Premium
Acid‐Base Compensation During Incremental Ascent to High Altitude
Author(s) -
Zouboules Shaelynn M.,
Nysten Heidi,
Brutsaert Tom,
Nysten Cassandra,
O'Halloran Ken D.,
Steinback Craig D.,
Sherpa Mingma,
Day Trevor A.
Publication year - 2018
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2018.32.1_supplement.909.2
Subject(s) - effects of high altitude on humans , hypocapnia , acetazolamide , respiratory alkalosis , base excess , alkalosis , acid–base homeostasis , respiratory compensation , bicarbonate , metabolic alkalosis , respiratory acidosis , acidosis , hypoxic ventilatory response , altitude (triangle) , chemistry , medicine , respiratory system , metabolic acidosis , hypercapnia , anaerobic exercise , anatomy , physiology , geometry , mathematics
Ascent to high altitude, and the associated hypoxic ventilatory response, imposes an acid‐base challenge, namely chronic hypocapnia and respiratory alkalosis. The kidneys act to compensate for this respiratory alkalosis via bicarbonate (HCO 3 − ) excretion in urine to induce a compensatory metabolic acidosis. Although the importance of renal responsiveness through acid‐base modifications is well‐defined, the time course and extent of plasticity in this response during incremental ascent to altitude is unclear. Thus, we developed a practical index of renal reactivity (RR), indexing the relative change in arterial HCO 3 − concentration ([HCO 3 − ] a ; i.e., response) against the relative change in arterial partial pressure of CO 2 (PaCO 2 ; i.e., stimulus) during incremental ascent to high altitude (RR=Δ[HCO 3 − ] a /ΔPaCO 2 ). We sought to assess (1) if RR increased over time and with incremental ascent to high altitude and (2) if RR was correlated with relative changes in arterial pH (ΔpH a ) throughout ascent. During ascent to 5160 m over 10 days in the Nepal Himalaya, arterial blood was drawn from the radial artery for measurement of acid‐base variables (Abbott i‐STAT portable blood gas/electrolyte analyzer; CG4+ and CHEM8+ cartridges) in lowlanders at 1045/1400 m (baseline) and at four different altitudes following one‐night sleep: 3440 m (n=18), 3820 m (n=17), 4370 m (n=15) and 5160 m (n=13). At 3820 m (day five of altitude exposure) and higher, RR significantly increased and plateaued in comparison to 3440 m (day three of altitude exposure; P<0.04), suggesting plasticity in renal acid‐base compensation. At all four altitudes, we observed a strong correlation (range: r=−0.71 to −0.98; P<0.001) between RR and relative ΔpH a from baseline, suggesting that the RR index accurately quantified acid‐base responsiveness via renal mechanisms throughout ascent. In conclusion, renal acid‐base compensation mechanisms demonstrate plasticity and a unique time course during incremental ascent to high altitude, which was detected using a novel RR index. The extent of plasticity and plateau in renal responsiveness may predict severity of altitude illness or acclimatization at higher or more prolonged stays at altitude. Support or Funding Information This work was supported by (a) Alberta Government Student Temporary Employment Program, (b) Alberta Innovates Health Solutions Summer Studentship, and (c) Natural Sciences and Engineering Research Council of Canada Discovery grant. This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .