Effects of high altitude on humans

Climbing Mount Rainier.

The effects of high altitude on humans are considerable. The percentage saturation of hemoglobin with oxygen determines the content of oxygen in our blood. After the human body reaches around 2,100 m (7,000 feet) above sea level, the saturation of oxyhemoglobin begins to plummet.^[1] However, the human body has both short-term and long-term adaptations to altitude that allow it to partially compensate for the lack of oxygen. Athletes use these adaptations to help their performance. There is a limit to the level of adaptation: mountaineers refer to the altitudes above 8,000 metres (26,000 ft) as the "death zone", where no human body can acclimatize.

Effects as a function of altitude

The human body functions best at sea level, where the atmospheric pressure is 101,325 Pa or 1013.25 millibars (or 1 atm, by definition). The concentration of oxygen (O₂) in sea-level air is 20.9%, so the partial pressure of O₂ (PO₂) is about 21.2 kPa. In healthy individuals, this saturates hemoglobin, the oxygen-binding red pigment in red blood cells.^[2]

Atmospheric pressure decreases exponentially with altitude while the O₂ fraction remains constant to about 100 km, so pO₂ decreases exponentially with altitude as well. It is about half of its sea-level value at 5,000 m (16,000 ft), the altitude of the Everest Base Camp, and only a third at 8,848 m (29,029 ft), the summit of Mount Everest.^[3] When PO₂ drops, the body responds with altitude acclimatization.^[4]

Mountain medicine recognizes three altitude regions that reflect the lowered amount of oxygen in the atmosphere:^[5]

• High altitude = 1,500–3,500 metres (4,900–11,500 ft)
• Very high altitude = 3,500–5,500 metres (11,500–18,000 ft)
• Extreme altitude = above 5,500 metres (18,000 ft)

Travel to each of these altitude regions can lead to medical problems, from the mild symptoms of acute mountain sickness to the potentially fatal high altitude pulmonary edema (HAPE) and high altitude cerebral edema (HACE). The higher the altitude, the greater the risk.^[6] Research also indicates elevated risk of permanent brain damage in people climbing to extreme altitudes.^[7] Expedition doctors commonly stock a supply of dexamethazone, or "dex," to treat these conditions on site.^[8]

Humans have survived for two years at 5,950 m (19,520 ft) [475 millibars of atmospheric pressure], which appears to be near the limit of the permanently tolerable highest altitude.^[9] At extreme altitudes, above 7,500 m (24,600 ft) [383 millibars of atmospheric pressure], sleeping becomes very difficult, digesting food is near-impossible, and the risk of HAPE or HACE increases greatly.^[6][10][11]

Death zone

The summit of Mount Everest is in the death zone

Finally, the death zone, in mountaineering, refers to altitudes above a certain point where the amount of oxygen is not high enough to sustain human life. This point is generally tagged as 8,000 m (26,000 ft) [less than 356 millibars of atmospheric pressure].^[12] The term "death zone" was originally coined by Edouard Wyss-Dunant, a Swiss doctor, in his 1952 book, The Mountain World.^[13]

Many deaths in high-altitude mountaineering have been caused by the effects of the death zone, either directly (loss of vital functions) or indirectly (wrong decisions made under stress, physical weakening leading to accidents). In the "death zone", no human body can acclimatize. The body uses up its store of oxygen faster than it can be replenished. An extended stay in the zone without supplementary oxygen will result in deterioration of bodily functions, loss of consciousness and, ultimately, death.^[14][15][16]

Scientists at the High Altitude Pathology Institute in Bolivia dispute the existence of a death zone, based on observation of extreme tolerance to hypoxia in patients with Chronic mountain sickness and normal fetuses in-utero, both of which present PaO2 levels similar to those at the summit of Mount Everest.^[17][18]

The summit of K2 is in the death zone

Acclimatization to altitude

The human body can adapt to high altitude through immediate and long-term acclimatization. At high altitude, in the short term, the lack of oxygen is sensed by the carotid bodies, which causes an increase in the breathing rate (hyperventilation). However, hyperventilation also causes the adverse effect of respiratory alkalosis, inhibiting the respiratory center from enhancing the respiratory rate as much as would be required. Inability to increase the breathing rate can be caused by inadequate carotid body response or pulmonary or renal disease.^[1][19]

