Effect of conditioning and deconditioning stimuli on metabolically determined blood flow in humans and implications for congestive heart failure.
Peripheral blood vessels do not dilate normally in congestive heart failure (CHF). The mechanisms responsible for this impairment are not well understood. In this review, a group of studies performed over the past 3 years aimed at examining these mechanisms further are described. These studies suggest that in CHF, fluid retention has a negative effect on vasodilator capacity, thereby limiting peak forearm blood flow. A second mechanism is described that is slowly reversing and not directly dependent on cardiac function; it is believed that this mechanism may be related to the vascular deconditioning associated with severe CHF. This postulate is based on studies that have shown that peak vasodilator capacity is higher in the trained arms of tennis players, that improved vasodilator capacity can be induced by a localized unilateral training program, and that vasodilator capacity is reduced by localized deconditioning. Furthermore, the level of conditioning on vasodilator capacity may be mediated by chronic changes in blood flow. Further studies are necessary to confirm these relations.
Department of Medicine, Milton S. Hershey Medical Center, Pennsylvania State University, Hershey 17033.
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D001783:Blood Flow Velocity; D001794:Blood Pressure; D001808:Blood Vessels / Q000033:anatomy & histology; D004231:Diuresis; D005542:Forearm; D006333:Heart Failure / Q000503:physiopathology*; D006801:Humans; D009132:Muscles / Q000098:blood supply*; D005082:Physical Exertion; D010991:Plethysmography; D012039:Regional Blood Flow; D014664:Vasodilation