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Original Research: Pulmonary Vascular Disease |

Chemoreceptor Responsiveness at Sea Level Does Not Predict the Pulmonary Pressure Response to High AltitudePulmonary Artery Pressure at High Altitude

Ryan L. Hoiland, BHK; Glen E. Foster, PhD; Joseph Donnelly, MBChB; Mike Stembridge, MSc; Chris K. Willie, PhD; Kurt J. Smith, MSc; Nia C. Lewis, PhD; Samuel J. E. Lucas, PhD; Jim D. Cotter, PhD; David J. Yeoman, BSc; Kate N. Thomas, BSc; Trevor A. Day, PhD; Mike M. Tymko, BHSc; Keith R. Burgess, MD; Philip N. Ainslie, PhD
Author and Funding Information

From the Centre for Heart, Lung and Vascular Health (Messrs Hoiland, Smith, and Tymko and Drs Foster, Willie, Lewis, and Ainslie), School of Health and Exercise Sciences, University of British Columbia–Okanagan, Kelowna, BC, Canada; Division of Neurosurgery (Dr Donnelly), Department of Clinical Neuroscience, University of Cambridge, Cambridge, England; Department of Physiology (Drs Donnelly and Lucas and Ms Thomas) and School of Physical Education (Drs Lucas and Cotter), Sport and Exercise Sciences, University of Otago, Dunedin, New Zealand; Cardiff School of Sport (Mr Stembridge), Cardiff Metropolitan University, Cardiff, Wales; School of Sport, Exercise and Rehabilitation Sciences (Dr Lucas), University of Birmingham, Birmingham, England; Department of Cardiology (Mr Yeoman), Dunedin School of Medicine, University of Otago, Dunedin, New Zealand; Department of Biology (Dr Day), Faculty of Science and Technology, Mount Royal University, Calgary, AB, Canada; and Peninsula Sleep Laboratory (Dr Burgess) and Department of Medicine (Dr Burgess), University of Sydney, Sydney, NSW, Australia.

CORRESPONDENCE TO: Ryan L. Hoiland, BHK, Centre for Heart, Lung and Vascular Health, School of Health and Exercise Sciences, University of British Columbia–Okanagan, 3333 University Way, Kelowna, BC, V1V 1V7, Canada; e-mail: ryanleohoiland@gmail.com


FUNDING/SUPPORT: These studies were carried out within the framework of the Ev-K2-CNR Project in collaboration with the Nepal Academy of Science and Technology as foreseen by the memorandum of understanding between Nepal and Italy and contributions from the Italian National Research Council. The work in this project was supported by a Canada Research Chair, a Natural Sciences and Engineering Research Council of Canada (NSERC) Discovery Grant, the Otago Medical Research Foundation, and the Department of Physiology (University of Otago). Dr Willie is supported by a Vanier Canada graduate scholarship, and Ms Thomas and Mr Smith are supported by the NSERC Alexander Graham Bell Canada Graduate Scholarship and Heart and Stroke Foundation of Canada doctoral and postdoctoral fellowship, respectively. Dr Donnelly is supported by a Woolf Fisher scholarship.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians. See online for more details.


Chest. 2015;148(1):219-225. doi:10.1378/chest.14-1992
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BACKGROUND:  The hypoxic ventilatory response (HVR) at sea level (SL) is moderately predictive of the change in pulmonary artery systolic pressure (PASP) to acute normobaric hypoxia. However, because of progressive changes in the chemoreflex control of breathing and acid-base balance at high altitude (HA), HVR at SL may not predict PASP at HA. We hypothesized that resting oxygen saturation as measured by pulse oximetry (Spo2) at HA would correlate better than HVR at SL with PASP at HA.

METHODS:  In 20 participants at SL, we measured normobaric, isocapnic HVR (L/min · −%Spo2−1) and resting PASP using echocardiography. Both resting Spo2 and PASP measures were repeated on day 2 (n = 10), days 4 to 8 (n = 12), and 2 to 3 weeks (n = 8) after arrival at 5,050 m. These data were also collected at 5,050 m in life-long HA residents (ie, Sherpa [n = 21]).

RESULTS:  Compared with SL, Spo2 decreased from 98.6% to 80.5% (P < .001), whereas PASP increased from 21.7 to 34.0 mm Hg (P < .001) after 2 to 3 weeks at 5,050 m. Isocapnic HVR at SL was not related to Spo2 or PASP at any time point at 5,050 m (all P > .05). Sherpa had lower PASP (P < .01) than lowlanders on days 4 to 8 despite similar Spo2. Upon correction for hematocrit, Sherpa PASP was not different from lowlanders at SL but was lower than lowlanders at all HA time points. At 5,050 m, although Spo2 was not related to PASP in lowlanders at any point (all R2 ≤ 0.05, P > .50), there was a weak relationship in the Sherpa (R2 = 0.16, P = .07).

CONCLUSIONS:  We conclude that neither HVR at SL nor resting Spo2 at HA correlates with elevations in PASP at HA.

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