Extracellular bicarbonate and non-bicarbonate buffering against lactic acid during and after exercise

Defense of extracellular pH constancy against lactic acidosis can be estimated from changes (Δ) in lactic acid ([La]), [HCO ₃ ⁻ ], pH and PCO₂ in blood plasma because it is equilibrated with the interstitial fluid. These quantities were measured in earlobe blood during and after incremental bicycle exercise in 13 untrained (UT) and 21 endurance-trained (TR) males to find out if acute and chronic exercise influence the defense. During exercise the capacity of non-bicarbonate buffers (β_nbi = −Δ[La] · ΔpH⁻¹ − Δ[HCO ₃ ⁻ ] · ΔpH⁻¹) available for the extracellular fluid (mainly hemoglobin, dissolved proteins and phosphates) amounted to 32 ± 2(SEM) and 20 ± 2 mmol l⁻¹ in UT and TR, respectively (P < 0.02). During recovery β_nbi decreased to 14 (UT) and 12 (TR) mmol l⁻¹ (both P < 0.001) corresponding to values previously found at rest by in vivo CO₂ titration. Bicarbonate buffering (β_bi) amounted to 44–48 mmol l⁻¹ during and after exercise. The large exercise β_nbi seems to be mainly caused by an increasing concentration of all buffers due to shrinking of the extracellular volume, exchange of small amounts of HCO ₃ ⁻ or H⁺ with cells and delayed HCO ₃ ⁻ equilibration between plasma and interstitial fluid. Increase of [HCO ₃ ⁻ ] during titration by these mechanisms augments total β and thus the calculated β_nbi more than β_bi because it reduces ΔpH and Δ[HCO ₃ ⁻ ] at constant Δ[La]. The smaller rise in exercise β_nbi in TR than UT may be caused by an increased extracellular volume and an improved exchange of La⁻, HCO ₃ ⁻ and H⁺ between trained muscles and blood.