Exercise-induced activation of coagulation in subjects with activated protein C resistance

In the healthy individual intensive physical exercise leads to a minor activation of blood coagulation that appears to be balanced by a concomitant activation of the fibrinolytic system. This study tested the hypothesis that vigorous exercise might give rise to an exaggerated activation of coagulation in subjects with resistance to activated protein C (APC). Molecular markers of thrombin (prothrombin fragment 1 + 2, thrombin–antithrombin III complexes) and fibrin formation (fibrinopeptide A), as well as markers of the fibrinolytic activity (plasmin–antiplasmin complexes, D-dimers), were determined in nine asymptomatic male individuals with APC resistance [age, 18 ± 3 years; maximal oxygen consumption, 56.7 ± 2.7 ml/kg per min (mean ± standard deviation)] and in nine male control subjects (age, 19 ± 4 years; maximal oxygen consumption, 56.2 ± 3.2 ml/kg per min) after 1 h of running to exhaustion. Baseline levels of prothrombin fragment 1 + 2 were higher in individuals with APC resistance than in controls [0.67 ± 0.06 nmol/l (mean ± standard error) versus 0.48 ± 0.01 nmol/l; P < 0.05]. In response to exercise, hemostatic variables significantly increased in both groups to a similar small extent. Likewise, exercise-induced changes of fibrinolytic variables in subjects with APC resistance paralleled those observed in controls. In summary, exhaustive running in subjects with APC resistance does not provoke an abnormal hemostatic or fibrinolytic response, suggesting that vigorous exercise does not imply an increased risk for thrombosis in young male subjects with APC resistance.