Thrombin generation after physical exercise

Prisco, Domenico; Paniccia, Rita; Guarnaccia, Vincenzo; Olivo, Giuseppe; Taddei, Tamara; Boddi, Maria; Gensini, Gian Franco

doi:10.1016/0049-3848(93)90013-e

Cited by 37 publications

(18 citation statements)

References 17 publications

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“…Indeed, exercise (bicycle ergometry) activity resulted in elevated F 1+2 , TAT and fibrinopeptide A, established markers of TG [170]. Further direct clinical evidence linking physical exercise with TG was found in this study, showing that exercise training not only influences the hemostatic system per se, but also leads to significant TG and fibrin formation independent of the type of physical activity [171]. However, other investigators found no evidence that exercise training affects F 1+2 , but enhances TAT and fibrinopeptide A release [172][173][174], and that these changes could not be attributed solely to aspirin pretreatment during the repeated exercise [174].…”

Section: Markers Of Tgsupporting

confidence: 51%

Biomarkers and Exercise Training: A Possible Missing Link between Physical Activity and Mortality Benefit in Patients with Heart Failure

Serebruany¹,

Davis

Meister

et al. 2001

Heart Drug

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Knowledge of the pathogenesis of congestive heart failure (CHF) has improved greatly in recent years. Nevertheless, this disease still causes high morbidity and mortality in the Western world. In particular, there have been many advancements in our understanding, treatment and prophylaxis of CHF in recent years, yet the incidence of this disease continues to rise. Due to the staggering numbers of patients afflicted, CHF is becoming the most expensive burden on the health care system. The relationship between the deterioration of cardiac function and ongoing ischemic events has not been fully investigated and could conceivably be both monitored and modulated via various biomarkers. Recent data also indicate that heart failure is associated with altered hemostasis, i.e. a prothrombotic state which can lead to complications arising from occlusive and/or thromboembolic phenomena. Although the incidence of overt and clinically apparent thrombotic events is low, it is possible that subclinical events contribute to the increasing morbidity and mortality from this disease. These subclinical events may include silent ischemic events or microinfarcts which are being recognized as contributing to the progression of heart failure. As far as nonpharmacologic approaches to heart failure are concerned, the use of uniform exercise training regimens in heart failure is still a very controversial topic. Before more definitive recommendations can be made regarding the justification of such procedures, further large-scale studies investigating the effects of physical exercise on the development and progression of heart failure are needed. Furthermore, these studies must have sufficient statistical power to detect effects on clinical outcomes, specifically mortality. The purpose of this review article is to bridge the gap between biomarkers, exercise training and heart failure by discussing our current knowledge of different markers of platelet activation, thrombin generation, inflammation, endothelial dysfunction and myocardial necrosis in CHF patients undertaking physical exercise.

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Section: Markers Of Tgsupporting

confidence: 51%

Biomarkers and Exercise Training: A Possible Missing Link between Physical Activity and Mortality Benefit in Patients with Heart Failure

Serebruany¹,

Davis

Meister

et al. 2001

Heart Drug

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“…The effect of exercise on thrombosis may also be influenced by the type of exercise. For example, running and treadmill exercise were associated with stronger thrombin generation than found during a bicycle ergometer exertion, probably because the treadmill exercise is associated with a higher degree of tissue damage with enhanced tissue factor-mediated activation of coagulation (17,19,25).…”

Section: Discussionmentioning

confidence: 99%

Strenuous but not moderate exercise increases the thrombotic tendency in healthy sedentary male volunteers

Cadroy

Pillard

Sakariassen

et al. 2002

Journal of Applied Physiology

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Cadroy, Yves, Fabien Pillard, Kjell S. Sakariassen, Claire Thalamas, Bernard Boneu, and Daniel Riviere. Strenuous but not moderate exercise increases the thrombotic tendency in healthy sedentary male volunteers. J Appl Physiol 93: 829-833, 2002; 10.1152/japplphysiol.00206. 2002.-We have investigated the effect of moderate and strenuous exercise on experimental arterial thrombus formation in men. Thrombogenesis was measured in 15 sedentary healthy male volunteers at rest or immediately after two standardized exercise tests performed for 30 min on a bicycle ergometer. The exercises were performed at a constant load corresponding to either 50 or 70% maximal oxygen uptake. Thrombus formation was induced ex vivo by exposing a collagen-coated coverslip in a parallel plate perfusion chamber to native nonanticoagulated blood for 3 min. The shear rate at the collagen surface was 2,600 s Ϫ1 . Platelet and fibrin deposition was quantified by immunoenzymatic methods. The results show that moderate exercise did not affect arterial thrombus formation. In contrast, platelet thrombus formation on collagen was increased on the average by 20% after 30 min at 70% maximal oxygen uptake (P ϭ 0.03). Fibrin deposition on collagen remained unchanged with ex-

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“…It may be hypothesized that the coagulation system is also activated after ' stress '. Increased formation of thrombin after physical exercise has been shown previously [8,9] but data on effects of mental stress and catecholamines on the generation of thrombin are scarce. Thrombin is not only central to coagulation but is also a very potent platelet agonist, which may influence platelet function in vivo.…”

Section: Introductionmentioning

confidence: 99%

Activation of haemostasis by exercise, mental stress and adrenaline: effects on platelet sensitivity to thrombin and thrombin generation

Wallén

Goodall

et al. 1999

Clinical Science

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A B S T R A C TStress-induced activation of haemostasis may be involved in the triggering of acute coronary syndromes. We compared the effects of mental stress, dynamic exercise and adrenaline infusion on platelet sensitivity to thrombin using flow-cytometric analysis of platelet fibrinogen binding in whole blood, and platelet aggregability using filtragometry ex vivo, in healthy volunteers. Furthermore, we assessed thrombin generation [prothrombin fragment 1j2 (F1j2) and thrombin-antithrombin complexes in plasma] and thrombin activity (fibrinopeptide A in plasma). Exercise (bicycle ergometry) enhanced thrombin-induced platelet fibrinogen binding (P 0.05) and platelet aggregability (P 0.01), and elevated F1j2, thrombin-antithrombin complexes and fibrinopeptide A (P 0.05 for all three). Adrenaline infusion enhanced thrombin-induced platelet fibrinogen binding and platelet aggregability (P 0.05), and elevated thrombin-antithrombin complexes (P 0.05), whereas F1j2 and fibrinopeptide A levels were not significantly affected. Mental stress increased platelet sensitivity to high concentrations of thrombin only, and produced small increases in levels of thrombin-antithrombin complexes. Time control experiments showed no important changes with repeated measurements during rest. Platelet responses to exercise and adrenaline were reversible, with recovery 60 min later. Thus, heavy exercise and high levels of adrenaline reversibly increased platelet aggregability and platelet sensitivity to thrombin, and enhanced thrombin formation ; the effects were most pronounced during exercise. Mental stress only weakly affected these parameters.

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Thrombin generation after physical exercise

Cited by 37 publications

References 17 publications

Biomarkers and Exercise Training: A Possible Missing Link between Physical Activity and Mortality Benefit in Patients with Heart Failure

Biomarkers and Exercise Training: A Possible Missing Link between Physical Activity and Mortality Benefit in Patients with Heart Failure

Strenuous but not moderate exercise increases the thrombotic tendency in healthy sedentary male volunteers

Activation of haemostasis by exercise, mental stress and adrenaline: effects on platelet sensitivity to thrombin and thrombin generation

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