Key result
Preconditioning with physical exercise prior to hypobaric hypoxia mitigated hypoxia-induced hypercoagulation, significantly prolonging platelet aggregation and prothrombin times (p=0.000).
Why the study?
Extreme environmental factors disrupt organ systems including hemostasis, creating a need to evaluate the hemostatic response to hypobaric hypoxia and whether exercise preconditioning can mitigate associated abnormalities.
Does preconditioning with physical exercise prevent hypercoagulation in rats exposed to hypobaric hypoxia?
Does preconditioning with physical exercise prevent hypercoagulation in rats exposed to hypobaric hypoxia?
p-value: p=<0.001
Physical exercise preconditioning mitigates the hypercoagulable state and suppression of anticoagulant/fibrinolytic activity induced by acute hypobaric hypoxia in rats.
BACKGROUND: Exposure to multiple extreme environmental factors disrupts the function of multiple organ systems, including the hemostatic system. Identifying safe and effective strategies to enhance the body’s adaptive capacity can help mitigate or prevent stress-related consequences. AIM: This study aimed to assess the response of the hemostatic system to a single 24-h exposure to hypobaric hypoxia and evaluate the potential of preconditioning with physical exercise to correct associated abnormalities. MATERIAL AND METHODS: The experiment involved 60 sexually mature male rats. Group 1 (n = 24) served as the control. Rats in group 2 (n = 12) underwent daily 2-h treadmill walking at a speed of 6–8 m/s for 30 days. Those in group 3 (n = 12) were exposed to a single 24-h hypobaric hypoxia episode by placing the rats in a hypobaric chamber at 0.55 kgf/cm2, simulating an altitude of 6,500 m above sea level. Group 4 rats (n = 12) received a 2-h daily exercise regimen for 30 days prior to a 24-h exposure to hypobaric hypoxia. Platelet aggregation activity, plasma coagulation, and the activity of anticoagulant and fibrinolytic systems were evaluated in all groups using diagnostic test kits (Technologia-Standart, Russia). Statistical analysis was performed using the software Statistica 10. Data were tested for statistical significance of differences using the Student t test and the nonparametric Mann–Whitney U test. RESULTS: A 24-h hypobaric hypoxia activated both the platelet and plasma arms of hemostasis, as shown by significantly shortened platelet aggregation time (p = 0.000), silica clotting time (p = 0.006), and prothrombin time (p = 0.008). Additionally, antithrombin III levels significantly declined (p = 0.000) and fibrin-lysis time lengthened (p = 0.001) relative to those of the controls. Preconditioning physical training followed by hypoxic exposure resulted in hypocoagulation, manifested as a significant prolongation of platelet aggregation time (p = 0.000), silica clotting time (p = 0.011), kaolin clotting time (p = 0.000), and prothrombin time (p = 0.000). Furthermore, antithrombin III concentration significantly increased (p = 0.000) and fibrin clot lysis time significantly decreased (p = 0.002) relative to those of the untrained animals exposed to hypoxia alone. CONCLUSION: A single episode of hypoxic stress is characterized by hypercoagulation at all stages of the coagulation cascade, accompanied with suppression of plasma anticoagulant and fibrinolytic activity, which is mitigated by prior physical training.
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Алексеева et al. (2024) studied Hypobaric hypoxia (n=60). Physical exercise preconditioning vs. Hypoxia alone (no exercise) was evaluated on Hemostatic parameters (platelet aggregation time, silica clotting time, kaolin clotting time, prothrombin time) (p=<0.001). Preconditioning with physical exercise prior to hypobaric hypoxia mitigated hypoxia-induced hypercoagulation, significantly prolonging platelet aggregation and prothrombin times (p=0.000).
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