Managing Cardiometabolic Risk

Exercise and Thrombosis

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An acute bout of heavy exercise has long been known as a potential trigger for myocardial infarction (102). Although there are discrepancies in the literature, a prior systematic review concluded that acute exercise can trigger a cardiovascular event by inducing a prothrombotic state associated with abnormal fibrinolysis and augmented platelet aggregation (99). However, a number of factors can influence the effect of acute exercise on thrombosis, such as baseline fitness and exercise intensity (99). For example, a number of studies (103, 104) have shown that while acute moderate-intensity (55-65% VO₂max) exercise can improve fibrinolysis and reduce platelet adhesiveness and aggregation, high intensity (80% VO₂max) exercise can have the opposite effect by increasing blood coagulation and platelet adhesion and aggregation. In addition, while the enhanced fibrinolytic response due to acute exercise is highly transient, the hypercoaguable state appears to be more persistent post exercise, providing an ideal environment for clot formation (105).

Reference

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99. Lee KW and Lip GY. Effects of lifestyle on hemostasis, fibrinolysis, and platelet reactivity: a systematic review. Arch Intern Med 2003; 163: 2368-92.

102. Tofler GH, Stone PH, Maclure M, et al. Analysis of possible triggers of acute myocardial infarction (the MILIS study). Am J Cardiol 1990; 66: 22-7.

103. Weiss C, Welsch B, Albert M, et al. Coagulation and thrombomodulin in response to exercise of different type and duration. Med Sci Sports Exerc 1998; 30: 1205-10.

104. Wang JS, Jen CJ, Kung HC, et al. Different effects of strenuous exercise and moderate exercise on platelet function in men. Circulation 1994; 90: 2877-85.

105. Hegde SS, Goldfarb AH and Hegde S. Clotting and fibrinolytic activity change during the 1 h after a submaximal run. Med Sci Sports Exerc 2001; 33: 887-92.

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