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 (PaO2 ) 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
(PaCO2 ) is decreased due to hypoxic hyperventilation
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
PaO2 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. PaO2 and PaCO2 ) 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 PaO2
reaches levels