Summary. Persons adapt to altitude by producing more RBCs to counter the
desaturation caused by the lower PO2. Altitude residents who spent their
growing years at altitude show a rather complete adaptation as seen in their
arterial oxygen content and VO2 max values. Lowlanders who arrive as adults
show only a modest adaptation

What is the effect of immediate exposure to altitude?
• Decrease in VO2 max upon ascent to 2300 m (9-22%); 3100 m (14-
24%); 4000 m (25-34%). Why such variability? Could be due to the
degree of saturation of hemoglobin.
• Remember arterial desaturation already discussed … the additional
impact of altitude can worsen this effect

What about training at altitude?
• 28 day study at 2300 m found VO2 max to increase 1-8%. Other
studies have reported no improvement. Why the variability? Could
be due to the training state before arriving at altitude

What about when athletes return to sea level after exposure to
altitude training?
• Some have higher VO2max upon return to low altitude, while others do
not. Why? Initial conditioning state; a “detraining” effect because one
cannot train as intensely at altitude … should you live high and train
low? Results are mixed, there are “responders and non-responders”

Bottom line for improving performance – live high enough to evoke
an increase in RBCs, train low enough to maintain training intensity.
High altitude climbing includes the stress of altitude, cold,
radiation
• Barometric pressure at Mt Everest Summit is approx 250 mmHg.
VO2 max estimated at approx 15 ml kg min.
• What does the arterial saturation of Hb depend on ?? As such,
successful climbers can hyperventilate well, and decrease their
pCO2 content, and increase their pO2 content
• Other factors that are essential for success in climbing … being
able to contend with a severe loss of appetite, Operation Everest
II subjects had a decrease in caloric expenditure of 43% over 40
day exposure to hypoxia, and a weight loss of approx 7 kg