High-intensity interval training recuperates capacity of endogenous thrombin generation in heart failure patients with reduced ejection fraction.
Thromb Res. 2020 Jan 15;187:159-165
Authors: Hsu CC, Fu TC, Huang SC, Wang JS
OBJECTIVE: Consumptive coagulopathy is associated with increased mortality in patients with heart failure (HF). Physical activity influences the risk of major vascular thrombotic events. This study investigates how high-intensity interval training (HIIT) affects the capacity of endogenous thrombin generation (TG) by modulating circulatory procoagulant microparticles (MPs) in HF patients.
METHODS: Thirty-eight HF patients with reduced ejection fraction (HFrEF) and 38 age- and gender-matched normal counterparts (NC) were recruited into this study. The HFrEF group performed HIIT (3-min intervals at 40% and 80%VO2peak) on a bicycle ergometer for 30 min/day, 3 days/week for 12 weeks, whereas the NC group did not receive any form of intervention. Plasma TG kinetics, procoagulant MPs, coagulation-related factors, and oxidative stress/proinflammatory status were analyzed.
RESULTS: The HFrEF group exhibited (i) less endogenous thrombin potential (ETP) and TG rate, (ii) lower concentration/activity of tissue factor (TF) and counts of TF-rich MPs derived from blood cells, and (iii) higher vascular endothelial shedding and plasma myeloperoxidase and interleukin-6 concentrations, compared to the NC group did. However, HIIT elevated TG rate and TF concentration/activity in plasma, as well as, TF-rich MP counts derived from blood cells in patients with HFrEF. Moreover, the exercise regimen also decreased vascular endothelial shedding and plasma myeloperoxidase and interleukin-6 concentrations in HFrEF patients.
CONCLUSION: HFrEF reduces the capacity of endogenous TG in plasma, which is associated with decreased (or consumed) circulatory procoagulant MP levels. However, HIIT alleviates HFrEF-declined endogenous TG capacity and vascular endothelial damage through recuperating TF-related coagulation activity and suppressing oxidative stress/proinflammatory status.
PMID: 32004876 [PubMed – as supplied by publisher]