The effects of chronic acid loads in normal man: further evidence for the participation of bone mineral in the defense against chronic metabolic acidosis.

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Abstract
We carried out metabolic balance studies in 5 normal subjects to investigate the nature of the buffers utilized in the defense against chronic NH4Cl acidosis and to determine the mechanisms responsible for the ultimate disposal of the administered acid. Initially, as in studies of acute metabolic acidosis, acid was retained and appeared to titrate extra- and intracellular buffer systems. As acid retention continued, intracellular and bone buffers and, finally, bone mineral alone, appeared to provide additional buffer reserves. When the acid load was stopped, extra- and intracellular buffers appeared to be promptly restored, but less than 1/3 the observed Ca losses were replaced during observations that lasted as long as 42 days after NH4Cl loading was stopped. The constant whole food diets used in these experiments provided a significant quantity of potential alkali as combustible anions, and during acid loading the fecal excretion of organic anions declined significantly. During NH4Cl loading, net fixed acid producion was increased by an average of 3,425 meq. Most of this acid load was excreted by the kidneys, but at the end of 12 recovery days an average of 193 meq of the acid fed had not been excreted in the urine, despite the return of the serum HCO3- to stable control levels. The simultaneous Ca balances averaged -185 meq, supporting the previous suggestion that bone mineral is an important buffer reservoir in the defense against chronic metabolic acidosis.

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