Exercise-induced shear stress is associated with changes in plasma von Willebrand factor in older humans

Gonzales, Joaquin U.; Thistlethwaite, John R.; Thompson, Benjamin C.; Scheuermann, Barry W.

doi:10.1007/s00421-009-1074-x

Cited by 12 publications

(6 citation statements)

References 19 publications

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“…Conversely, vWF is not a marker specific to cellular damage, as it is partially stored in Weibel-Palade bodies and is released in response to various vascular stimuli (8,9,16,33,74). Both endothelial glycoproteins TM and vWF have previously been shown to increase with exercise (10,27,33,58). In our study, there were equivalent increases in TM following both exercise bouts, suggesting slight disruption of endothelial cell membranes independent of exercise intensity.…”

Section: Discussionmentioning

confidence: 40%

The effects of moderate and high-intensity exercise on circulating markers of endothelial integrity and activation in young, healthy men

Sapp

Evans

Eagan

et al. 2019

Journal of Applied Physiology

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Endothelial function typically exhibits a hormetic response to exercise. It is unknown whether endothelial damage occurs in response to acute exercise and could be a contributing mechanism. We sought to determine the effects of acute exercise on endothelial-derived circulating factors proposed to reflect endothelial integrity and activation. Young, healthy men ( n = 10) underwent 30-min moderate continuous (MOD) and high-intensity interval (HII) cycling exercise bouts. Venous blood samples were taken immediately before and after exercise for quantification of circulating endothelial cells (CECs), circulating angiogenic cells (CACs), apoptotic and activated endothelial microvesicles (EMVs), thrombomodulin (TM), von Willebrand factor (vWF), syndecan-1, and circulating microRNAs (ci-miRs) 126–3p and 126–5p. Endothelial function was assessed by flow-mediated dilation (FMD) of the brachial artery before, 10 min after, and 60 min after exercise. Numbers of CECs and EMVs were unchanged by either exercise bout ( P > 0.05). Numbers of all measured CAC subtypes decreased in response to MOD (21%–34%, P < 0.05), whereas only CD31+/34+/45dim/− CACs decreased following HII (21%, P < 0.05). TM and syndecan-1 increased with both exercise intensities (both ~20%, P < 0.05). HII, but not MOD, increased vWF (88%, P < 0.001), ci-miR-126–3p (92%, P = 0.009) and ci-miR-126–5p (110%, P = 0.01). The changes in several circulating factors correlated with changes in FMD following either one or both intensities. Changes in circulating factors do not support the concept of exercise-induced endothelial cell denudation, apoptosis, or activation, though slight disruption of endothelial glycocalyx and membrane integrity may occur. A related loss of mechanotransduction along with mechanisms underlying endothelial activation and ci-miR-126 secretion may relate to changes in endothelial function. NEW & NOTEWORTHY Using circulating endothelial-derived factors, we show that endothelial denudation, apoptosis, and activation do not appear to increase, whereas disrupted endothelial glycocalyx and membrane integrity may occur during both high-intensity interval and moderate intensity cycling. Increases in factors nonspecific to endothelial damage, including von Willebrand factor and microRNA-126, occurred only after high-intensity interval exercise. These results shed light on the hypothesis that disrupted endothelial integrity contributes to the endothelial function response to exercise.

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Section: Discussionmentioning

confidence: 40%

The effects of moderate and high-intensity exercise on circulating markers of endothelial integrity and activation in young, healthy men

Sapp

Evans

Eagan

et al. 2019

Journal of Applied Physiology

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“…), in additional to hormonal and nutrient status and responsiveness. 37,48,111,128,129 On the contrary, age-related changes can also be seen as a natural state of aging, given that the same changes occur in all of us, and that healthy centenarians also show such changes. 14,111 Finally, the finding that the levels of several hemostasis markers change with aging has several implications for laboratories undertaking such testing, and namely: (1) to utilize age-adjusted normal ranges for some tests (e.g., for D-dimer), (2) to consider the consequence on previous diagnoses (e.g., "mild type 1" VWD, where VWF test results may "normalize" with aging), and (3) to consider the effect of these changes on the (perceived) therapeutic efficacy of antithrombotic medications such as aspirin.…”

