Ryan L Hoiland1, Glen E Foster2, Joseph Donnelly3, Mike Stembridge2, Chris K Willie2, Kurt J Smith2, Nia C Lewis2, Samuel J E Lucas4, Jim D Cotter5, David J Yeoman6, Kate N Thomas7, Trevor A Day8, Mike M Tymko2, Keith R Burgess9, Philip N Ainslie2. 1. Centre for Heart, Lung and Vascular Health, School of Health and Exercise Sciences, University of British Columbia-Okanagan, Kelowna, BC, Canada. Electronic address: ryanleohoiland@gmail.com. 2. Centre for Heart, Lung and Vascular Health, School of Health and Exercise Sciences, University of British Columbia-Okanagan, Kelowna, BC, Canada. 3. Division of Neurosurgery, Department of Clinical Neuroscience, University of Cambridge, Cambridge, England; Department of Physiology, Sport and Exercise Sciences, University of Otago, Dunedin, New Zealand. 4. Department of Physiology, Sport and Exercise Sciences, University of Otago, Dunedin, New Zealand; School of Physical Education, Sport and Exercise Sciences, University of Otago, Dunedin, New Zealand; School of Physical Education, Sport and Exercise Sciences, University of Otago, Dunedin, New Zealand; School of Sport, Exercise and Rehabilitation Sciences, University of Birmingham, Birmingham, England. 5. School of Physical Education, Sport and Exercise Sciences, University of Otago, Dunedin, New Zealand. 6. Department of Cardiology, Dunedin School of Medicine, University of Otago, Dunedin, New Zealand. 7. Department of Physiology, Sport and Exercise Sciences, University of Otago, Dunedin, New Zealand. 8. Department of Biology, Faculty of Science and Technology, Mount Royal University, Calgary, AB, Canada. 9. Cardiff School of Sport (Mr Stembridge), Cardiff Metropolitan University, Cardiff, Wales; Peninsula Sleep Laboratory, University of Sydney, Sydney, NSW, Australia; Department of Medicine, University of Sydney, Sydney, NSW, Australia.
Abstract
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.
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.
Authors: Marzieh Fatemian; Mari Herigstad; Quentin P P Croft; Federico Formenti; Rosa Cardenas; Carly Wheeler; Thomas G Smith; Maria Friedmannova; Keith L Dorrington; Peter A Robbins Journal: J Physiol Date: 2015-06-05 Impact factor: 5.182
Authors: Christopher K Willie; Michael Stembridge; Ryan L Hoiland; Michael M Tymko; Joshua C Tremblay; Alexander Patrician; Craig Steinback; Jonathan Moore; James Anholm; Prajan Subedi; Shailesh Niroula; Chris J McNeil; Ali McManus; David B MacLeod; Philip N Ainslie Journal: PLoS One Date: 2018-10-31 Impact factor: 3.240