flow regulation and altitude acclimatization Glen E. Foster School of Human Kinetics, University of British Columbia, Vancouver, Canada
Email: glen.foster@ubc.ca
Travel to high altitude for the lowland
dweller unmasks a complicated array of physiological mechanisms responsible for acclimatization (Dempsey & Forster, 1982). First, the reduction in both the barometric pressure and the arterial partial pressure for oxygen (P aO2 ) stimulates an increase in ventilation, the magnitude of which depends upon the individual ventilatory sensitivity to hypoxia. Then, the arterial partial pressure for carbon dioxide (P aCO2 ) is decreased due to hypoxic hyper- ventilation resulting in respiratory alkalosis. As time at altitude increases over the next 1–2 weeks, acid–base balance is normalized by renal excretion of bicarbonate, and P aO2 is improved by increases in the ventilatory sensitivity to hypoxia and polycythaemia. This simplified overview of altitude acclimatization highlights two major controlling factors for cerebral blood flow (CBF): (1) changes in arterial blood gases (i.e. P aO2 and P aCO2 ) and (2) changes in pH. The brain, notably a vital organ, relies upon an adequate supply of blood and delivery of oxygen for its normal operation. Therefore, CBF is regulated not only to maintain oxygen delivery but also to maintain cerebral tissue pH (or cerebral spinal fluid (CSF) pH). Interestingly, the cerebral circulation is relatively insensitive to hypoxia, only increasing CBF when P aO2 reaches levels <50 mmHg. Conversely, CBF is highly sensitive to changes in P aCO2 (and pH), decreasing CBF during hypocapnia and increasing CBF with hypercapnia. This property of the cerebral circulation may dampen changes in CSF pH and provides a unique point of respiratory integration. It can be appreciated that oscillations in CSF pH in the region responsible for central chemoreception would directly affect ventilation. Taking this one step further, the individual magnitude of the