Aerobic exercise training reduces arterial stiffness in metabolic syndrome.
David A Donley, Sara B Fournier, Brian L Reger, Evan DeVallance, Daniel E Bonner, I Mark Olfert, Jefferson C Frisbee, Paul D Chantler
Author Information
David A Donley: Division of Exercise Physiology, School of Medicine, West Virginia University, Morgantown, West Virginia;
Sara B Fournier: Division of Exercise Physiology, School of Medicine, West Virginia University, Morgantown, West Virginia; Center for Cardiovascular and Respiratory Sciences, School of Medicine, West Virginia University, Morgantown, West Virginia; and.
Brian L Reger: Division of Exercise Physiology, School of Medicine, West Virginia University, Morgantown, West Virginia;
Evan DeVallance: Division of Exercise Physiology, School of Medicine, West Virginia University, Morgantown, West Virginia; Center for Cardiovascular and Respiratory Sciences, School of Medicine, West Virginia University, Morgantown, West Virginia; and.
Daniel E Bonner: Division of Exercise Physiology, School of Medicine, West Virginia University, Morgantown, West Virginia;
I Mark Olfert: Division of Exercise Physiology, School of Medicine, West Virginia University, Morgantown, West Virginia; Center for Cardiovascular and Respiratory Sciences, School of Medicine, West Virginia University, Morgantown, West Virginia; and.
Jefferson C Frisbee: Center for Cardiovascular and Respiratory Sciences, School of Medicine, West Virginia University, Morgantown, West Virginia; and Department of Physiology and Pharmacology, School of Medicine, West Virginia University, Morgantown, West Virginia.
Paul D Chantler: Division of Exercise Physiology, School of Medicine, West Virginia University, Morgantown, West Virginia; Center for Cardiovascular and Respiratory Sciences, School of Medicine, West Virginia University, Morgantown, West Virginia; and pchantler@hsc.wvu.edu.
The metabolic syndrome (MetS) is associated with a threefold increase risk of cardiovascular disease (CVD) mortality partly due to increased arterial stiffening. We compared the effects of aerobic exercise training on arterial stiffening/mechanics in MetS subjects without overt CVD or type 2 diabetes. MetS and healthy control (Con) subjects underwent 8 wk of exercise training (ExT; 11 MetS and 11 Con) or remained inactive (11 MetS and 10 Con). The following measures were performed pre- and postintervention: radial pulse wave analysis (applanation tonometry) was used to measure augmentation pressure and index, central pressures, and an estimate of myocardial efficiency; arterial stiffness was assessed from carotid-femoral pulse-wave velocity (cfPWV, applanation tonometry); carotid thickness was assessed from B-mode ultrasound; and peak aerobic capacity (gas exchange) was performed in the seated position. Plasma matrix metalloproteinases (MMP) and CVD risk (Framingham risk score) were also assessed. cfPWV was reduced (P < 0.05) in MetS-ExT subjects (7.9 ± 0.6 to 7.2 ± 0.4 m/s) and Con-ExT (6.6 ± 1.8 to 5.6 ± 1.6 m/s). Exercise training reduced (P < 0.05) central systolic pressure (116 ± 5 to 110 ± 4 mmHg), augmentation pressure (9 ± 1 to 7 ± 1 mmHg), augmentation index (19 ± 3 to 15 ± 4%), and improved myocardial efficiency (155 ± 8 to 168 ± 9), but only in the MetS group. Aerobic capacity increased (P < 0.05) in MetS-ExT (16.6 ± 1.0 to 19.9 ± 1.0) and Con-ExT subjects (23.8 ± 1.6 to 26.3 ± 1.6). MMP-1 and -7 were correlated with cfPWV, and both MMP-1 and -7 were reduced post-ExT in MetS subjects. These findings suggest that some of the pathophysiological changes associated with MetS can be improved after aerobic exercise training, thereby lowering their cardiovascular risk.
