Aerobic exercise training reduces arterial stiffness in metabolic syndrome

Abstract

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.

Keywords: arterial stiffness; exercise training; metabolic syndrome.

Copyright © 2014 the American Physiological Society.

Figures

Fig. 1.

Example of central pressure waveform. The systolic (SBP) and diastolic blood pressures (DBP) are the peak and trough of the pressure waveform. Augmentation pressure (AP) is the pressure added to the forward wave by the reflected wave (P1-P2), whereas augmentation index is the ratio between AP and central pulse pressure (PP = SBP − DBP). The dicrotic notch represents closure of the aortic valve and is used to calculate ejection duration (ED). Time to wave reflection is calculated at the point of rise in the initial ejection wave to the onset of the reflected wave. Travel time (Tr) represents the time taken for the forward pressure wave from the aorta to the reflection site and back. SBP-to-DBP shifts were assessed by the SBP (shaded area) and DBP (open area) pressure-time integrals. DT, diastolic time interval.

Fig. 2.

Relationship between peak aerobic capacity (V̇o2peak) and arterial markers, namely, carotid femoral pulse wave velocity (A), carotid intima medial thickness (B), augmentation pressure (C), and brachial (bSBP) and central SBP (cSBP; D).

Fig. 3.

Relationship between the change (postintervention-preintervention values) in V̇o2peak and carotid femoral pulse wave velocity.