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This Article Full Text Full Text (PDF) All Versions of this Article: 295/4/H1794    most recent 131.2008v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Hunt, B. E. Articles by Weiss, J. W. Search for Related Content PubMed PubMed Citation Articles by Hunt, B. E. Articles by Weiss, J. W.

Baroreflex responsiveness during ventilatory acclimatization in humans

¹Department of Kinesiology, School of Public Health and Health Sciences, University of Massachusetts, Amherst, Massachusetts; ²Pulmonary and Sleep Research Laboratory, Division of Pulmonary, Critical Care and Sleep Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts; and ³Laboratoire du Sommeil, Laboratoire HP2 (Hypoxie PathoPhysiologie), Centre Hospitalier Universitaire de Grenoble, Grenoble, France

Submitted 7 February 2008 ; accepted in final form 25 August 2008

We tested the hypothesis that the decline in muscle sympathetic activity during and after 8 h of poikilocapnic hypoxia (Hx) was associated with a greater sympathetic baroreflex-mediated responsiveness. In 10 healthy men and women (n = 2), we measured beat-to-beat blood pressure (Portapres), carotid artery distension (ultrasonography), heart period, and muscle sympathetic nerve activity (SNA; microneurography) during two baroreflex perturbations using the modified Oxford technique before, during, and after 8 h of hypoxia (84% arterial oxygen saturation). The integrated baroreflex response [change of SNA (SNA)/change of diastolic blood pressure (DBP)], mechanical (diastolic diameter/DBP), and neural (SNA/diastolic diameter) components were estimated at each time point. Sympathetic baroreflex responsiveness declined throughout the hypoxic exposure and further declined upon return to normoxia [pre-Hx, –8.3 ± 1.2; 1-h Hx, –7.2 ± 1.0; 7-h Hx, –4.9 ± 1.0; and post-Hx: –4.1 ± 0.9 arbitrary integrated units (AIU)·min^–1·mmHg^–1; P < 0.05 vs. previous time point for 1-h, 7-h, and post-Hx values]. This blunting of baroreflex-mediated efferent outflow was not due to a change in the mechanical transduction of arterial pressure into barosensory stretch. Rather, the neural component declined in a similar pattern to that of the integrated reflex response (pre-Hx, –2.70 ± 0.53; 1-h Hx, –2.59 ± 0.53; 7-h Hx, –1.60 ± 0.34; and post-Hx, –1.34 ± 0.27 AIU·min^–1·µm^–1; P < 0.05 vs. pre-Hx for 7-h and post-Hx values). Thus it does not appear as if enhanced baroreflex function is primarily responsible for the reduced muscle SNA observed during intermediate duration hypoxia. However, the central transduction of baroreceptor afferent neural activity into efferent neural activity appears to be reduced during the initial stages of peripheral chemoreceptor acclimatization.

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