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J Appl Physiol 105: 1692, 2008; doi:10.1152/japplphysiol.zdg-8198.2008
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LETTER TO THE EDITOR

Comments on Baker et al.'s "Quantitative analysis of serum sodium concentration after prolonged running in the heat"

TO THE EDITOR: Baker et al. (1) tested the Nguyen-Kurtz equation's (4) predictive powers for serum [Na]. Briefly, the N-K equation is a mass-balance approach to predicting changes in serum [Na]. Given a starting serum [Na] and total body water and then accounting for changes in body water, sodium, and potassium, a new serum sodium concentration can be predicted. Interestingly, Baker et al. found that the changes in serum [Na] were less than predicted when serum [Na] both increased and decreased. An explanation for such "damping" can be found in the original Edelman et al. (2) equation. This observationally based equation had serum sodium concentration equal to the sum of exchangeable sodium and potassium divided by total body water, minus a term to which Edelman et al. gave the numerical value of 23.8 meq/l. Edelman et al. thought that this term represented the store of osmotically inactive sodium. Recent studies (4, 10) in which addition of significant quantities of sodium did not change either body water or osmolality have led Titze et al. (9, 10) to further investigate osmotic activation and inactivation of sodium. Titze et al. found that for rats, skin is a reservoir for osmotically inactive sodium (9). On the basis of studies of athletes for whom mass balance of water and sodium can be estimated, with both normal and hyponatremic values for serum [Na], Noakes et al. (6) proposed that osmotic activation and inactivation are part of homeostatic control that buffers changes in serum sodium concentration during prolonged exercise. Baker et al.'s findings may represent the first demonstration of osmotic activation and inactivation in controlled experimental conditions.

On a separate point, Baker et al. conclude that their findings do not support the idea that if weight is maintained in endurance exercise, body water has increased. A combination of three factors accounts for body water increase when weight is maintained: oxidation (without replacement) of fuel (3); water produced by oxidation of fuel (0.6 g water for every g carbohydrate oxidized) (7); and release of water complexed to stored glycogen (8). Under the conditions of this experiment, none of these factors is expected to be significant. The fuel required to complete the 18-km run in the trial, plus additional run to exhaustion (maximum, an extra 5–6 km) is ~1,200 kcal, or ~250 g CHO (3). The water produced in such oxidation, at the rate of 0.6 g water/g CHO, is ~150 g (0.150 liters). Regarding the release of glycogen-complexed water, this is expected to be significant only when a sufficient amount of stored glycogen is consumed. Unless the subjects tapered and purposefully loaded glycogen, this seems unlikely. Thus their experiments were inadequate to test the hypothesis that weight maintenance means addition of body water. Experiments in which more work is performed are required to test this hypothesis.

FOOTNOTES


Address for reprint requests and other correspondence: L. B. Weschler, 161 Richdale Rd., Colts Neck, NJ 07722 (e-mail: weschler1{at}verizon.net)

REFERENCES

  1. Baker LB, Lang JA, Kenney WL. Quantitative analysis of serum sodium concentration after prolonged running in the heat. J Appl Physiol 105: 91–99, 2008. First published May 1, 2008; doi:10.1152/japplphysiol.00130.2008.[Abstract/Free Full Text]
  2. Edelman IS, Leibman J, O'Meara MP, Birkenfeld LW. Interrelations between serum sodium concentration, serum osmolarity and total exchangeable sodium, total exchangeable potassium and total body water. J Clin Invest 37: 1236–1256, 1958.[Web of Science][Medline]
  3. Glace BW, Murphy CA, McHugh MP. Food intake and electrolyte status of ultramarathoners competing in extreme heat. J Am Coll Nutr 21: 553–559, 2002.[Abstract/Free Full Text]
  4. Heer M, Baisch F, Kropp J, Gerzer R, Drummer C. High dietary sodium chloride consumption may not induce body fluid retention in humans. Am J Physiol Renal Physiol 278: F585–F595, 2000.[Abstract/Free Full Text]
  5. Kurtz I, Nguyen MK. A simple quantitative approach to analyzing the generation of the dysnatremias. Clin Exp Nephrol 7: 138–143, 2003.[CrossRef][Medline]
  6. Noakes TD, Sharwood K, Speedy D, Hew T, Reid S, Dugas J, Almond C, Wharam P, Weschler L. Three independent biological mechanisms cause exercise-associated hyponatremia: evidence from 2,135 weighed competitive athletic performances. Proc Natl Acad Sci USA 102: 18550–18555, 2005.[Abstract/Free Full Text]
  7. Pivarnik JM, Leeds EM, Wilkerson JE. Effects of endurance exercise on metabolic water production and plasma volume. J Appl Physiol 56: 613–618, 1984.[Abstract/Free Full Text]
  8. Sherman WM, Plyley MJ, Sharp RL, Van Handel PJ, McAllister RM, Fink WJ, Costill DL. Muscle glycogen storage and its relationship with water. Int J Sports Med 3: 22–24, 1982.[Web of Science][Medline]
  9. Titze J, Lang R, Ilies C, Schwind KH, Kirsch KA, Dietsch P, Luft FC, Hilgers KF. Osmotically inactive skin Na+ storage in rats. Am J Physiol Renal Physiol 285: F1108–F1117, 2003.[Abstract/Free Full Text]
  10. Titze J, Maillet A, Lang R, Gunga HC, Johannes B, Gauquelin-Koch G, Kihm E, Larina I, Gharib C, Kirsch KA. Long-term sodium balance in humans in a terrestrial space station simulation study. Am J Kidney Dis 40: 508–516, 2002.[CrossRef][Web of Science][Medline]

Louise B. Weschler


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J Appl Physiol, November 1, 2008; 105(5): 1693 - 1693.
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