Time of day and short‐duration high‐intensity exercise influences on coagulation and fibrinolysis

Zadow, Emma K.; Kitic, Cecilia M.; Wu, Sam; Fell, James C.; Adams, Murray J.

doi:10.1080/17461391.2017.1420237

Cited by 20 publications

(19 citation statements)

References 59 publications

(100 reference statements)

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“…To investigate diurnal rhythms in response to exercise completed at different times of the day, three separate investigations 13,16,96 have employed similar exercise protocols with varying exercise intensities over two different time points (►Table 2), while a single investigation has examined the influence of a shorter-duration, high-intensity bout of exercise over five individual time points. 14 The findings of Szymanski and Pate 96 mirrored the diurnal rhythms previously reported for tissue plasminogen activator (t-PA) and plasminogen activator inhibitor-1 (PAI-1), with both markers significantly increased post exercise (p < 0.05), with greater concentrations observed immediately following evening exercise (p < 0.001). In contrast to Szymanski and Pate, 97 Siahkouhian and associates 13 failed to demonstrate the time of day response in markers of coagulation and fibrinolysis following both morning and evening exercise, despite significant increases (p < 0.05) in post exercise plasma concentrations of hemostasis.…”

Section: Hemostasis Exercise and Time Of Daysupporting

confidence: 67%

“…numerous factors, including the study population assessed with regard to training status; age and gender [11][12][13] ; the exercise type, intensity, and duration 6,9,14 ; and the time of the day the exercise is performed. [15][16][17] Although exerciseinduced hemostatic activation may not be detrimental to most individuals, approximately 1 in 1,000 athletes 12,18 may experience a post-exercise-related thromboembolic incident, similar to that of the general population, albeit in the absence of exercise.…”

mentioning

confidence: 99%

“…[19][20][21][22] To achieve competitive success, athletes are frequently exposed to many acquired thrombogenic risk factors associated with hypercoagulability, including long-haul travel, dehydration, postexercise hemoconcentration, and polycythemia. 23 Furthermore, athletes are exposed to acquired "athlete-specific" risk factors including exercise (duration and intensity), trauma, and the time of the day at which exercise is performed, [14][15][16] potentially enhancing the risk for VTE. When these factors are considered in conjunction with genetic predispositions to hypercoagulability present in some athletes, an overall increased risk for VTE is present.…”

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confidence: 99%

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Acquired and Genetic Thrombotic Risk Factors in the Athlete

Zadow

Adams

Kitic

et al. 2018

Semin Thromb Hemost

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While athletes are often considered the epitome of health due to their physique and lowered potential for metabolic and cardiovascular diseases, they may also be at risk for the onset and development of venous thromboembolism (VTE). In an attempt to achieve and remain competitive, athletes are frequently exposed to numerous athlete-specific risk factors, which may predispose them to VTE through the disruption of factors associated with Virchow's triad (i.e., hypercoagulability, venous stasis, and vessel wall injury). Indeed, hypercoagulability within an athletic population has been well documented to occur due to a combination of multiple factors including exercise, dehydration, and polycythemia. Furthermore, venous stasis within an athletic population may occur as a direct result of prolonged periods of immobilization experienced when undertaking long-distance travels for training and competition, recovery from injury, and overdevelopment of musculature. While all components of Virchow's triad are disrupted, injury to the vessel wall has emerged as the most important factor contributing to thrombosis formation within an athletic population, due to its ability to influence multiple hemostatic mechanisms. Vessel wall injury within an athletic population is often related to repetitive microtrauma to the venous and arterial walls as a direct result of sport-dependent trauma, in addition to high metabolic rates and repetitive blood monitoring. Although disturbances to Virchow's triad may not be detrimental to most individuals, approximately 1 in 1,000 athletes will experience a potentially fatal post-exercise thrombotic incidence. When acquired factors are considered in conjunction with genetic predispositions to hypercoagulability present in some athletes, an overall increased risk for VTE is present.

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Section: Hemostasis Exercise and Time Of Daysupporting

confidence: 67%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Acquired and Genetic Thrombotic Risk Factors in the Athlete

Zadow

Adams

Kitic

et al. 2018

Semin Thromb Hemost

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“…Repetitive Exercise On each of three subsequent days, the participants cycled approximately 80 km over the course of 4 hours, always at the same time of day to take into account possible diurnal effects. 24 Submaximal exercise intensity was achieved by cycling in a hilly landscape, covering a total of 800 height meters, with a maximum slope of 10%, inducing 90 to 95% intensity for approximately 10 minutes when climbing hills, and > 75% intensity between hills.…”

Section: Appendix: Methodology For the Pilot Studymentioning

confidence: 99%

“…21,22 Altogether, these changes result in a shift toward a transient hypercoagulable state, 23 that depends at least partly on exercise intensity. 24 Whereas moderate exercise enhances fibrinolytic activity, strenuous exercise (corresponding to 80-100% of the maximal heart rate) induces a more procoagulant state, causing an enhanced risk of thrombotic events, especially in untrained individuals. [25][26][27] Contrary to acute high-intensity exercise, regular training at moderate intensity is associated with a lower overall risk of adverse cardiovascular events.…”

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confidence: 99%

Effects of Repeated Bouts of Exercise on the Hemostatic System

Vorm

Huskens

Kicken

et al. 2018

Semin Thromb Hemost

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Physical activity is beneficial for health, for example, by lowering the risk of cardiovascular events. However, vigorous exercise is associated with the occurrence of thromboembolic events and sudden cardiac death, in particular in untrained individuals. Whereas acute exercise is known to cause a hypercoagulable state, repeated exposure to (strenuous) exercise by means of training may actually condition the hemostatic response to exercise. To date, the effects of exercise training on blood coagulability and the underlying mechanisms have yet to be fully discerned. In this review, the authors provide an overview of existing literature on how training programs and training status influence hemostasis in healthy individuals. Furthermore, they present data of a pilot study in which we studied the effects of repetitive submaximal intensity cycling on procoagulant and anticoagulant processes. It is known that factor VIII (FVIII) and von Willebrand factor (VWF) increase after exercise, but we found that this increase in FVIII and VWF (antigen, propeptide, and VWF in active conformation) was smaller on each of three subsequent days, suggesting either adaptation of endothelial activation or exhaustion of endothelial VWF supplies. With respect to thrombin generation, elevated FVIII significantly increased the thrombin generation peak but not the endogenous thrombin potential. In contrast, platelet activation in terms of P-selectin expression after stimulation with protease-activated receptor-1 and glycoprotein VI agonists decreased after exercise and did not recover, indicating exhaustion of the platelet response to repetitive exercise.

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