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Cardiovascular and cerebrovascular responses to acute isocapnic and poikilocapnic hypoxia in humans

Departments of Physiology and Biophysics and Clinical Neurosciences, Hotchkiss Brain Institute and the Libin Cardiovascular Institute, Faculty of Medicine and Faculty of Kinesiology, University of Calgary, Calgary, Alberta, Canada

Submitted 22 May 2007 ; accepted in final form 19 November 2007

We examined the cardiovascular and cerebrovascular responses to acute isocapnic (IH) and poikilocapnic hypoxia (PH) in 10 men (25.7 ± 4.2 yr, mean ± SD). Heart rate (HR), mean arterial pressure (MAP), and mean peak middle cerebral artery blood flow velocity (P) were measured continuously during two randomized protocols of 20 min of step IH and PH (45 Torr). HR was elevated during both IH (P < 0.01) and PH (P < 0.01), with no differences observed between conditions. MAP was modestly elevated across all time points during IH but only became elevated after 5 min during PH. During IH, P was elevated from baseline throughout the exposure with a consistent hypoxic sensitivity of 0.34 cm·s^–1·%desaturation^–1 (P < 0.05). The P response to PH was biphasic with an initial decrease from baseline occurring at 79 ± 23 s, followed by a subsequent elevation, becoming equivalent to the IH response by 10 min. The nadir of the PH response exhibited a hypoxic sensitivity of –0.24 cm·s^–1·%desaturation^–1. When expressed in relation to end-tidal PCO₂, a sensitivity of –1.08 cm·s^–1·Torr^–1 was calculated, similar to previously reported sensitivities to euoxic hypocapnia. Cerebrovascular resistance (CVR) was not changed during IH. During PH, an initial increase in CVR was observed. However, CVR returned to baseline by 20 min of PH. These data show the cerebrovascular response to PH consists of an early hypocapnia-mediated response, followed by a secondary increase, mediated predominantly by hypoxia.

cerebral blood flow; blood pressure; heart rate; hypocapnia