The consequential positive energy balance of modern lifestyles, frequently characterized by physical inactivity and unhealthy diet intake, is a major cause for insulin resistance and the metabolic syndrome. The liver, as a key metabolic tissue, develops obesity-related complications. Nonalcoholic fatty liver disease (NAFLD) is associated with increased incidence of cerebrovascular and cardiovascular accidents. The aim of the present work was to investigate the effects of swimming exercise on the prothrombotic factors and fibrinolytic activity of the blood in a rat model of NAFLD. Forty rats were randomly divided into four groups (n=10 for each). Group 1 rats, fed with standard laboratory chow for 15 weeks, were used as control (Con). Group 2 rats (Con+Ex) were fed a standard laboratory chow for 15 weeks and obliged to swimming exercise from the 11th week to the 15th week. Group 2 rats fed a high-cholesterol diet with 10% fructose solution (HCFD) for 15 weeks. Rats in group 4 (HCFD+Ex), fed with high-cholesterol diet with 10% fructose solution (HCFD) for 15 weeks and obliged to swimming exercise from the 11th week to the 15th week. At the end of experiments, after 15 weeks, blood samples were humanely taken in a single sampling episode by cardiac puncture under terminal ether anaesthesia. Serum glucose, insulin, lipogram, plasminogen activator inhibitor-1 (PAI-1), fibrinogen, von Willibrand factor (vW factor), Fibrin degration products (FDPs), endothelin-1 (ET-1), intercellular adhesion molecule (ICAM), and vascular cell adhesion molecule (VCAM) were assayed. Platelet count, bleeding time, clotting time, prothrombin time (PT), activated partial thromboplastin time (aPTT) and adenosine diphosphate (ADP) platelet aggregation were measured. Data are expressed as mean±S.D. and significance (P<0.05) tested with ANOVA. HCFD fed rats showed a significant increase in systolic blood pressure from 122±5 to 144±8 mmHg, with increased body weight by 21% compared to control rats. They had significantly higher plasma glucose, insulin, lipid profile and HOMA-IR. PAI-1 increased significantly from 36.33±3.52 to 57.04±5.75 ng.ml-1 and fibrinogen from 188.34±12.51 to 350.38±26.92 mg.dl-1. HCFD rats had also higher FDPs, vW factor, ET-1, ICAM, VCAM, and platelet aggregation, with shorter bleeding time by 25%, clotting time by 27%, PT by 29% and aPTT by 35% versus control rats. In contrast, swimming exercise significantly decreased the gained body weight by 15%, glucose by 30%, insulin by 35%, and lipid profile compared to HCFD group. In response to exercise PAI-1 decreased to 42.14±4.26 ng.ml-1. Fibrinogen, FDPs, vW factor, ET-1, ICAM, VCAM, platelet aggregation decreased to normal values with normalization of bleeding time, clotting time, PT and aPTT. It could, therefore, be concluded that NAFLD increases the prothrombotic markers and platelets adhesion and aggregation. Swimming ameliorates the hypercoagulable hypofibrinolytic state induced by HCFD in a rat model of NAFLD.