The impact of metabolic syndrome and endothelial dysfunction on exercise-induced cardiovascular changes.

OBJECTIVE

There is limited information regarding the synergistic or additive effects of metabolic syndrome (MS) and endothelial dysfunction (ED) on cardiovascular disease (CVD). Altered cardiovascular responses to exercise have been shown to predict future cardiovascular events as well as assess autonomic function. The present study evaluated the impact of MS and brachial artery reactivity (a proxy of ED) on peak exercise-induced cardiovascular changes.

DESIGN AND

METHODS

Individuals (n = 303) undergoing a standard nuclear medicine exercise stress test were assessed for MS. Participants underwent a Forearm Hyperaemic Reactivity test and were considered to have dysfunctional reactivity if their rate of uptake ratio (RUR) was <3.55. Resting and peak blood pressure (BP) and heart rate (HR) were measured. Reactivity was calculated as the difference between peak and resting measures.

RESULTS

Analyses, adjusting for age, sex, resting HR, total metabolic equivalents (METs), and a history of major CVD, revealed a main effect of MS (F = 5.51, η(2) = 0.02, P = 0.02) and RUR (F = 6.69, η(2) = 0.02, P = 0.01) on HR reactivity, such that patients with MS and/or poor RUR had reduced HR reactivity. There were no interactive effects of RUR and MS. There were no effects of RUR or MS on systolic BP (SBP) or diastolic BP (DBP) reactivity or rate pressure product (RPP) reactivity.

CONCLUSIONS

The presence of decreased HR reactivity among participants with MS or poor brachial artery reactivity, combined with the lack of difference in other exercise-induced cardiovascular changes, indicates that these patients may have some degree of parasympathetic dysregulation. Further longitudinal studies are needed to understand the long-term implications of MS and endothelial abnormalities in this context.