Coronavirus (COVID-19), Coagulation, and Exercise: Interactions That May Influence Health Outcomes.

The proinflammatory cytokine storm associated with coronavirus disease 2019 (COVID-19) negatively affects the hematological system, leading to coagulation activation and endothelial dysfunction and thereby increasing the risk of venous and arterial thrombosis. Coagulopathy has been reported as associated with mortality in people with COVID-19 and is partially reflected by enhanced D-dimer levels. Poor vascular health, which is associated with the cardiometabolic health conditions frequently reported in people with severer forms of COVID-19, might exacerbate the risk of coagulopathy and mortality. Sedentary lifestyles might also contribute to the development of coagulopathy, and physical activity participation has been inherently lowered due to at-home regulations established to slow the spread of this highly infectious disease. It is possible that COVID-19, coagulation, and reduced physical activity may contribute to generate a "perfect storm," where each fuels the other and potentially increases mortality risk. Several pharmaceutical agents are being explored to treat COVID-19, but potential negative consequences are associated with their use. Exercise is known to mitigate many of the identified side effects from the pharmaceutical agents being trialled but has not yet been considered as part of management for COVID-19. From the limited available evidence in people with cardiometabolic health conditions, low- to moderate-intensity exercise might have the potential to positively influence biochemical markers of coagulopathy, whereas high-intensity exercise is likely to increase thrombotic risk. Therefore, low- to moderate-intensity exercise could be an adjuvant therapy for people with mild-to-moderate COVID-19 and reduce the risk of developing severe symptoms of illness that are associated with enhanced mortality.

Acquired and Genetic Thrombotic Risk Factors in the Athlete.

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.

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

Exercise has been demonstrated to have considerable effects upon haemostasis, with activation dependent upon the duration and intensity of the exercise bout. In addition, markers of coagulation and fibrinolysis have been shown to possess circadian rhythms, peaking within the morning (0600-1200 h). Therefore, the time of day in which exercise is performed may influence the activation of the coagulation and fibrinolytic systems. This study aimed to examine coagulation and fibrinolytic responses to short-duration high-intensity exercise when completed at different times of the day. Fifteen male cyclists (VO2max: 60.3 ± 8.1 ml kg-1 min-1) completed a 4-km cycling time trial (TT) on five separate occasions at 0830, 1130, 1430, 1730 and 2030. Venous blood samples were obtained pre- and immediately post-exercise, and analysed for tissue factor (TF), tissue factor pathway inhibitor (TFPI), thrombin-anti-thrombin complexes (TAT) and D-Dimer. Exercise significantly increased plasma concentrations of TF (p < .0005), TFPI (p < .0006), TAT complexes (p < .0012) and D-Dimer (p < .0003). There was a time-of-day effect in pre-exercise TF (p = .004) and TFPI (p = .031), with 0830 greater than 1730 (p .001), while 1730 was less than 2030 h (p = .008), respectively. There was no significant effect of time of day for TAT (p = .364) and D-Dimer (p = .228). Power output, TT time and heart rate were not significantly different between TTs (p > .05); however, percentage VO2max was greater at 1730 when compared to 2030 (p = .04). Due to a time-of-day effect present within TF, peaking at 0830, caution should be applied when prescribing short-duration high-intensity exercise bout within the morning in populations predisposed to hypercoagulability.