Int J Sports Med 2001; 22(5): 337-343
DOI: 10.1055/s-2001-15649
Physiology and Biochemistry

© Georg Thieme Verlag Stuttgart · New York

Platelet Activation Through Triathlon Competition in Ultra-Endurance Trained Athletes: Impact of Thrombin and Plasmin Generation and Catecholamine Release

M. Möckel1 , N. V. Ulrich2 , G.  Heller3  Jr. , L. Röcker4 , R. Hansen5 , H. Riess1 , H. Patscheke6 , T. Störk7 , U. Frei1 , A. Ruf6
  • 1Department of Medicine, Charité/Campus Virchow-Klinikum, Humboldt University Berlin, Germany
  • 2Department of Cardiology, Charité/Campus Mitte, Humboldt University Berlin, Germany
  • 3Institute for Medical Sociology and Social Medicine, University of Marburg, Germany
  • 4Department of Physiology, Free University Berlin, Germany
  • 5Institute for Clinical Chemistry, Charité/Campus Virchow-Klinikum, Humboldt University Berlin, Germany
  • 6Institute for Medical Laboratory Diagnostics, Klinikum Karlsruhe, Germany
  • 7Department of Cardiology, Karl Olga Hospital, Stuttgart, Germany
Further Information

Publication History

Publication Date:
31 December 2001 (online)

The aims of this study were to evaluate whether platelets are activated during strenuous exercise in healthy athletes. Also, to determine the impact of plasmin and thrombin activity and catecholamine release. Previous studies have shown activation of the hemostatic system after competitive exercise, but platelet activation was thought to be absent in trained athletes. The impact of thrombin and other potent platelet activators is still a matter for debate. We examined 30 healthy triathletes during a triathlon competition. Flow cytometric detection of CD62p (P-selectin) was used to measure in vivo activation of platelets. Platelet-leukocyte aggregates were also determined. Thrombin concentration was assessed by the thrombin-antithrombin III complex (TAT) and the fibrinolytic state was characterised by the plasmin-α2-antiplasmin complex (PAP). Catecholamines were measured by means of high-pressure liquid chromatography. CD62p rose from baseline (2.3 %) to 3.4 % and was still elevated after 2 hours (3.1 %, p = 0.0133). Platelet-leukocyte aggregates were elevated 30 min after exercise (4.3 % vs 3.6 %) and decreased significantly after 60 min (2.9 %, p = 0.008). TAT increased from 3.9 μg/l to 8.3 μg/l after competition and to 5.4 μg/l 2 hours later (p < 0.001). PAP increased 10-fold from 350 μg/l to 3267 μg/l after the triathlon and was still elevated after 2 hours (1074 μg/l, p < 0.001). No linear correlation was found between the hemostatic markers, catecholamines and platelet activation. Platelets, coagulation and fibrinolysis are activated by competitive exercise in athletes, whereby fibrinolytic changes are pronounced. Mechanisms of platelet activation during exercise include phenomena other than plasmatic hemostatic factors and catecholamines.

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Dr. med. Martin Möckel, M. D.

Dept. of Cardiology

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13353 Berlin
Germany


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