Trans-cerebral HCO 3 - and PCO 2 exchange during acute respiratory acidosis and exercise-induced metabolic acidosis in humans.

This study investigated trans-cerebral internal jugular venous-arterial bicarbonate ([HCO 3 - ]) and carbon dioxide tension (PCO 2 ) exchange utilizing two separate interventions to induce acidosis: 1) acute respiratory acidosis via elevations in arterial PCO 2 (PaCO 2 ) (n = 39); and 2) metabolic acidosis via incremental cycling exercise to exhaustion (n = 24). During respiratory acidosis, arterial [HCO 3 - ] increased by 0.15 ± 0.05 mmol ⋅ l -1 per mmHg elevation in PaCO 2 across a wide physiological range (35 to 60 mmHg PaCO 2 ; P < 0.001). The narrowing of the venous-arterial [HCO 3 - ] and PCO 2 differences with respiratory acidosis were both related to the hypercapnia-induced elevations in cerebral blood flow (CBF) (both P < 0.001; subset n = 27); thus, trans-cerebral [HCO 3 - ] exchange (CBF × venous-arterial [HCO 3 - ] difference) was reduced indicating a shift from net release toward net uptake of [HCO 3 - ] (P = 0.004). Arterial [HCO 3 - ] was reduced by -0.48 ± 0.15 mmol ⋅ l -1 per nmol ⋅ l -1 increase in arterial [H + ] with exercise-induced acidosis (P < 0.001). There was no relationship between the venous-arterial [HCO 3 - ] difference and arterial [H + ] with exercise-induced acidosis or CBF; therefore, trans-cerebral [HCO 3 - ] exchange was unaltered throughout exercise when indexed against arterial [H + ] or pH (P = 0.933 and P = 0.896, respectively). These results indicate that increases and decreases in systemic [HCO 3 - ] - during acute respiratory/exercise-induced metabolic acidosis, respectively - differentially affect cerebrovascular acid-base balance (via trans-cerebral [HCO 3 - ] exchange).