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,CO   2) 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,CO   2–minute ventilation relation shifted to higher and P   a,CO   2with 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.