Date of Graduation


Document Type


Degree Type



School of Medicine


Exercise Physiology

Committee Chair

Paul D. Chantler

Committee Co-Chair

Randall W. Bryner

Committee Member

I. Mark Olfter


Background: Arterial dysfunction, due in part to arterial stiffening, is recognized as a surrogate end point for cardiovascular disease (CVD) and predicts the risk of future CV events. The metabolic syndrome (MetS) is a clustering of risk factors associated with increased stiffening and carotid artery thickening. Aerobic exercise is a well-established therapy that reduces CV events, and has proven to be an effective intervention against arterial stiffening and pathological wall remodeling in the healthy, hypertensive, and diabetic population.;Aims: The purpose of this thesis was to examine the impact of aerobic exercise training on arterial stiffness and wall remodeling in MetS individuals. We hypothesized that an 8-week exercise intervention would decrease stiffness and reduce carotid wall thickness, compared to inactive MetS participants.;Methods: We compared arterial stiffness (pulse wave velocity: PWV), carotid wall thickness (cIMT), central pulse pressure (cPP), and peak aerobic capacity (VO2peak) between healthy subjects (n=15) and MetS individuals (n=21), free of CV events. Further, we examined how 8 weeks of aerobic exercise training in MetS individuals (n=11) altered the above parameters, compared to MetS individuals (n=9) who remained inactive. Two MetS participants did not finish the 8-week intervention and were only included in the baseline analysis. Cross-sectional comparisons were analyzed using two-tailed independent t-tests. The intervention data was analyzed using repeated measures analysis of variance.;Results: Carotid-femoral PWV (PWVcf) and cPP were 26% (P=0.001) and 33% (p<0.05) higher, respectively; in MetS individuals compared to healthy controls, and cIMT was 13% (p<0.05) greater in the MetS group. There was no significant difference between the trained and non-trained group in all baseline indexes. The major finding of this study was that 8 weeks of aerobic exercise significantly attenuated PWVcf (8.1 +/- 0.5 vs. 7.2 +/- 0.4 m/s, p<0.05) in the trained group, and no change was observed in the non-trained group (8.0 +/- 0.5 vs. 7.9 +/- 0.3 m/s, p=0.51). Carotid IMT did not change in the trained or non-trained group (0.58 +/- 0.03 vs. 0.58 +/- 0.03 mm, p=0.78 and 0.59 +/- 0.05 vs. 0.61 +/- 0.05 mm, p=0.92). Another discovery was the trained group increased VO 2peak (16.0 +/- 1.4 vs. 18.2 +/-1.7 ml/kg/min, p=0.05), and no change was seen in the non-trained group (19.0 +/- 1.9 vs. 18.7 +/- 1.3 ml/kg/min, p=0.76). Further, PWVcf and cPP were both negatively correlated (r=-.40 and r=-.51, p<0.01 for both) with VO2peak.;Conclusions: Although the mechanisms underlying the improvement in arterial elasticity are not fully understood, there is strong evidence supporting an association with the improvement in peak aerobic capacity. Cross-sectional examination revealed increased stiffening and blunted VO2peak in the MetS individuals. Negative correlation was established between composite measures of stiffness and VO2peak. Following the aerobic exercise intervention, the trained group improved cardiorespiratory fitness, while reducing arterial stiffness. These are novel findings that indicate chronic, aerobic exercise is an effective therapeutic intervention that decreases arterial stiffness, but does not attenuate carotid wall thickening in the MetS.