Viviane M Conraads1, Nele Pattyn2, Catherine De Maeyer3, Paul J Beckers4, Ellen Coeckelberghs5, Véronique A Cornelissen6, Johan Denollet7, Geert Frederix8, Kaatje Goetschalckx9, Vicky Y Hoymans10, Nadine Possemiers11, Dirk Schepers12, Bharati Shivalkar13, Jens-Uwe Voigt14, Emeline M Van Craenenbroeck15, Luc Vanhees16. 1. Department of Cardiology, Antwerp University Hospital, Edegem, Belgium; University of Antwerp, Antwerp, Belgium. 2. Department of Rehabilitation Sciences, KU Leuven, Leuven, Belgium. Electronic address: nele.pattyn@faber.kuleuven.be. 3. Department of Cardiology, Antwerp University Hospital, Edegem, Belgium; University of Antwerp, Antwerp, Belgium. Electronic address: catherine.demaeyer@uza.be. 4. Department of Cardiology, Antwerp University Hospital, Edegem, Belgium; University of Antwerp, Antwerp, Belgium. Electronic address: paul.beckers@uza.be. 5. Department of Rehabilitation Sciences, KU Leuven, Leuven, Belgium. Electronic address: ellen.coeckelberghs@faber.kuleuven.be. 6. Department of Rehabilitation Sciences, KU Leuven, Leuven, Belgium. Electronic address: veronique.cornelissen@faber.kuleuven.be. 7. Department of Cardiology, Antwerp University Hospital, Edegem, Belgium; CoRPS-Centre of Research on Psychology in Somatic diseases, Tilburg University, Tilburg, The Netherlands. Electronic address: j.denollet@uvt.nl. 8. Department of Cardiology, Antwerp University Hospital, Edegem, Belgium; Laboratory of Cellular and Molecular Cardiology, Antwerp University Hospital, Edegem, Belgium. Electronic address: geert.frederix@uza.be. 9. Department of Rehabilitation Sciences, KU Leuven, Leuven, Belgium; Department of Cardiovascular Diseases, University Hospitals of Leuven, Leuven, Belgium. Electronic address: kaatje.goetschalckx@uzleuven.be. 10. Department of Cardiology, Antwerp University Hospital, Edegem, Belgium; University of Antwerp, Antwerp, Belgium; Laboratory of Cellular and Molecular Cardiology, Antwerp University Hospital, Edegem, Belgium. Electronic address: vicky.hoymans@uza.be. 11. Department of Cardiology, Antwerp University Hospital, Edegem, Belgium. Electronic address: nadine.possemiers@uza.be. 12. Department of Rehabilitation Sciences, KU Leuven, Leuven, Belgium. Electronic address: dirk.schepers@uzleuven.be. 13. Department of Cardiology, Antwerp University Hospital, Edegem, Belgium; University of Antwerp, Antwerp, Belgium. Electronic address: bharati.shivalkar@uza.be. 14. Department of Cardiovascular Diseases, University Hospitals of Leuven, Leuven, Belgium. Electronic address: jens.uwe.voigt@gmx.net. 15. Department of Cardiology, Antwerp University Hospital, Edegem, Belgium; University of Antwerp, Antwerp, Belgium; Laboratory of Cellular and Molecular Cardiology, Antwerp University Hospital, Edegem, Belgium. Electronic address: emeline.vancraenenbroeck@uantwerpen.be. 16. Department of Rehabilitation Sciences, KU Leuven, Leuven, Belgium; Department of Cardiovascular Diseases, University Hospitals of Leuven, Leuven, Belgium. Electronic address: luc.vanhees@faber.kuleuven.be.
Abstract
BACKGROUND:Exercise-based cardiac rehabilitation increases peak oxygen uptake (peak VO₂), which is an important predictor of mortality in cardiac patients. However, it remains unclear which exercise characteristics are most effective for improving peak VO₂ in coronary artery disease (CAD) patients. Proof of concept papers comparing Aerobic Interval Training (AIT) and Moderate Continuous Training (MCT) were conducted in small sample sizes and findings were inconsistent and heterogeneous. Therefore, we aimed to compare the effects of AIT and Aerobic Continuous Training (ACT) on peak VO₂, peripheral endothelial function, cardiovascular risk factors, quality of life and safety, in a large multicentre study. METHODS:Two-hundred CAD patients (LVEF >40%, 90% men, mean age 58.4 ± 9.1 years) were randomized to a supervised 12-week cardiac rehabilitation programme of three weekly sessions of either AIT (90-95% of peak heart rate (HR)) or ACT (70-75% of peak HR) on a bicycle. Primary outcome was peak VO₂; secondary outcomes were peripheral endothelial function, cardiovascular risk factors, quality of life and safety. RESULTS:Peak VO₂ (ml/kg/min) increased significantly in both groups (AIT 22.7 ± 17.6% versus ACT 20.3 ± 15.3%; p-time<0.001). In addition, flow-mediated dilation (AIT+34.1% (range -69.8 to 646%) versus ACT+7.14% (range -66.7 to 503%); p-time<0.001) quality of life and some other cardiovascular risk factors including resting diastolic blood pressure and HDL-C improved significantly after training. Improvements were equal for both training interventions. CONCLUSIONS: Contrary to earlier smaller trials, we observed similar improvements in exercise capacity and peripheral endothelial function following AIT and ACT in a large population of CAD patients.
RCT Entities:
BACKGROUND: Exercise-based cardiac rehabilitation increases peak oxygen uptake (peak VO₂), which is an important predictor of mortality in cardiac patients. However, it remains unclear which exercise characteristics are most effective for improving peak VO₂ in coronary artery disease (CAD) patients. Proof of concept papers comparing Aerobic Interval Training (AIT) and Moderate Continuous Training (MCT) were conducted in small sample sizes and findings were inconsistent and heterogeneous. Therefore, we aimed to compare the effects of AIT and Aerobic Continuous Training (ACT) on peak VO₂, peripheral endothelial function, cardiovascular risk factors, quality of life and safety, in a large multicentre study. METHODS: Two-hundred CAD patients (LVEF >40%, 90% men, mean age 58.4 ± 9.1 years) were randomized to a supervised 12-week cardiac rehabilitation programme of three weekly sessions of either AIT (90-95% of peak heart rate (HR)) or ACT (70-75% of peak HR) on a bicycle. Primary outcome was peak VO₂; secondary outcomes were peripheral endothelial function, cardiovascular risk factors, quality of life and safety. RESULTS: Peak VO₂ (ml/kg/min) increased significantly in both groups (AIT 22.7 ± 17.6% versus ACT 20.3 ± 15.3%; p-time<0.001). In addition, flow-mediated dilation (AIT+34.1% (range -69.8 to 646%) versus ACT+7.14% (range -66.7 to 503%); p-time<0.001) quality of life and some other cardiovascular risk factors including resting diastolic blood pressure and HDL-C improved significantly after training. Improvements were equal for both training interventions. CONCLUSIONS: Contrary to earlier smaller trials, we observed similar improvements in exercise capacity and peripheral endothelial function following AIT and ACT in a large population of CAD patients.
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