Extracellular pH defense against lactic acid in normoxia and hypoxia before and after a Himalayan expedition

Abstract

The extracellular pH defense against the lactic acidosis resulting from exercise can be estimated from the ratios −Δ[La] · ΔpH⁻¹ (where Δ[La] is change in lactic acid concentration and ΔpH is change in pH) and Δ[HCO₃ ⁻] · ΔpH⁻¹ (where Δ[HCO₃ ⁻] is change in bicarbonate concentration) in blood plasma. The difference between −Δ[La] · ΔpH⁻¹ and Δ[HCO₃ ⁻] · ΔpH⁻¹ yields the capacity of available non-bicarbonate buffers (mainly hemoglobin). In turn, Δ[HCO₃ ⁻] · ΔpH⁻¹ can be separated into a pure bicarbonate buffering (as calculated at constant carbon dioxide tension) and a hyperventilation effect. These quantities were measured in 12 mountaineers during incremental exercise tests before, and 7–8 days (group 1) or 11–12 days (group 2) after their return from a Himalayan expedition (2800–7600 m altitude) under conditions of normoxia and acute hypoxia. In normoxia −Δ[La] · ΔpH⁻¹ amounted to [mean (SEM)] 92 (6) mmol · l⁻¹ before altitude, of which 19 (4), 48 (1) and 25 (3) mmol · l⁻¹ were due to hyperventilation, bicarbonate and non-bicarbonate buffering, respectively. After altitude −Δ[La] · ΔpH⁻¹ was increased to 128 (12) mmol · l⁻¹ (P < 0.01) in group 1 and decreased to 72 (5) mmol · l⁻¹ in group 2 (P < 0.05), resulting mainly from apparent large changes of non-bicarbonate buffer capacity, which amounted to 49 (14) mmol · l⁻¹ in group 1 and to 10 (2) mmol · l⁻¹ in group 2. In acute hypoxia the apparent increase in non-bicarbonate buffers of group 1 was even larger [140 (18) mmol · l⁻¹]. Since the hemoglobin mass was only modestly elevated after descent, other factors must play a role. It is proposed here that the transport of La⁻ and H⁺ across cell membranes is differently influenced by high-altitude acclimatization.