In addition, at high altitude, the heart beats faster; the stroke volume is slightly decreased; and non-essential bodily functions are suppressed, resulting in a decline in food digestion efficiency (as the body suppresses the digestive system in favor of increasing its cardiopulmonary reserves).^[20]

Full acclimatization, however, requires days or even weeks. Gradually, the body compensates for the respiratory alkalosis by renal excretion of bicarbonate, allowing adequate respiration to provide oxygen without risking alkalosis. It takes about four days at any given altitude and is greatly enhanced by acetazolamide.^[19] Eventually, the body has lower lactate production (because reduced glucose breakdown decreases the amount of lactate formed), decreased plasma volume, increased hematocrit (polycythemia), increased RBC mass, a higher concentration of capillaries in skeletal muscle tissue, increased myoglobin, increased mitochondria, increased aerobic enzyme concentration, increase in 2,3-BPG, hypoxic pulmonary vasoconstriction, and right ventricular hypertrophy.^[1] Pulmonary artery pressure increases in an effort to oxygenate more blood.

Full hematological adaptation to high altitude is achieved when the increase of red blood cells reaches a plateau and stops. The length of full hematological adaptation can be approximated by multiplying the altitude in kilometers by 11.4 days. For example, to adapt to 4,000 metres (13,000 ft) of altitude would require around 46 days.^[21] The upper altitude limit of this linear relationship has not been fully established.^[17][9]

Altitude and athletic performance

Main article: Altitude training

For athletes, high altitude produces two contradictory effects on performance. For explosive events (sprints up to 400 metres, long jump, triple jump) the reduction in atmospheric pressure means there is less resistance from the atmosphere and the athlete's performance will generally be better at high altitude.^[22] For endurance events (races of 5,000 metres or more), the predominant effect is the reduction in oxygen, which generally reduces the athlete's performance at high altitude. Sports organizations acknowledge the effects of altitude on performance: the International Association of Athletics Federations (IAAF), for example, have ruled that performances achieved at an altitude greater than 1,000 metres will not be approved for record purposes.

Athletes can also take advantage of altitude acclimatization to increase their performance.^[4] The same changes that help the body cope with high altitude increase performance back at sea level. However, this may not always be the case. Any positive acclimatization effects may be negated by a de-training effect as the athletes are usually not able to exercise with as much intensity at high altitudes compared to sea level.

This conundrum led to the development of the altitude training modality known as "Live-High, Train-Low", whereby the athlete spends many hours a day resting and sleeping at one (high) altitude, but performs a significant portion of their training, possibly all of it, at another (lower) altitude. A series of studies conducted in Utah in the late 1990s by researchers Ben Levine, Jim Stray-Gundersen, and others, showed significant performance gains in athletes who followed such a protocol for several weeks.^[23][24] Other studies have shown performance gains from merely performing some exercising sessions at altitude, yet living at sea level.^[25]

The performance-enhancing effect of altitude training could be due to increased red blood cell count,^[26] more efficient training,^[27] or changes in muscle physiology.^[28][29]

See also

• Altitude sickness
• Altitude tent
• Armstrong's limit the altitude/pressure at which water boils in the lungs at body temperature
• Gamow bag
• 1996 Mount Everest disaster
• 2008 K2 disaster
• Hypoxemia
• Hypoxia (medical)
• Organisms at high altitude

