title: Interaction between the ventilatory and cerebrovascular responses to hypo- and hypercapnia at rest and during exercise.
abstract: 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 (VE) relation shifted to higher VE and P(a,CO(2)) 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.
authors.affiliation: Department of Integrative Physiology, University of North Texas Health Science Center, 3500 Camp Bowie Boulevard, Fort Worth, TX 76107, USA. sogoh@hsc.unt.edu
authors.forename: Shigehiko
authors.initials: S
authors.lastname: Ogoh
authors.forename: Naoyuki
authors.initials: N
authors.lastname: Hayashi
authors.forename: Masashi
authors.initials: M
authors.lastname: Inagaki
authors.forename: Philip N
authors.initials: PN
authors.lastname: Ainslie
authors.forename: Tadayoshi
authors.initials: T
authors.lastname: Miyamoto
mesh_terms: D001921:Brain / Q000098:blood supply*; D015444:Exercise / Q000502:physiology*; D006801:Humans; D006935:Hypercapnia / Q000378:metabolism*; D016857:Hypocapnia; D008297:Male; D010100:Oxygen / Q000378:metabolism; D055815:Young Adult
chemical_list: D010100:Oxygen