Section: Resultsmentioning

confidence: 99%

Aging Hemostasis: Changes to Laboratory Markers of Hemostasis As We Age—A Narrative Review

Favaloro

Franchini

Lippi

2014

Semin Thromb Hemost

107

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The incidence of venous thromboembolism (VTE) is well recognized to increase with aging. Concurrently, the plasma concentrations of many coagulation factors (e.g., fibrinogen, factor [F] V, FVII, FVIII, and FIX) increase with aging, as does von Willebrand factor (VWF), thrombin generation, and platelet activation. Data are conflicting regarding age-related changes in the natural anticoagulants, including protein C, protein S, and antithrombin. Changes are also observed with components of the fibrinolytic pathway. All in all, aging is associated with a variety of hemostasis changes that on balance reflects a heightened procoagulant status compared with earlier age. It has to be recognized that as this occurs in the otherwise normal general population, this can also be considered a normal phenomenon of progressive life. An element of this heightened procoagulant status may reflect ongoing inflammatory processes, given some markers, notably FVIII and fibrinogen, are acute phase reactants. A variety of acquired prothrombotic risk factors (e.g., cancer, autoimmune disorders, and diabetes) also gradually develop with aging, some of which may induce profound abnormalities of hemostasis, and confound the age-related changes in hemostasis, as well as their influence on thrombotic risk. In this article, we review the changes in hemostasis markers measurable within many hemostasis laboratories, and consider many of the important implications for clinical and laboratory practice. Apart from representing an increased thrombotic risk, additional considerations entail the potential need (1) to utilize age-adjusted normal ranges (e.g., for D-dimer), (2) to consider the consequence on previous diagnoses (e.g., "mild type 1" von Willebrand disease [VWD], where VWF test results may "normalize" with aging), and (3) to consider the effect of these changes of risk factors on the (perceived) therapeutic efficacy of antithrombotic medications such as aspirin.

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“…Secondly, exercise, e.g. due to climbing or walking to a higher altitude induces an increase in von Willebrand factor and factor VIII (FVIII), causing an exercise-increased haemostatic response leading to a prothrombotic phenotype [ 20 – 23 ].…”

Section: Introductionmentioning

confidence: 99%

Hypoxia Induces a Prothrombotic State Independently of the Physical Activity

et al. 2015

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Hypoxia (oxygen deprivation) is known to be associated with deep vein thrombosis and venous thromboembolism. We attempted to get a better comprehension of its mechanism by going to high altitude, thereby including the potential contributing role of physical activity. Two groups of 15 healthy individuals were exposed to hypoxia by going to an altitude of 3900 meters, either by climbing actively (active group) or transported passively by cable car (passive group). Both groups were tested for plasma fibrinogen, von Willebrand factor and factor VIII levels, fibrinolysis, thrombin generating capacity, heart rate, oxygen saturation levels and blood pressure. As a control for the passive group, 7 healthy volunteers stayed immobile in bed for 7 days at normoxic conditions. The heart rate increased and oxygen saturation levels decreased with increasing altitude. Fibrinolysis and fibrinogen levels were not affected. Factor VIII and von Willebrand factor levels levels increased significantly in the active group, but not in the passive group. Plasma thrombin generation remained unchanged in both the active and passive group with increasing altitude and during 7 days of immobility in healthy subjects. However, by applying whole blood thrombin generation, we found an increased peak height and endogenous thrombin potential, and a decreased lagtime and time-to-peak with increasing levels of hypoxia in both groups. In conclusion, by applying whole blood thrombin generation we demonstrated that hypoxia causes a prothrombotic state. As thrombin generation in plasma did not increase, our results suggest that the cellular part of the blood is involved in the prothrombotic phenotype induced by hypoxia.

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Exercise-induced shear stress is associated with changes in plasma von Willebrand factor in older humans

Cited by 12 publications

References 19 publications

The effects of moderate and high-intensity exercise on circulating markers of endothelial integrity and activation in young, healthy men

The effects of moderate and high-intensity exercise on circulating markers of endothelial integrity and activation in young, healthy men

Aging Hemostasis: Changes to Laboratory Markers of Hemostasis As We Age—A Narrative Review

Hypoxia Induces a Prothrombotic State Independently of the Physical Activity

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