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Updated: Aug 20, 2025
A Real-World High-Intensity Interval Training Protocol for Cardiorespiratory Fitness Improvement
Published on: February 22, 2022
Haemostasis and fibrinolysis after regular high-intensity interval training in patients with coronary artery disease:
Jacobina Kristiansen1,2,3, Erik Lerkevang Grove4,5, Tórur Sjúrðarson6,7
1Department of Medicine, National Hospital of the Faroe Islands, Torshavn, Faroe Islands.
Insights
Regular exercise in coronary artery disease (CAD) patients did not improve blood clotting or clot breakdown. High-intensity exercise for 12 weeks showed no significant changes in platelet aggregation, thrombin generation, or fibrinolysis.
Area of Science:
- Cardiology
- Exercise Physiology
- Hemostasis
Background:
- Coronary artery disease (CAD) patients exhibit prothrombotic tendencies.
- Regular exercise is known to reduce cardiovascular mortality in stable CAD.
- The precise mechanisms behind exercise's cardioprotective effects, particularly on hemostasis, remain unclear.
Purpose of the Study:
- To investigate if regular exercise can inhibit platelet aggregation and thrombin generation.
- To determine if regular exercise can increase fibrinolysis in patients with CAD.
- To elucidate the hemostatic mechanisms underlying the benefits of exercise in CAD.
Main Methods:
- A randomized controlled trial involving 169 stable CAD patients.
- Intervention group: 12 weeks of supervised high-intensity exercise training.
- Control group: Standard care. Assessed platelet aggregation, thrombin generation, and fibrinolysis at baseline and 12 weeks.
Main Results:
- 142 patients completed the study (64 exercise, 78 standard care).
- No significant between-group differences were observed in adenosine diphosphate-induced platelet aggregation.
- No significant differences in endogenous thrombin potential or 50% clot lysis time were found between groups after 12 weeks.
Conclusions:
- Twelve weeks of high-intensity whole-body endurance exercise did not alter platelet aggregation in stable CAD patients.
- The study found no significant effect of this exercise regimen on thrombin generation.
- High-intensity exercise did not enhance fibrinolysis in this patient cohort over 12 weeks.
Abstract:
IntroductionPatients with coronary artery disease (CAD) have prothrombotic changes compared with healthy individuals. Regular exercise reduces cardiovascular mortality in patients with stable CAD. However, the underlying mechanism for the beneficial effect is unknown. We investigated whether regular exercise would inhibit platelet aggregation and thrombin generation and increase fibrinolysis in patients with CAD.
Materials And Methods:
Patients with CAD were randomised 1:1 to a supervised high-intensity exercise training programme or standard care for 12 weeks. Blood samples were obtained at baseline and after 6 and 12 weeks. Platelet aggregation was evaluated with the Multiplate Analyser, thrombin generation using the calibrated automated thrombogram and fibrinolysis employing a clot lysis assay.
Results:
A total of 169 stable patients with CAD were randomised, and 142 patients (67±9 years, 83% males) completed the study; 64 in the exercise group and 78 in the standard care group. All but one patients received single antiplatelet therapy. From baseline to 12 weeks postintervention (Δ), no significant between-group differences were found in adenosine diphosphate-induced platelet aggregation (Δ-15 aggregation units (AU), AU×min, 95% CI -70 to 40 in the exercise group and Δ-26 AU×min, 95% CI -77 to 26 in the standard care group, p=0.44); endogenous thrombin potential (medians: Δ-5%, 95% CI -12 to 3 in the exercise group and Δ-6%, 95% CI -13 to 1 in the standard care group, p=0.26); nor in 50% clot lysis time (medians: Δ-9%, 95% CI -23 to 7 in the exercise group and Δ-17%, 95% CI -29 to -3 in the standard care group, p=0.60).
Conclusions:
Twelve weeks of high-intensity whole-body endurance exercise did not affect platelet aggregation, thrombin generation or fibrinolysis in patients with stable CAD.
Trial Registration Number:
NCT04268992.
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