The Acute and Chronic Effects of Resistance and Aerobic Exercise in Hemostatic Balance: A Brief Review

Abstract

Hemostatic balance refers to the dynamic balance between blood clot formation (coagulation), blood clot dissolution (fibrinolysis), anticoagulation, and innate immunity. Although regular habitual exercise may lower the incidence of cardiovascular diseases (CVD) by improving an individual’s hemostatic profile at rest and during exertion, vigorous exercise may increase the risk of sudden cardiac death and venous thromboembolism (VTE). This literature review aims to investigate the hemostatic system’s acute and chronic adaptive responses to different types of exercise in healthy and patient populations. Compared to athletes, sedentary healthy individuals demonstrate similar post-exercise responses in platelet function and coagulatory and fibrinolytic potential. However, hemostatic adaptations of patients with chronic diseases in regular training is a promising field. Despite the increased risk of thrombotic events during an acute bout of vigorous exercise, regular exposure to high-intensity exercise might desensitize exercise-induced platelet aggregation, moderate coagulatory parameters, and up-regulate fibrinolytic potential via increasing tissue plasminogen activator (tPA) and decreasing plasminogen activator inhibitor (PAI-1) response. Future research might focus on combining different types of exercise, manipulating each training characteristic (frequency, intensity, time, and volume), or investigating the minimal exercise dosage required to maintain hemostatic balance, especially in patients with various health conditions.

Immunomodulatory effects of exercise in cancer prevention and adjuvant therapy: a narrative review

“…Nonetheless, intensity can be the rate-limiting factor for physical activity–mediated positive effects. Some studies report that high-intensity physical activity (<75% VO 2 max) led to CTC–platelet aggregation ( Wang et al, 2022 ; Skouras et al, 2023 ), while moderate physical activity (50%–74% VO 2 max) prevented both adhesiveness and aggregation of platelets ( Barale et al, 2023 ).…”

Impact of Physical Exercise on Platelets: Focus on Its Effects in Metabolic Chronic Diseases

“…Considering this, acute exercise without chronic adaptation may paradoxically interfere with platelet responsiveness in a detrimental way through reduced NO bioavailability and ox-LDL generation [ 75 ]. Nevertheless, the exact effect of an acute bout of exercise on platelet function is still unclear [ 86 , 87 ].…”

“…The mechanisms underlying these different effects on thrombotic processes involve platelets, fibrinolytic, and coagulation activity. Specifically, acute but light exercise (under 49% VO 2 max) increases fibrinolytic activity but does not interfere with platelet reactivity and coagulation, while if moderate, acute exercise (50–74% VO 2 max) inhibits platelet reactivity and enhances fibrinolysis without modifying the coagulation system; whereas if vigorous, acute exercise (more than 75% VO 2 max) activates both platelets and the coagulation system, besides promoting fibrinolytic activity [ 87 , 133 ]. Thus, on the one side, the adaptation to moderate-intensity exercise attenuates platelet reactivity and increases fibrinolysis at rest; on the other side, during strenuous exercise, it limits enhanced platelet reactivity and sustains hyper-fibrinolytic activity.…”

“…On the basis of these results, the authors postulated that vigorous aerobic exercise might be a suitable strategy to protect obese women from thrombotic events. Indeed, this assertion has been confuted in favor of regular exposure to high-intensity exercise in order to desensitize against exercise-induced platelet aggregation, attenuate coagulatory parameters, and up-regulate fibrinolytic potential [ 87 ]. In another study, obese subjects underwent moderate-intensity exercise on a treadmill (at 60% of their VO 2 max), and the results showed changes in size distribution and cell origin of extracellular vesicles (EVs) [ 190 ].…”

Exercise Effects on Health-Related Quality of Life (HRQOL), Muscular Function, Cardiorespiratory Function, and Body Composition in Smokers: A Narrative Review

“…A recent study revealed the biomechanical changes that occur in smokers with a significant abnormality in the HR response [37]. In smokers during exercise, signals from the cardiac parasympathetic blockade cause the stimulation of mechanoreceptors to inhibit the stimulation of the activation of parasympathetic activity resulting in a drastic inverse outcome of its effects [27,35].…”