The precise mechanisms underlying EIAH are not
known at present. A number of physiologic theories
implicate inadequate hyperventilatory compensation
and widened A-aDO2 gradient, but definitive
evidence is lacking.
Current hypotheses on the role of ventilatory
compensation tend to focus on ventilatory drive
during exercise. As metabolic demand increases
during exercise, individuals are expected to exhibit
elevated ventilation to compensate for the gas
exchange requirements. During heavy exercise, an
increase in PAO2 is required to maintain the level to
correct for lower venous PO2 and reduced pulmonary
red blood cell transit time (1). Relative
hypoventilation, defined as alveolar ventilation below
the rate required to maintain arterial blood gases at
physiologically normal levels (11), is characterized
by PAO235 mmHg (12). In
healthy untrained individuals, the ventilatory capacity
of the lungs is viewed as overbuilt for exercise, being
able to maintain blood gases when approaching VO2
max. However, endurance-trained athletes are able to
achieve significantly higher metabolic rates that
cannot be matched by compensatory
hyperventilation, which leads to relative
hypoventilation (5).