References

1. ^ ^{a b c} Young, Andrew J; Reeves, John T. (2002). "Human Adaptation to High Terrestrial Altitude". Medical Aspects of Harsh Environments. 2. Washington, DC. http://www.bordeninstitute.army.mil/published_volumes/harshEnv2/HE2ch21.pdf. Retrieved 2009-01-05. 
2. ^ "Hypoxia, Oxygen, and Pulse Oximetry" (PDF). FlightState Pulse Oximeter. http://www.flightstat.nonin.com/documents/Hypoxia,%20Oxygen%20and%20Pulse%20Oximetry.pdf. Retrieved 2006-12-29. 
3. ^ "Introduction to the Atmosphere". PhysicalGeography.net. http://www.physicalgeography.net/fundamentals/7d.html. Retrieved 2006-12-29. 
4. ^ ^{a b} Muza, SR; Fulco, CS; Cymerman, A (2004). "Altitude Acclimatization Guide". US Army Research Inst. of Environmental Medicine Thermal and Mountain Medicine Division Technical Report (USARIEM–TN–04–05). http://archive.rubicon-foundation.org/7616. Retrieved 2009-03-05. 
5. ^ "Non-Physician Altitude Tutorial". International Society for Mountain Medicine. http://www.ismmed.org/np_altitude_tutorial.htm. Retrieved 22 December 2005. 
6. ^ ^{a b} Cymerman, A; Rock, PB. Medical Problems in High Mountain Environments. A Handbook for Medical Officers. USARIEM-TN94-2. US Army Research Inst. of Environmental Medicine Thermal and Mountain Medicine Division Technical Report. http://archive.rubicon-foundation.org/7976. Retrieved 2009-03-05. 
7. ^ Fayed, N; Modrego, P.J.; Morales, H (2006). "Evidence of brain damage after high-altitude climbing by means of magnetic resonance imaging,". The American Journal of Medicine (Elsevier) 119 (2): 168. http://www.cns.nyu.edu/events/spf/SPF_papers/fayed2006evidence.pdf. 
8. ^ Krakauer, Jon (1999), Into Thin Air: A Personal Account of the Mt. Everest Disaster, New York: Anchor Books/Doubleday, ISBN 9780385494786 
9. ^ ^{a b} West, JB (2002). "Highest permanent human habitation". High Altitude Medical Biology 3 (4): 401–7. doi:10.1089/15270290260512882. PMID 12631426. 
10. ^ Rose MS, Houston CS, Fulco CS, Coates G, Sutton JR, Cymerman A (December 1988). "Operation Everest. II: Nutrition and body composition". J. Appl. Physiol. 65 (6): 2545–51. PMID 3215854. http://jap.physiology.org/content/65/6/2545.long. Retrieved 2009-03-05. 
11. ^ Kayser B (October 1992). "Nutrition and high altitude exposure". Int J Sports Med 13 Suppl 1: S129–32. doi:10.1055/s-2007-1024616. PMID 1483750. 
12. ^ "Everest:The Death Zone". Nova. PBS. 1998-02-24. http://www.pbs.org/wgbh/nova/transcripts/2506everest.html. 
13. ^ Schott, Ben (2010-01-09). "Death Zone". New York Times. http://schott.blogs.nytimes.com/2010/04/28/death-zone/. 
14. ^ Darack, Ed (2002). Wild winds: adventures in the highest Andes. p. 153. ISBN 9781884980817. http://books.google.com/?id=z2WPzJHpfLEC&pg=RA1-PA153&dq=%22death+zone%22#v=onepage&q=%22death%20zone%22&f=false. 
15. ^ Huey, Raymond B.; Xavier Eguskitza (2 July 2001). "Limits to human performance: elevated risks on high mountains". J. Experimental Biology 204 (18): 3115–9. PMID 11581324. http://jeb.biologists.org/content/204/18/3115.abstract. 
16. ^ Grocott, Michael P.W.; Daniel S. Martin, Denny Z.H. Levett, Roger McMorrow, Jeremy Windsor, Hugh E. Montgomery (2009). "Arterial Blood Gases and Oxygen Content in Climbers on Mount Everest". N Engl J Med 360 (2): 140–9. doi:10.1056/NEJMoa0801581. PMID 19129527. http://content.nejm.org/cgi/reprint/360/2/140. 
17. ^ ^{a b} Zubieta-Castillo, G.; Zubieta-Calleja, GR, Zubieta-Calleja, L. Zubieta-Castillo, Nancy (2008). "Facts that Prove that Adaptation to life at Extreme Altitude (8842m) is possible". In Adaptation Biology and Medicine 5 (Suppl 5): 348–355. 
