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, PaCO2 and ventilation (V˙E) were measured during progressively increasing work rate exercise in 16 normal subjects. (V˙E) increased with [H+]a, the latter attributable to PaCO2 increase below the lactic acidosis threshold (LAT) (ΔV˙E/Δ[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 (V˙E) 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.

► Arterial hydrogen ion ([H+]a) is tightly regulated during exercise (nanomolar range). ► VE increases with increasing [H+]a maintaining homeostasis and minimizing pH change. ► Below lactic acidosis threshold (LAT), (V˙E) increased 15 L/min/nanomol [H+]a increase. ► Above LAT, (V˙E) of CO2 from aerobic metabolism and HCO3- buffering regulated [H+]a. ► Increased (V˙E) regulates [H+]a above and below LAT by controlled exhalation of CO2.