Ventilatory regulation of arterial H(+) (pH) during exercise

Abstract

We hypothesized that exercise ventilation and arterial H(+) ([H(+)]a) are mutually interactive, [H(+)]a stimulating V(E) and V(E) regulating [H(+)]a increase. Fifty-five patients were studied, 10 normal and 45 with cardio-respiratory disorders. Each patient underwent cardiopulmonary exercise testing with simultaneous serial arterial blood gas and pH measurements. Subsequently, they were classified into one of 7 clinical groups: (1) normal, (2) exercise-induced hypoxemia (PaO2<50mmHg), (3) exercise-induced myocardial ischemia, (4) heart failure, (5) COPD, (6) interstitial lung disease, and (7) pulmonary vasculopathy. The average resting pHa was 7.42 or 7.43 for each group. At anaerobic (lactic acidosis) threshold (AT), [H(+)]a increased due to PaCO2 increase (+2mmHg), primarily. At peak exercise, [H(+)]a increased further due to arterial HCO3(-) decrease. In summary, [H(+)]a appears to be closely regulated at rest to AT and further to peak exercise by CO2 elimination from the venous return. No evidence was observed for over-ventilation of CO2, causing the arterial blood to become more alkaline during exercise in the patient groups studied.

Keywords: Acid–base regulation; Arterial pH; Exercise; Hypoxemia; Physiological dead space/tidal volume ratio; Ventilation–arterial H(+) interaction.