18. ^ http://zuniv.net/pub/Everest2.pdf
19. ^ ^{a b} Harris, N Stuart; Nelson, Sara W (16 Apr 2008). "Altitude Illness – Cerebral Syndromes". eMedicine Specialties > Emergency Medicine > Environmental. http://emedicine.medscape.com/article/768478-overview. 
20. ^ Westerterp, Klaas (June 1, 2001). "Energy and Water Balance at High Altitude". News in Physiological Sciences 16 (3): 134–7. PMID 11443234. http://physiologyonline.physiology.org/content/16/3/134.full. 
21. ^ Zubieta-Calleja, G. R.; Paulev, P-E., Zubieta-Calleja, L. Zubieta-Castillo, G. (2007). "Altitude adaptation through hematocrit change". Journal of Physiology and Pharmacology: an Official Journal of the Polish Physiological Society 58 (Suppl 5(Pt 2)): 811–18. ISSN 0867-5910. 
22. ^ Ward-Smith, AJ (1983). "The influence of aerodynamic and biomechanical factors on long jump performance". Journal of Biomechanics 16 (8): 655–8. doi:10.1016/0021-9290(83)90116-1. PMID 6643537. 
23. ^ Levine, BD; Stray-Gundersen, J (July 1997). ""Living high-training low": effect of moderate-altitude acclimatization with low-altitude training on performance". Journal of Applied Physiology 83 (1): 102–12. PMID 9216951. http://jap.physiology.org/content/83/1/102.long. Retrieved 2009-01-05. 
24. ^ Stray-Gundersen, J; Chapman, RF; Levine, BD (September 2001). ""Living high-training low" altitude training improves sea level performance in male and female elite runners". Journal of Applied Physiology 91 (3): 1113–20. PMID 11509506. http://jap.physiology.org/content/91/3/1113.long. Retrieved 2009-01-05. 
25. ^ Dufour, SP; Ponsot E, Zoll J, Doutreleau S, Lonsdorfer-Wolf E, Geny B, Lampert E, Flück M, Hoppeler H, Billat V, Mettauer B, Richard R, Lonsdorfer J. (April 2006). "Exercise training in normobaric hypoxia in endurance runners. I. Improvement in aerobic performance capacity". Journal of Applied Physiology 100 (4): 1238–48. doi:10.1152/japplphysiol.00742.2005. PMID 16540709. http://jap.physiology.org/content/100/4/1238.long. Retrieved 2009-01-05. 
26. ^ Levine, BD; Stray-Gundersen, J (November 2005). "Point: positive effects of intermittent hypoxia (live high:train low) on exercise performance are mediated primarily by augmented red cell volume". Journal of Applied Physiology 99 (5): 2053–5. doi:10.1152/japplphysiol.00877.2005. PMID 16227463. http://jap.physiology.org/content/99/5/2053.long. Retrieved 2009-01-05. 
27. ^ Gore, CJ; Hopkins, WG (November 2005). "Counterpoint: positive effects of intermittent hypoxia (live high:train low) on exercise performance are not mediated primarily by augmented red cell volume". Journal of Applied Physiology 99 (5): 2055–7; discussion 2057–8. doi:10.1152/japplphysiol.00820.2005. PMID 16227464. http://jap.physiology.org/content/99/5/2055.full. Retrieved 2009-01-05. 
28. ^ Bigard, AX; Brunet, A; Guezennec, CY; Monod, H (1991). "Skeletal muscle changes after endurance training at high altitude". Journal of Applied Physiology 71 (6): 2114–21. PMID 1778900. 
29. ^ Ponsot, E; Dufour SP, Zoll J, Doutrelau S, N'Guessan B, Geny B, Hoppeler H, Lampert E, Mettauer B, Ventura-Clapier R, Richard R. (April 2006). "Exercise training in normobaric hypoxia in endurance runners. II. Improvement of mitochondrial properties in skeletal muscle". J. Appl. Physiol. 100 (4): 1249–57. doi:10.1152/japplphysiol.00361.2005. PMID 16339351. http://jap.physiology.org/content/100/4/1249.long. Retrieved 2009-03-05. 

External links

• Physiology at MCG 4/4ch7/s4ch7_32
• IPPA, High Altitude Pathology Institute.