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J Am Coll Cardiol, 2001; 38:1313-1319 © 2001 by the American College of Cardiology Foundation |
a Department of Internal Medicine, University of Innsbruck, Innsbruck, Austria
Manuscript received April 3, 2001; revised manuscript received June 21, 2001, accepted July 13, 2001.
* Reprint requests and correspondence: Dr. Hannes Gaenzer, Department of Internal Medicine, University of Innsbruck, Anichstrasse 35, 6020 Innsbruck, Austria
hannes.gaenzer{at}uibk.ac.at
OBJECTIVES
We sought to analyze diameter changes of conduit arteries in response to whole-body exercise and hypothesized that this response might be endothelium-dependent and, therefore, impaired in smokers.
BACKGROUND
Hyperemia and coincident vasodilation are pivotal mechanisms for meeting the increased metabolic demands of active muscle tissue during physical exercise, but studies in humans are sparse.
METHODS
We studied diameter and blood flow of the femoral and brachial arteries in response to a submaximal bicycle exercise test in 10 nonsmoking and 8 smoking healthy male subjects. During an exercise period of 40 min the investigated conduit arteries were periodically scanned in longitudinal sections by high-resolution ultrasound. In the same subjects flow-mediated dilation (FMD) of the brachial artery was recorded by inducing an ischemia through a forearm-occluding cuff.
RESULTS
In response to exercise the diameter of the femoral artery significantly increased in both nonsmokers and smokers, with a diminished response in smokers (9.2 ± 1.9% vs. 4.8 ± 1.6%, p < 0.001). Flow-mediated dilation of the brachial artery induced by forearm occlusion was also reduced in smoking subjects, revealing a strong correlation between these different methods of FMD (exercise vs. forearm ischemia) (r = 0.88, p < 0.001). In contrast, blood flow increase of the femoral artery was similar in nonsmoking and smoking subjects (392 ± 77% vs. 382 ± 109%, p = NS).
CONCLUSIONS
Conduit arteries react with a flow-mediated dilation in response to whole-body exercise. The impairment of this vasodilation observed in smokers was strongly related to a decrease of endothelium-dependent dilation induced by forearm ischemia, indicating that endothelial dysfunction represents the underlying mechanism.
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