Alterations of Fibrinolysis and Blood Coagulation Induced by Exercise, and the Role of Beta-Adrenergic-Receptor Stimulation

Cohen, R. L.; Epstein, S E; Cohen, LawrenceS.; Dennis, Lewis H.

doi:10.1016/s0140-6736(68)91760-1

Cited by 115 publications

(62 citation statements)

References 21 publications

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“…Catecholamines are known to affect fibrinolysis by stimulating endothelial cells to release t-PA, 8 as well as stimulating coagulation by liberating factor VIII and vWF into the bloodstream. 7,34 During exercise, release of t-PA begins when 50% of maximal exercise intensity is reached, whereas factor VIII and vWF are not liberated until 95% to 100% of maximal oxygen consumption is achieved. 2 In the presence of atherosclerosis in our study, signs of enhanced coagulation were already observed as a consequence of exercise with mean maximal intensity of 76%.…”

Section: Discussionmentioning

confidence: 99%

Physical Exertion Induces Thrombin Formation and Fibrin Degradation in Patients With Peripheral Atherosclerosis

Mustonen

Lepäntalo

Lassila

1998

ATVB

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Section: Discussionmentioning

confidence: 99%

Physical Exertion Induces Thrombin Formation and Fibrin Degradation in Patients With Peripheral Atherosclerosis

Mustonen

Lepäntalo

Lassila

1998

ATVB

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“…The current study suggests that the mechanism(s) responsible for maintaining fibrinogen level constant during and after exercise also serves to blunt the increase in plasma viscosity, which would otherwise occur as a consequence of hemoconcentration. Increased fibrinolytic activity during exercise maintains fibrinogen concentration at or near pre-exercise levels (Blattler el al., 1979;Clement and Shepherd, 1976;Cohen et al, 1968) and may play a significant role in attenuating the effect of hemoconcentration on plasma viscosity and reducing the magnitude of the increase in viscous resistance during recovery from exercise. Accordingly, at a given arterial pressure and degree of arteriolar vasoconstriction, blood flow and oxygen delivery are better maintained.…”

Section: Discussionmentioning

confidence: 99%

Effects of exercise on plasma viscosity in athletes and sedentary normal subjects

Letcher

Pickering

Chien

et al. 1981

Clinical Cardiology

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Summary:To assess the immediate and long-term effects of exercise on factors regulating blood flow, we measured plasma viscosity (qP) and plasma renin activity (PRA) in 17 trained runners and 16 sedentary healthy subjects before and 10 min after graded treadmill exercise. Resting vP was lower in runners primarily because of significantly lower fibrinogen concentration. Compared to nonrunners with similar 24-h urine electrolyte excretion rates, runners were characterized by lower PRA at rest. In view of the overall correlation between heart rate and PRA before exercise, reduced adrenergic tone was probably a major factor contributing to the lower PRA in runners. After exercise, plasma viscosity and PRA exceeded control levels, and were similar in magnitude in runners and sedentary subjects. Changes in plasma viscosity were less than expected from the degree of hemoconcentration, primarily because enhanced fibrinolysis maintained fibrinogen level constant. To the extent that plasma viscosity affects viscous flow resistance, the results suggest that tissue perfusion and oxygen delivery rate at rest are greater in trained runners than in sedentary subjects, but these variables become similar after maximum exertion.

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“…Strenuous exerciseinduced hyper-coagulability as reflected by an increasing of FVIII concentration and shortening of activated partial thromboplastin time (APPT) [60,61] suggests that this activation occurs though the intrinsic, but not the extrinsic coagulation pathway. The b-adrenergic pathway has been implicated as a pathway potentially mediating an exercise-induced increase in FVIII levels as b-blockade blunts this increase [62]. Some investigations showed that aerobic and anaerobic exercise increases plasmin formation, possibly by increasing plasminogen activator (t-PA) and reducing plasminogen activator inhibitor (PAI-1) [34,63], thereby accelerating the blood fibrinolysis rate and enhancing fibrin degradation.…”

Section: Effects Of Acute Exercisementioning

confidence: 99%

Exercise prescription and thrombogenesis

Wang

2006

J Biomed Sci

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SummaryLifestyle habits, such as exercise, may significantly influence risk of major vascular thrombotic events. The risk of primary cardiac arrest has been shown to transiently increase during vigorous exercise, whereas regular moderate-intensity exercise is associated with an overall reduced risk of cardiovascular diseases. What are the mechanisms underlying these paradoxical effects of vigorous exercise versus exercise training on thrombotic modification? This review analyzes research regarding effects and their underlying mechanisms of acute exercise, endurance training, and deconditioning on platelets, coagulation, and fibrinolysis. Evidence suggests that (i) light, acute exercise ( £ 49% VO 2 max ) does not affect platelet reactivity and coagulation and increases fibrinolytic activity; (ii) moderate, acute exercise (50$74% VO 2max ) suppresses platelet reactivity and enhances fibrinolysis, which remains unchanged in the coagulation system; and, (iii) strenuous, acute exercise ( ‡ 75% VO 2max ) enhances both platelet reactivity and coagulation, simultaneously promoting fibrinolytic activity. Therefore, moderate exercise is likely a safe and effective exercise dosage for minimizing risk of cardiovascular diseases by inducing beneficial anti-thrombotic changes. Moreover, moderate-intensity exercise training reduces platelet reactivity and enhances fibrinolysis at rest, also attenuating enhanced platelet reactivity and augmenting hyper-fibrinolytic activity during strenuous exercise. However, these favorable effects of exercise training on thrombotic modification return to a pretraining state after a period of deconditioning. These findings can aid in determining appropriate exercise regimes to prevent early thrombotic events and further hinder the cardiovascular disease progression. Benefits and risks associated with exercise in cardiovascular diseasesIncreased physical activity [1] and cardiorespiratory fitness [2] are associated with a reduced risk of fatality from coronary heart disease, as well as other causes. Moreover, increased studies have demonstrated that regular moderate-intensity physical activity is associated with health benefits, even when aerobic fitness (e.g., maximal oxygen uptake, VO 2max ) remains unchanged [3] Conversely, clinical investigations conferred that strenuous, acute exercise can enhance risk of major vascular thrombotic events and transiently increase incidence of primary cardiac arrest [9,10]. The incidence of cardiovascular complications during exercise is substantially greater for those with cardiovascular disease than for healthy

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Alterations of Fibrinolysis and Blood Coagulation Induced by Exercise, and the Role of Beta-Adrenergic-Receptor Stimulation

Cited by 115 publications

References 21 publications

Physical Exertion Induces Thrombin Formation and Fibrin Degradation in Patients With Peripheral Atherosclerosis

Physical Exertion Induces Thrombin Formation and Fibrin Degradation in Patients With Peripheral Atherosclerosis

Effects of exercise on plasma viscosity in athletes and sedentary normal subjects

Exercise prescription and thrombogenesis

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