Time Course and Magnitude of Ventilatory and Renal Acclimatization Following Rapid Ascent and Residence to 3800m over Nine Days

Future Physiology 2020 (Virutal) (2020) Proc Physiol Soc 46, PC0136

Poster Communications: Time Course and Magnitude of Ventilatory and Renal Acclimatization Following Rapid Ascent and Residence to 3800m over Nine Days

Jordan Bird1, Glen Foster2, Caroline Rickards3, Jack Leacy4, David Burns4, Ken O'Halloran4, Nick Jendzjowsky5, Richard Wilson5, Craig Steinback6, Peter Ondrus6, Trevor Day1

1 Department of Biology, Faculty of Science and Technology, Mount Royal University, Calgary, Canada 2 Centre for Heart, Lung, and Vascular Health, School of Health and Exercise Sciences, University of British Columbia, Kelowna, Canada 3 Cerebral & Cardiovascular Physiology Laboratory, Department of Physiology & Anatomy, University of North Texas Health Science Center, Fort Worth, Texas, The United States of America 4 Department of Physiology, School of Medicine, College of Medicine and Health, University College Cork, Cork, Ireland 5 Hotchkiss Brain Institute, Cumming School of Medicine, University of Calgary, Calgary, Canada 6 Neurovascular Health Laboratory, Faculty of Kinesiology, Sport, and Recreation, University of Alberta, Edmonton, Canada

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Rapid ascent to high altitude imposes an acute hypoxia and acid-base challenge. Several interrelated acclimatization processes work to counter these perturbations, in part through ventilatory and renal systems. Specifically, a hypoxic ventilatory response (HVR) improves oxygenation, but elicits acute hypocapnia and respiratory alkalosis. In response, the kidney tubules eliminate bicarbonate, eliciting a compensatory relative metabolic acidosis, protecting arterial pH(a). However, the time course and magnitude of these acclimatization processes are highly variable between-individuals and between organ systems. Using a previously developed metric of renal reactivity (RR) that indexes the relative change in arterial bicarbonate concentration (∆[HCO3-]a; i.e., renal response) over the relative change in arterial pressure of CO2 (∆PaCO2; i.e., renal stimulus), we aimed to assess whether: (a) RR magnitude increased with duration at altitude and (b) whether RR was inversely correlated with relative changes in pH (∆pHa) with time spent at altitude. Resident lowlanders (n=16) were tested at 1045m (day 0) prior to ascent, and on days D2 and D9 upon arrival and during residence at 3800m. On days 0, 2 and 9, arterial blood draws from the radial artery were obtained to measure and/or calculate blood gas variables PaO2, [Hb], SaO2 and CaO2, and acid-base variables PaCO2, [HCO3-]a and pHa. RR increased from D2 to D9 (P=0.056), suggesting plasticity in renal acid-base compensatory mechanisms. We observed a strong negative correlation between RR and ∆pHa from baseline on D2 and D9 (r≤−0.95; P<0.00001). The high variability in blood gas and acid-base variables on D2 suggests three distinct phenotypes for how individuals acclimatize within the first 24 hours of altitude exposure: (a) no HVR, and thus no renal compensation, (b) HVR with no renal compensation and (c) HVR with renal compensation. Our study highlights the differential time course and magnitude of ventilatory and renal acclimatization following rapid ascent and residence at high altitude.



Where applicable, experiments conform with Society ethical requirements.

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