Abstract | Background: Exercise is widely accepted to exert beneficial effect on human health in prevention and treatment of cardiovascular diseases (CVD). However, a paradox has emerged where exercise has been documented to result in pathological activation of platelets contributing to the development of CVDs. Aims: This study is aimed at understanding the exact molecular mechanisms that governs the differentiation between pathological and physiological activation of platelets. Methods: The potential effects of exercise on platelet activation are studied using an in vitro model that simulates exercise induced activation of platelets using whole blood samples and low concentrations of agonists (epinephrine, TRAP/thrombin receptor-activating peptide, serotonin). The levels of platelet activation are analysed using flow cytometry method. Results: The use of the low concentrations of individual agonists did not result in significant platelet activation as shown by the expression of CD62P. The addition of 1 µM TRAP led to 3.0% ±1.1% (P=0.9549) CD62P positive platelets compared to level of expression in the absence of agonists (3.1% ±1.3%). The presence of 10 µM serotonin resulted in 5.2% ±2.4% activated platelets compared to no agonist conditions (P=0.9999). The 5 µM epinephrine led to a modest, non-significant activation (12.1% ±6.9%) compared to no agonist levels (P=0.9519). However, the combination of agonists showed a striking synergy and a significant increase in platelet activation 50.87% ±25.81 (P=0.0044) compared to no agonist levels. Summary/Conclusion: Preliminary results using in vitro model showed that a combination of agonists that are likely to be present during physiological exercise act synergistically to trigger a strong platelet activation. Whether similar process indeed occurs during in vivo conditions will be investigated in the future study. |
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