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

This study investigated trans-cerebral internal jugular venous-arterial bicarbonate ([HCO]) and carbon dioxide tension (PCO) exchange utilizing two separate interventions to induce acidosis: 1) acute respiratory acidosis via elevations in arterial PCO (PaCO) (n = 39); and 2) metabolic acidosis via incremental cycling exercise to exhaustion (n = 24). During respiratory acidosis, arterial [HCO] by 0.15 ± 0.05 mmol ⋅ l per mmHg elevation in PaCO across a wide physiological range (35 to 60 mmHg PaCO; P < 0.001). The of the venous-arterial [HCO] and PCO 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] exchange (CBF × venous-arterial [HCO] difference) was reduced indicating a shift from net release toward net uptake of [HCO] (P = 0.004). Arterial [HCO] was by -0.48 ± 0.15 mmol ⋅ l per nmol ⋅ l increase in arterial [H] with exercise-induced acidosis (P < 0.001). There was no relationship between the venous-arterial [HCO] difference and arterial [H] with exercise-induced acidosis or CBF; therefore, trans-cerebral [HCO] 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] - during acute respiratory/exercise-induced metabolic acidosis, respectively - differentially affect cerebrovascular acid-base balance (via trans-cerebral [HCO] exchange).