Passive leg movement in chronic obstructive pulmonary disease: evidence of locomotor muscle vascular dysfunction

Author:

Ives Stephen J.123,Layec Gwenael12,Hart Corey R.12,Trinity Joel D.12,Gifford Jayson R.124,Garten Ryan S.125,Witman Melissa A. H.126,Sorensen Jacob R.4ORCID,Richardson Russell S.127

Affiliation:

1. Geriatric Research, Education, and Clinical Center, George E. Whalen Department of Veterans Affairs Medical Center, Salt Lake City, Utah

2. Division of Geriatrics, Department of Internal Medicine, University of Utah, Salt Lake City, Utah

3. Health and Human Physiological Sciences Department, Skidmore College, Saratoga Springs, New York

4. Department of Exercise Sciences, Brigham Young University, Provo, Utah

5. Department of Kinesiology and Health Sciences, Virginia Commonwealth University, Richmond, Virginia

6. Department of Kinesiology and Applied Physiology, University of Delaware, Wilmington, Delaware

7. Department of Nutrition and Integrative Physiology, University of Utah, Salt Lake City, Utah

Abstract

Utilizing both the single and continuous passive leg movement (PLM) models, which induce nitric oxide (NO)-dependent hyperemia, this study provides evidence of vascular dysfunction in the locomotor muscle of patients with chronic obstructive pulmonary disease (COPD), independent of central hemodynamics. This impaired hyperemia may be the result of an oxidant-mediated attenuation in NO bioavailability. In addition to clearly dysfunctional lungs, vascular dysfunction in locomotor muscle may contribute to the exercise intolerance associated with COPD and increased cardiovascular disease risk.

Funder

Office of Extramural Research, National Institutes of Health

U.S. Department of Veterans Affairs

Publisher

American Physiological Society

Subject

Physiology (medical),Physiology

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