Good bye "lactic acid"; hello lactate and acid.

TO THE EDITOR: I benefited from reading this Point:Counterpoint discussion (2, 3) and some of the papers cited therein and was shocked to learn that the construct of “lactic acidosis” has been questioned before (4). However, it is clear (from Ref. 1) that the reduction of pyruvate to lactate consumes two protons, and as Robergs et al. (4) have said, the production of lactate retards the development of acidosis and is definitely not the cause of it. My renewed understanding is that the proximate cause of metabolic acidosis in cells is a decline in ratio of [ATP] to [ADP] in the face of normal levels of ATP. Under anerobic conditions accompanied by a declining energy charge, the production of lactate is a homeostatic mechanism serving to regenerate NAD so that glycolysis can continue to energize the cell. I am uncomfortable continuing to use the term “lactic acidosis” just because the development of acidosis from ATP hydrolysis and the rise in cellular lactate is temporally aligned. As Robergs et al. (4) have noted, it is also clear why muscle pH does not drop during anerobic exercise in patients with McArdle’s disease (5); because less ATP is produced, the amount of acid generated is also less. One would also expect that the arguments raised by Robergs (4) apply equally to entities such as “ketoacidosis”—the formation of ketoacid anions is a response to falling energy charge and is not certainly the actual cause of acidosis.