The effect of chronic metabolic acidosis and alkalosis on ventilation during exercise and hypoxia

Abstract

Resting and exercise ventilation (Pl O 2 = 95, 150, and 400 mm Hg) were measured on 3 healthy young men during 6 chronic acid-base conditions: I) normal, 2) metabolic acidosis (5–7 days), 3) metabolic alkalosis (5–7 days), 4) chronic hypoxia (Pl O 2 = 95 for 64 hr and, 5) and 6) chronic hypoxia super-imposed on chronic metabolic acidosis and alkalosis. After 5–7 days of metabolic acidosis, all resting and exercise ventilations were uniformly increased 20%, above normal pH conditions (ΔpHa=0.1, ΔPa CO 2 = 6 mm Hg). On the other hand, after 5–7 days of metabolic alkalosis, ventilation was reduced slightly from normal (ΔpHa=0.04, ΔPa CO 2 = 3 mm Hg). After 64 hr of normal chronic hypoxia, ventilation was uniformly increased 20 % above control (ΔPa CO 2 = 5–7 mm Hg). When chronic hypoxia was super-imposed on metabolic acidosis and/or alkalosis, there was a slightly greater ventilatory change than during normal chronic hypoxia (2 mm Hg greater Pa CO 2 reduction). Two specific findings were discussed. Firstly, the exercise stimulus to ventilation interacted with the H +, the acute hypoxia, and the chronic hypoxia stimuli. One observed consequence of the interaction was arterial pH homeostasis between each rest and work condition. Secondly, ventilation was the same during 3 specific conditions: a) chronic hypoxia superimposed on metabolic alkalosis (pHa=7.480), b) normal chronic hypoxia (pHa = 7.409) and c) axute hypoxia during metabolic acidosis (pHa = 7.301). According to current theories on regulation of ventilation, cerebral spinal fluid (CSF) pH would have been relatively most acid during condition (a). If this conclusion is correct, then chronic hypoxia must disrupt the normal relationship between arterial and CSF pH during chronic metabolic acidosis and alkalosis.