The effects of exercise and catecholamines on platelet reactivity or coagulation and fibrinolysis appear to be inconsistent. This may be partly due to the methods employed in previous studies. In the present study, we investigated the effects of acute aerobic exercise and catecholamines on the thrombotic status by a novel in vitro method, shear-induced hemostatic plug formation (hemostatometry), using nonanticoagulated (native) blood. Aerobic exercise (60% maximal O2 consumption) was performed by healthy male volunteers for 20 min, and the effect on platelet reactivity and coagulation was assessed by performing hemostatometry before and immediately after exercise. Exercise significantly increased shear-induced platelet reactivity, coagulation, and catecholamine levels. The effect of catecholamines on platelet reactivity and coagulation was assessed in vitro by adding catecholamines to blood collected in the resting state. The main findings of the present study are that elevation of circulating norepinephrine at levels that are attained during exercise causes platelet hyperreactivity and a platelet-mediated enhanced coagulation. This may be a mechanism of an association of aerobic exercise with thrombotic risk.

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This is the first laboratory evaluation of a new instrument, designed to test both platelet function and thrombolytic activity from a native blood sample, in vitro. The inventor assumed that the reduction and arrest of blood flow was due to activation, aggregation and stabilized thrombus formation by shear-activated platelets, and that re-establishment of flow was due to thrombolysis. Morphologic and functional studies presented here confirm these mechanisms. In vitro tests provided incontestable evidence for the principal role of platelets in the obstruction of flow (occlusion time) and for thrombolysis as the principal mechanism underlying the restoration of blood flow (lysis time). In addition to aggregation, it is the explosive generation of thrombin by shear-activated platelets that results in the formation of an occlusive haemostatic thrombus. Anticoagulation of blood completely prevented occlusion. Platelet-rich thrombus formation (occlusion time) was dose-dependently inhibited by monoclonal antibody against platelet glycoprotein (GP) Ib (6B4 and 12E4), aurin tricarboxylic acid, monoclonal antibody against platelet GPIIb/IIIa (MA-16N7C2 and abciximab), a synthetic GPIIb/IIIa antagonist (TAK-029), thrombin inhibitor (argatroban), and anti-von Willebrand factor, but not by anti-fibrinogen. Plasminogen activator streptokinase (Varidase) and tissue-type plasminogen activator (Monteplase) dose-dependently enhanced thrombolysis (lysis time) without affecting platelet function (occlusion time). The test is specific for thrombolysis. The plasmin inhibitor tranexamic acid prevented plasminogen activator-induced thrombolysis, while inhibition of clot retraction by cytochalasin B did not affect the lysis time. This rapid and sensitive global test of platelet function and thrombolytic activity could be of great value both in research and in clinical practice.

Platelets play a crucial role in the pathogenesis of acute cardiac events, such as angina, myocardial infarction and sudden death. It is believed that regular low-intensity exercise can reduce, while high-intensity exercise may provoke acute cardiac events. The aim of the present study was to investigate the effect of acute exercise both at low and high intensities on the ventilatory threshold (VT), platelet reactivity and coagulation before and after exercise. Platelet reactivity and coagulation were measured under flow condition, using native blood, by hemostatometry. Seven healthy young men (age: 20–29 years) performed bicycle ergometer exercise for 30 min at intensities of 90% (Ex-VT90% or approximately 55% VO_2max) and 130% (Ex-VT130% or 80% VO_2max) of individual VT. Blood cell counts, hematocrit, blood lactic acid and plasma catecholamine levels were slightly but significantly increased after Ex-VT90% and markedly after Ex-VT130% after 30 min exercise. Subsequent to the exercise, the elevated blood cell counts decreased to the resting levels both at Ex-VT90% and at Ex-VT130%. Platelet reactivity to shear stress and dynamic coagulation were significantly enhanced immediately and 30 min after Ex-130%VT. In contrast, no significant changes occurred in those of Ex-90%VT. The present study suggests that high-intensity exercise-induced platelet hyperreactivity and hypercoagulable state may pose an increased risk for acute, sometimes fatal cardiac event. On the other hand, our findings support the view that low-intensity exercise does not present a risk of thrombosis.

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We used a new test (the Görög Thrombosis Test) for assessing the effect of aging, smoking and exercise habits on the overall thrombotic status including platelet reactivity and spontaneous thrombolytic activity of 30 healthy young males (mean, 21.1 +/- 0.4 years) and 34 elderly males (64.5 +/- 1.1 years). The occlusion time (OT) and the lysis time (LT) were measured from a single native blood sample. The OT is an index of platelet activation and subsequent occlusive thrombus formation by high shear stress, while the LT is an index of the resumption of blood flow due to thrombolysis. The LTs in the elderly group were significantly longer than in the young group (P < 0.001). The LTs of elderly smokers were significantly longer than those of non-smokers (P < 0.001). Exercise did not affect the LT significantly. Platelet reactivity to shear stress (OT) was not affected either by aging, smoking or exercise habits. Suppressed spontaneous thrombolytic activity in elderly males and smokers could be a mechanism of acute thrombotic events in these people.

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