(Thrombogenic Responses to Exercise Modalities: A Strategy for Managing the Atherothrombotic (A Systematic Review

The dysregulation of the dynamic interplay between blood coagulation and fibrinolysis systems is a critical axis in the pathophysiology of atherothrombotic events. This systematic review aims to elucidate the cellular, molecular, and hemodynamic mechanisms governing the regulation of the thrombogenic profile in response to various exercise modalities, specifically identifying the thresholds that either stabilize or trigger thrombosis. By analyzing the reciprocal effects of diverse training modalities on key procoagulant and fibrinolytic markers, this study explores the biological mechanisms ranging from gene expression to systemic vascular hemodynamic changes. Findings indicate that chronic training, particularly combined modalities, promotes the stabilization of the thrombogenic response by reducing fibrinolysis inhibitors and enhancing clot dissolution capacity through the optimization of endothelial function. Conversely, acute exercise, especially at maximal intensities, is characterized by a "vascular danger window"—a transient prothrombotic state that increases thrombotic risk. However, the lack of homogeneity in research protocols and the neglect of the "fibrinolysis paradox" at high intensities have hindered a precise interpretation of these effects. Based on the theory of "Hemostatic Engineering," vascular stability is a function of a personalized dose-response pattern that respects critical intensity thresholds. Consequently, a transition from generalized exercise prescriptions toward "Precision Sports Medicine" is imperative to optimize the thrombogenic response and ensure hemodynamic safety in both clinical and athletic populations.

کلیدواژه ها:

Thrombosis ، Fibrinolysis ، Blood Coagulation ، Exercise ، Vascular Endothelium ، Atherothrombosis