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(Hypertension. 2006;48:560.)
© 2006 American Heart Association, Inc.

Editorial Commentaries

Too Much Is Not Enough

Hypertension and Sympathetic Vasoconstriction in Contracting Muscles

Michael J. Joyner

From the Department of Anesthesiology, Mayo Clinic, Rochester, Minn.

Correspondence to Michael J. Joyner, Department of Anesthesiology, Mayo Clinic, 200 First St SW, Rochester, MN 55905. E-mail joyner.michael@mayo.edu

An extract of the first 250 words of the full text is provided, because this article has no abstract.

When young healthy humans, and especially trained endurance athletes, perform activities like running, swimming, or cycling, mean arterial pressure (MAP) does not rise much.^1,2 At first glance, this seems counterintuitive, because in normal subjects, cardiac output can increase 4- to 5-fold during heavy exercise, and in elite male athletes, cardiac output values in excess of 40 L/min have been reported.³ The "failure" of MAP to rise is even more puzzling in light of the large exercise-mediated increases in vasoconstricting sympathetic outflow directed at most vascular beds.² In the athletes, stroke volume can reach 200 mL/beat, making the maintenance of MAP even more impressive. By contrast, in middle-aged subjects with hypertension, mean arterial blood pressure frequently rises markedly during exercise in spite of more modest increases in cardiac output and small stroke volumes.¹ How does this happen, and what insight does the article by Zhao et al⁴ from the Thomas laboratory at University of Texas Southwestern provide on this observation and related phenomenon?

First, young subjects are "protected" from a rise in MAP during exercise by marked peripheral vasodilation in the face of the increased sympathetic outflow. Because a high fraction of cardiac output during exercise is directed toward the active skeletal muscles, vasodilation in the exercising muscle is a key.^1,2 This is caused by marked metabolic vasodilation along with a local metabolite-mediated blunting of -adrenergic vasoconstriction (functional sympatholysis) in the active muscles.^5–7 Thus, diastolic pressure either remains relatively constant or can even fall dramatically in the athletes mentioned above. This . . . [Full Text of this Article]

Related Article:

Reactive Oxygen Species Impair Sympathetic Vasoregulation in Skeletal Muscle in Angiotensin II–Dependent Hypertension

Weiying Zhao, Scott A. Swanson, Jianfeng Ye, Xilong Li, John M. Shelton, Weiguo Zhang, and Gail D. Thomas
Hypertension 2006 48: 637-643. [Abstract] [Full Text] [PDF]