Arterial H+ regulation during exercise in humans

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 determine the precision with which [H(+)]a is regulated during exercise, [H(+)]a, PaCO(2) and ventilation ((V) over dot(E))were measured during progressively increasing work rate exercise in 16 normal subjects. ((V) over dot(E)) increased with [H(+)]a, the latter attributable to PaCO(2) increase below the lactic acidosis threshold (LAT) (Delta(V) over dot(E)/Delta[H(+)]a approximate to 15 L min(-1) nanomol(-1)). [H(+)]a and PaCO(2) increased, simultaneously, as work rate was increased below LAT. PaCO(2) reversed direction of change between MT and ventilatory compensation point (VCP). Above LAT, [H(+)]a increase relative to ((V) over dot(E)) increase was greater than below MT. PaCO(2) 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. (C) 2011 Elsevier B.V. All rights reserved.