It has been concluded from comparisons of base excess (BE) and lactic acid (La) concentration changes in blood during exercise-induced acidosis that more H+ than La- leave the muscle and enter interstitial fluid and blood. To examine this, we performed incremental cycle tests in 13 untrained males and measured acid-base status and [La] in arterialized blood, plasma, and red cells until 21 min after exhaustion. The decrease of actual BE (-deltaABE) was 2.2 +/- 0.5 (SEM) mmol l(-1) larger than the increase of [La]blood at exhaustion, and the difference rose to 4.8 +/- 0.5 mmol l(-1) during the first minutes of recovery. The decrease of standard BE (SBE), a measure of mean BE of interstitial fluid (if) and blood, however, was smaller than the increase of [La] in the corresponding volume (delta[La](if+blood)) during exercise and only slightly larger during recovery. The discrepancy between -deltaABE and delta[La]blood mainly results from the Donnan effect hindering the rise of [La]erythrocyte to equal values like [La]plasma. The changing Donnan effect during acidosis causes that Cl- from the interstitial fluid enter plasma and erythrocytes in exchange for HCO3(-). A corresponding amount of La- remains outside the blood. SBE is not influenced by ion shifts among these compartments and therefore is a rather exact measure of acid movements across tissue cell membranes, but changes have been compared previously to delta[La]blood instead to delta[La](if+blood). When performing correct comparisons and considering Cl-/HCO3(-) exchange between erythrocytes and extracellular fluid, neither the use of deltaABE nor of deltaSBE provides evidence for differences in H+ and La- transport across the tissue cell membranes.

Defense of extracellular pH constancy against lactic acidosis can be estimated from changes (Delta) in lactic acid ([La]), [HCO(3)(-)], pH and PCO(2) 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 (beta(nbi) = -Delta[La] . DeltapH(-1) - Delta[HCO(3)(-)] . DeltapH(-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 beta(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 CO(2) titration. Bicarbonate buffering (beta(bi)) amounted to 44-48 mmol l(-1) during and after exercise. The large exercise beta(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 beta and thus the calculated beta(nbi) more than beta(bi) because it reduces DeltapH and Delta[HCO(3)(-)] at constant Delta[La]. The smaller rise in exercise beta(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.

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