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• W1994461059 abstract "Dear Sir, Exhaustive running over 1 h leads to a minor activation of blood coagulation with increased plasma levels of markers of in vivo thrombin and fibrin formation that, however, do not exceed the range of normal values [1Weiss C. Seitel G. Bärtsch P. Coagulation and fibrinolysis after moderate and very heavy exercise in healthy male subjects.Med Sci Sports Exerc. 1998; 30: 246-51Crossref PubMed Scopus (93) Google Scholar]. That activation of coagulation with exercise appears to be balanced by a concomitant activation of fibrinolysis suggesting that there is most likely no increased risk of thrombosis with exercise [2Bärtsch P. Platelet activation with exercise and risk of cardiac events.Lancet. 1999; 354: 1747-8Abstract Full Text Full Text PDF PubMed Scopus (44) Google Scholar, 3Bourey R.E. Santoro S.A. Interactions of exercise, coagulation, platelets, and fibrinolysis – a brief review.Med Sci Sports Exerc. 1988; 20: 439-46Crossref PubMed Scopus (78) Google Scholar]. This study tested the hypothesis that exercise-induced activation of coagulation might be enhanced in subjects with thrombophilia. Therefore we examined the hemostatic response to exercise in six individuals with protein C (PC) deficiency [five male, one female; age: 26 ± 6 years (mean ± SD)], and in two individuals with anticardiolipin antibodies (ACA) (two males, aged 19 and 56 years), all of which were non-anticoagulated. Except for one subject with PC deficiency and one subject with ACA both having a history of thromboembolic complications, all subjects were asymptomatic. Participants of the study were subjected to a 1-h run on a treadmill at a velocity corresponding to an oxygen demand of 75–80% of maximum (anaerobic threshold), an exercise model that has been shown to induce significant increases of markers of thrombin (prothrombin fragment 1 + 2, PTF 1 + 2; thrombin–antithrombin III complexes, TAT) and fibrin formation (fibrinopeptide A, FPA) [1Weiss C. Seitel G. Bärtsch P. Coagulation and fibrinolysis after moderate and very heavy exercise in healthy male subjects.Med Sci Sports Exerc. 1998; 30: 246-51Crossref PubMed Scopus (93) Google Scholar, 4Weiss C. Welsch B. Albert M. Friedmann B. Strobel G. Jost J. Nawroth P. Bärtsch P. Coagulation and thrombomodulin in response to exercise of different type and duration.Med Sci Sports Exerc. 1998; 30: 1205-10Crossref PubMed Scopus (50) Google Scholar]. Plasma levels of PTF 1 + 2, TAT and of FPA as well as concentrations of fibrin degradation products (FbDP) as an indicator of in vivo fibrinolysis were measured with specific immunoassays before, during and after exercise testing as previously described [1Weiss C. Seitel G. Bärtsch P. Coagulation and fibrinolysis after moderate and very heavy exercise in healthy male subjects.Med Sci Sports Exerc. 1998; 30: 246-51Crossref PubMed Scopus (93) Google Scholar, 4Weiss C. Welsch B. Albert M. Friedmann B. Strobel G. Jost J. Nawroth P. Bärtsch P. Coagulation and thrombomodulin in response to exercise of different type and duration.Med Sci Sports Exerc. 1998; 30: 1205-10Crossref PubMed Scopus (50) Google Scholar]. Results of subjects with thrombophilia were compared with data obtained from nine healthy controls with normal values for protein C, protein S, antithrombin III, prolongation of aPTT by activated protein C, absence of ACA and without evidence of thromboembolic disease in their personal or family history (all were males, age: 19 ± 4 years). Anthropometric data and characteristics of exercise are summarized in Table 1.Table 1Clinical data and characteristics of exercise testing in eight subjects with thrombophilia and in nine control subjectsSubjects with thrombophilia (mean ± SD)Controls (mean ± SD)PSex, M/F7/19/0Age, years29 ± 1319 ± 4< 0.05BMI, kg m−225.4 ± 4.521.7 ± 1.3< 0.05Maximal heart rate, 1 min−1194 ± 13194 ± 11NSVO2 max, mL kg min−154.2 ± 11.156.2 ± 3.2NS1 h run Velocity, km h−110.0 ± 1.812.5 ± 1.2< 0.01 Heart ratemean, % heart ratemax92 ± 493 ± 4NS Mean plasma lactate, mmol L−14.5 ± 1.53.4 ± 0.8NS ΔFbDP, ng mL−1103 ± 6636 ± 47< 0.05BMI, body mass index; VO2 max, maximal oxygen consumption; ΔFbDP, exercise-induced increase of fibrin degradation products. P-values refer to Mann–Whitney U-tests. Open table in a new tab BMI, body mass index; VO2 max, maximal oxygen consumption; ΔFbDP, exercise-induced increase of fibrin degradation products. P-values refer to Mann–Whitney U-tests. Exercise testing in subjects with thrombophilia and in controls resulted in a mean heart rate between 92 and 93% of maximal heart rate, thus indicating that exercise intensity was comparable between groups. With the exception of one individual with ACA, plasma levels of hemostatic variables at rest were within the range for normal values and – as also shown by others [5Mannucci P.M. Tripodi A. Bottasso B. Baudo F. Finazzi G. De Stefano V. Palareti G. Manotti C. Mazzucconi M.G. Castaman G. Markers of procoagulant imbalance in patients with inherited thrombophilic syndromes.Thromb Haemost. 1992; 67: 200-2Crossref PubMed Scopus (77) Google Scholar]– did not allow reliable differentiation between subjects with thrombophilia and controls. One hour of exhaustive running in controls induced the known moderate increase of hemostatic variables [1Weiss C. Seitel G. Bärtsch P. Coagulation and fibrinolysis after moderate and very heavy exercise in healthy male subjects.Med Sci Sports Exerc. 1998; 30: 246-51Crossref PubMed Scopus (93) Google Scholar] with PTF 1 + 2 rising by 0.07 ± 0.03 (mean ± SE) nmol L−1 (P < 0.01), TAT complexes by 1.1 ± 0.4 ng mL−1 (P < 0.05), and FPA by 0.7 ± 0.2 ng mL−1 (P < 0.01) (Fig. 1). Minimal fibrin formation corresponded to an increase of fibrin degradation products (ΔFbDP) by 36 ± 14 ng mL−1 (P < 0.01) after exercise. In three subjects with PC deficiency and in both subjects with ACA, however, plasma levels of hemostatic variables increased to levels far above the 95% confidence interval of the control group (Fig. 1). Also the increase of fibrin degradation products with exercise was considerably greater in subjects with thrombophilia as compared with controls (Table 1) suggesting that the balance between hemostatic and fibrinolytic activation with exercise appears to be maintained yet on a higher level. The data demonstrate that intensive physical exercise leads to an exaggerated formation of thrombin and fibrin in distinct subjects with PC deficiency or ACA. It is noteworthy that both individuals with ACA, as a condition with a comparably high risk for thrombosis [6Seligsohn U. Lubetsky A. Genetic susceptibility to venous thrombosis.N Engl J Med. 2001; 344: 1222-31Crossref PubMed Scopus (749) Google Scholar], revealed an abnormal hemostatic response to exercise. As most of our subjects with thrombophilia were (still) asymptomatic, a selection of individuals with low risk for thrombosis cannot be ruled out entirely. Nevertheless it is conceivable that the abnormal increase of exercise-induced activation of coagulation reflects the clinical significance of the disorder and may occur in those subjects who have a greater risk for thrombosis. However, whether exercise testing is, indeed, capable of identifying individuals with a particular high risk for thrombosis with sufficient accuracy remains to be determined in prospective studies comprising a large number of subjects." @default.
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• W1994461059 date "2003-06-01" @default.
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• W1994461059 title "Exercise-induced activation of coagulation in thrombophilia" @default.
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