (IL-6) is secreted by contracting skeletal muscles, followed by an acute reactant release of C-reactive protein (CRP). Both CRP and IL-6 can stimulate monocyte tissue factor production, provoke platelet hyperreactivity, promote fibrinogen biosynthesis, and enhance microparticle formation and erythrocyte aggregability, thus triggering prothrombotic state. By contrast, regular exercise and physical activity are protective against all-cause mortality through suppressing pro-inflammatory cytokine production, enhancing anti-inflammatory mediators and antioxidant development, and promoting fibrinolytic activity. Low-load resistance exercise also plays an advantageous role in thrombogenesis by reducing inflammatory processes and potentiating fibrinolytic features. In the present review article, we provide an overview of the impact of different modes and intensities of physical activity on vascular inflammation and thrombogenesis.