Interaction between the ventilatory and cerebrovascular responses to hypo- and hypercapnia at rest and during exercise

Cerebrovascular reactivity to changes in the partial pressure of arterial carbon dioxide (P(a,CO2)) via limiting changes in brain [H(+)] modulates ventilatory control. It remains unclear, however, how exercise-induced alterations in respiratory chemoreflex might influence cerebral blood flow (CBF), in particular the cerebrovascular reactivity to CO(2). The respiratory chemoreflex system controlling ventilation consists of two subsystems: the central controller (controlling element), and peripheral plant (controlled element). In order to examine the effect of exercise-induced alterations in ventilatory chemoreflex on cerebrovascular CO(2) reactivity, these two subsystems of the respiratory chemoreflex system and cerebral CO(2) reactivity were evaluated (n = 7) by the administration of CO(2) as well as by voluntary hypo- and hyperventilation at rest and during steady-state exercise. During exercise, in the central controller, the regression line for the P(a,CO2)-minute ventilation ((V) over dot(E)) relation shifted to higher (V) over dot(E) and P(a,CO2) with no change in gain (P = 0.84). The functional curve of the peripheral plant also reset rightward and upward during exercise. However, from rest to exercise, gain of the peripheral plant decreased, especially during the hypercapnic condition (-4.1 +/- 0.8 to -2.0 +/- 0.2 mmHg l(-1) min(-1), P = 0.01). Therefore, under hypercapnia, total respiratory loop gain was markedly reduced during exercise (-8.0 +/- 2.3 to -3.5 +/- 1.0 U, P = 0.02). In contrast, cerebrovascular CO(2) reactivity at each condition, especially to hypercapnia, was increased during exercise (2.4 +/- 0.2 to 2.8 +/- 0.2% mmHg(-1), P = 0.03). These findings indicate that, despite an attenuated chemoreflex system controlling ventilation, elevations in cerebrovascular reactivity might help maintain CO(2) homeostasis in the brain during exercise.