Karlman Wasserman, William L Beaver, Xing-Guo Sun, William Stringer
Resting arterial H+ concentration ([H+]a) is in the nanomolar range (40+/-2 nm/L) while its production is in the millimolar range/min, with little variation from subject to subject. To determin the precision with which [H+]a is regulated during exercise, [H+]a, PaCO2 and ventilation (Ve) were measured during progressively increasing work rate exercise in 16 normal subjects. (Ve) increased with [H+]a, the latter attributable to PaCO2 increase below the lactic acidosis threshold (LAT) (DVe/D[H+]a ~15 L min-1 nanomol-1). [H+]a and PaCO2 increased, simultaneously, as work rate was increased below LAT. PaCO2 reversed direction of change between LAT and ventilatory compensation point (VCP). Above LAT, [H+]a increase relative to (Ve) increase was greater than below LAT. PaCO2 decreased above the LAT, while [H+]a continued to increase. Thus the exercise acidosis was converted from respiratory, below, to a metabolic, above the LAT. We conclude that [H+]a is increased and regulated over the full range of exercise, but with less sensitivity above the LAT.
Respiratory Physiology & Neurobiology 178 (2011) 191-195