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J Appl Physiol 105: 361, 2008; doi:10.1152/japplphysiol.00162.2008b
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POINT-COUNTERPOINT

Rebuttal from Drs. Böning and Maassen

Besides our criticism concerning SID we disagree with the following Counterpoint statements (6). First, "...arterial blood does not provide an ‘average’ representation of acid-base balance within the body." Concentration differences in venous outflow from organs are averaged in mixed venous blood being representative for 90% of the blood. After lung passage blood composition is unchanged except for gases since lung cell and interstitial volumes are too small to exert measurable effects on electrolytes. Therefore arterial blood represents nonrespiratory acid-base changes in blood, but of course not in the body.

Concerning BE we are astonished about some arguments since we have clearly discerned (1) in vitro (actual, ABE) and in vivo (standard, SBE) conditions. The BE concept is determination of added fixed acid by back-titration to pH 7.4 at constant PCO2 and O2 saturation using buffer values of blood with actual [Hb] (ABE) or diluted with interstitial fluid (assumed [Hb] 5 g/dl, SBE). This includes normal [2,3-diphosphoglycerate], which is constant during short exercise (4). Under pure in vitro conditions titration with lactic acid yields equal changes ({Delta}) of [La]blood and ABE (1, 3). When applying ABE to arterialized blood during exercise deviations of PCO2 from 40 mmHg are small, calculation errors for this effect being negligible. Not considered are changes in plasma [protein] and [phosphate] but this error is small. [Protein] increases by fluid shift to tissues even cause alkalosis (5), not acidosis (6) at constant PCO2.

The SBE concept has been confirmed by in vivo CO2 titrations (reviewed in Ref. 2). When calculating exercise-induced {Delta}SBE, changes of [Hb] are not considered, but deviations are not important for calculation. Therefore our results [near equality between –{Delta}ABE and {Delta}[La] + {Delta} [Cl–] in blood as well as between –{Delta}SBE and the average of {Delta}[La] in blood and interstitial fluid after exhaustion (1)] are not coincidental but evidence of lactic acid as cause of nonrespiratory acidosis. During exercise the effect of extracellular volume shrinking on [HCO3–] is additionally mirrored in changes of ABE and SBE.

The statement on nonexistence of the Donnan equilibrium holds only for cations. The Donnan equilibrium is an electrochemical equilibrium. In contrast to active cation pumps passive transporters like Cl– HCO3– exchangers or La– H+ cotransporters as well as enzymes (carboanhydrases) do not change the equilibrium but only shorten the time for regaining it after disturbances. For La– this lasts minutes and is often completed only during recovery (1).

REFERENCES

  1. Böning D, Klarholz C, Himmelsbach B, Hütler M, Maassen N. Causes of differences in exercise-induced changes of base excess and blood lactate. Eur J Appl Physiol 99: 163–171, 2007.[CrossRef][Web of Science][Medline]
  2. Böning D, Klarholz C, Himmelsbach B, Hütler M, Maassen N. Extracellular bicarbonate and non-bicarbonate buffering against lactic acid during and after exercise. Eur J Appl Physiol 100: 457–467, 2007.[CrossRef][Web of Science][Medline]
  3. Böning D, Maassen N. Blood osmolality in vitro: dependence on PCO2, lactic acid concentration, and O2 saturation. J Appl Physiol Respir 54: 118–122, 1983.
  4. Braumann KM, Böning D, Trost F. Bohr effect and slope of the oxygen dissociation curve after physical training. J Appl Physiol Respir Environ Exerc Physiol 52: 1524–1529, 1982.[Abstract/Free Full Text]
  5. Lang W, Zander R. Prediction of dilutional acidosis based on the revised classical dilution concept for bicarbonate. J Appl Physiol 98: 62–71, 2005.[Abstract/Free Full Text]
  6. Lindinger MI, Heigenhauser GJF. Counterpoint: Lactic acid is not the only physicochemical contributor to the acidosis of exercise. J Appl Physiol; doi:10.1152/japplphysiol.00162.2008a.[Free Full Text]




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