Matthew J Lawrence, Gareth Davies, Michael Nyberg, Janet Whitley, Vanessa Evans, Rhodri Williams, Ylva Hellsten, Phillip A Evans
Journal: Thrombosis research 2019;170():32-37
PMID: 30098458
BACKGROUND
The long term benefits of exercise on the cardiovascular status of a patient have been proven, however, their benefit/risk relationship with exercise intensity is unclear. Furthermore, many thromboembolic diseases such as myocardial infarction and ischaemic stroke are associated with profound catecholamine release. In this study we explore the relationship between catecholamine release and hemodynamic changes and their effect on coagulation.
MATERIALS AND METHODS
Twelve healthy recreationally active males were recruited. Local anesthesia was given and catheters were placed under aseptic conditions, in the femoral artery and vein of the experimental leg. The first experiment involved tyramine infusion into the femoral artery at a dose of 1.0 μmol·min·L leg volume. The second experiment involved single leg knee-extensor exercise performed at 30 W for 15 min. Venous blood was collected at each time point to assess clot microstructure using the d biomarker.
RESULTS AND CONCLUSIONS
Tyramine infusion causes a local noradrenaline release in the leg. The increase in noradrenaline was associated with a significant increase in clot microstructure formation (d increased from 1.692 ± 0.029 to 1.722 ± 0.047, p = 0.016). Additionally moderate intensity single leg knee extensor exercise, which minimally alters sympathetic activity, also induced an increases in d (from 1.688 ± 0.025 to 1.723 ± 0.023, p = 0.001). This suggests that exercise can alter clot microstructure formation both via an increase in catecholeamine levels and by factors related to muscle activity per se, such as increased blood flow and consequent shear. These findings have implications for recommendations of exercise in patients at risk of cardiovascular events.
Copyright © 2018 Elsevier Ltd. All rights reserved.
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