Human Physiology at Great Heights

This page is my understanding of the (mal)adaptations we go through when we travel to high places (mountains specifically are of interest). I've learned this information from three places: Places to buy these books can easily be found on the web. Houston's book is by far the best because it explains the underlying biological processes.

What's the problem?

Basically, going higher means that the outside air pressure decreases. This means the difference between oxygen pressure in the lungs (lung air sacks or alveoli) and the blood decreases. Thus the body's cells get less oxygen. There is a buffer of oxygen in the cells (myoglobin) but this won't last long. Moreover, anaerobic energy production is not very efficient, won't last long either, and produces harmful side products (lactic acid is one). The basic problem is therefore that not enough oxygen arrives at the cells (and carbon dioxide CO2 is not removed quickly enough):- this will kill you in minutes (unless your metabolic rate drops drastically, but this will only happen together with severe hypothermic (undercooling) reactions, so don't count on this!). Note that it is in fact the excess of CO2 rather than lack of oxygen that drives many of the actions the body takes.

What are the body's reactions?

The following table, taken from Houston's book, summarises the actions and results of the body when confronted with lower air pressure:
action intended result
1 increased breathing better exchange of oxygen & CO2 in alveoli
2 increased cardiac output move more blood (temporary)
3 increased red cell count more oxygen carriers
4 more tissue capillaries move blood closer to cells
5 increased myoglobin stores larger local oxygen buffers
6 increased urine output concentrate blood (temporary)

Point 1 increases the throughput of air so that more oxygen and CO2 are exchanged in the lungs. Now lack of oxygen leads to hyperventilation as the first adaptation. This in turns leads to a loss of CO2 from the blood, turning it alkaline. This acts as a brake on hyperventilation so that the extra oxygen intake is slowed; bad news. Another, slower, mechanism to keep the blood pH neutral is by secreting bicarbonate in the kidneys. Urine output is then increased, and more water must be drunk. Diamox inhibits the first mechanism, encouraging the second mechanism. Note that urinating more is an effect, not the cause!

Points 2 and 6 increase the throughput (liters circulated per minute) of the blood, but not the oxygen capacity. More oxygen arrives by moving the blood faster. This also increases the blood pressure (at least in the arteries between heart and lungs, and lungs and heart). Increased blood pressure is one of the factors that increases leakage of blood vessels leading to oedema in the lungs (high altitude pulmonary edema, or HAPE). Nifedipine lowers artery blood pressure and hence leakage. Higher blood pressure can also lead to cerebral oedema (HACE), haemorraging in the eyes, and perhaps elsewhere as well.

Point 3 increases the oxygen-carrying capacity of the blood: with the same circulation more oxygen arrives at cells. The blood will be thicker and harder to pump around. EPO (erythropoietin) is made to stimulate production of red blood cells.

Point 4 increases the efficiency of delivering oxygen to cells.

Point 5 only allows a temporary larger oxygen deficit at cells by enlarging local oxygen buffers (diving animals have large myoglobin stores, allowing them to not breathe fresh air for an hour or longer).

In all of these adaptations the lungs are the limiting factor to performance, not the heart.

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(2000-06-26)