Physiology of Extreme Altitude

2011 ◽  
Author(s):  
John B. West
Keyword(s):  
Extreme Altitude

Skeletal Muscle Adaptations to Prolonged Exposure to Extreme Altitude: A Role of Physical Activity?

2008 ◽  
Vol 9 (4) ◽  
pp. 311-317 ◽  
Author(s):  
Masao Mizuno ◽  
Gabrielle K Savard ◽  
Nils-Holger Areskog ◽  
Carsten Lundby ◽  
Bengt Saltin
Keyword(s):  
Physical Activity ◽  
Skeletal Muscle ◽  
Prolonged Exposure ◽  
Muscle Adaptations ◽  
Extreme Altitude ◽  
Skeletal Muscle Adaptations

Regional circulatory responses to hypocapnia and hypercapnia in bar-headed geese

1986 ◽  
Vol 250 (3) ◽  
pp. R499-R504 ◽  
Author(s):  
F. M. Faraci ◽  
M. R. Fedde
Keyword(s):  
Blood Flow ◽  
Regional Blood Flow ◽  
Muscle Blood Flow ◽  
Pectoral Muscle ◽  
Blood Flows ◽  
Arterial Blood ◽  
Blood Flow Reduction ◽  
Extreme Altitude ◽  
Anser Indicus ◽  
O2 Delivery

To investigate mechanisms that may allow birds to tolerate extreme high altitude (hypocapnic hypoxia), we examined the effects of severe hypocapnia and moderate hypercapnia on regional blood flow in bar-headed geese (Anser indicus), a species that flies at altitudes up to 9,000 m. Cerebral, coronary, and pectoral muscle blood flows were measured using radioactive microspheres, while arterial CO2 tension (PaCO2) was varied from 7 to 62 Torr in awake normoxic birds. Arterial blood pressure was not affected by hypocapnia but increased slightly during hypercapnia. Heart rate did not change during alterations in PaCO2. Severe hypocapnia did not significantly alter cerebral, coronary, or pectoral muscle blood flow. Hypercapnia markedly increased cerebral and coronary blood flow, but pectoral muscle blood flow was unaffected. The lack of a blood flow reduction during severe hypocapnia may represent an important adaptation in these birds, enabling them to increase O2 delivery to the heart and brain at extreme altitude despite the presence of a very low PaCO2.

Red cell function at extreme altitude on Mount Everest

1984 ◽  
Vol 56 (1) ◽  
pp. 109-116 ◽  
Author(s):  
R. M. Winslow ◽  
M. Samaja ◽  
J. B. West
Keyword(s):  
Cell Function ◽  
Blood Gases ◽  
Hemoglobin Concentration ◽  
Respiratory Alkalosis ◽  
Blood Collection ◽  
Red Cell ◽  
Arterial Blood ◽  
Extreme Altitude ◽  
2,3 Dpg

As part of the American Medical Research Expedition to Everest in 1981, we measured hemoglobin concentration, red cell 2,3-diphosphoglycerate (2,3-DPG), Po2 at which hemoglobin is 50% saturated (P50), and acid-base status in expedition members at various altitudes. All measurements were made in expedition laboratories and, with the exception of samples from the South Col of Mt. Everest (8,050 m), within 2 h of blood collection. In vivo conditions were estimated from direct measurements of arterial blood gases and pH or inferred from base excess and alveolar PCO2. As expected, increased 2,3-DPG was associated with slightly increased P50, when expressed at pH 7.4. Because of respiratory alkalosis, however, the subjects' in vivo P50 at 6,300 m (27.6 Torr) was slightly less than at sea level (28.1 Torr). The estimated in vivo P50 was progressively lower at 8,050 m (24.9 Torr) and on the summit at 8,848 m (19.4 Torr in one subject). Our data suggest that, at extreme altitude, the blood O2 equilibrium curve shifts progressively leftward because of respiratory alkalosis. This left shift protects arterial O2 saturation at extreme altitude.

Diseases of high terrestrial altitudes

2010 ◽  
pp. 1402-1408
Author(s):  
Andrew J. Pollard ◽  
Buddha Basnyat ◽  
David R. Murdoch
Keyword(s):  
High Altitude ◽  
Hypobaric Hypoxia ◽  
Cell Mass ◽  
Red Cell ◽  
Physiological Changes ◽  
Exposed Individual ◽  
Extreme Altitude ◽  
First Arrival ◽  
The Individual ◽  
Over Time

Ascent to altitudes above 2500 m leads to exposure to hypobaric hypoxia. This affects performance on first arrival at high altitude and disturbs sleep, but physiological changes occur over time to defend arterial and tissue oxygenation and allow the individual to adjust. This process of acclimatization includes (1) an increase in the rate and depth of breathing; and (2) an increase in red cell mass, and in red cell 2,3-diphosphoglycerate. Acclimatization is no longer possible at extreme altitude (>5800 m) and the exposed individual will gradually deteriorate....

Diseases of high terrestrial altitudes

2020 ◽  
pp. 1701-1709
Author(s):  
Tyler Albert ◽  
Erik R. Swenson ◽  
Andrew J. Pollard ◽  
Buddha Basnyat ◽  
David R. Murdoch
Keyword(s):  
Genetic Predisposition ◽  
Hypobaric Hypoxia ◽  
Cell Mass ◽  
Red Cell ◽  
Physiological Changes ◽  
Exposed Individual ◽  
Extreme Altitude ◽  
First Arrival ◽  
The Individual ◽  
Over Time

Ascent to altitudes above 2,500 m leads to exposure to hypobaric hypoxia. This affects performance on first arrival at high altitude and disturbs sleep, but physiological changes occur over time to defend arterial and tissue oxygenation and allow the individual to adjust. This process of acclimatization includes (1) an increase in the rate and depth of breathing; and (2) an increase in red cell mass, and in red cell 2,3-diphosphoglycerate. Acclimatization is no longer possible at extreme altitude (>5,800 m) and the exposed individual will gradually deteriorate. Altitude illness results from a failure to adjust to hypobaric hypoxia at altitude. Risk is increased by ascent to higher altitudes, by more rapid gain in altitude, and (in some people) genetic predisposition; the condition may be avoided in most cases by slow, graded ascent.

Free and total thyroid hormones in humans at extreme altitude

1995 ◽  
Vol 39 (1) ◽  
pp. 17-21 ◽  
Author(s):  
Minakshi Basu ◽  
K. Pal ◽  
A. S. Malhotra ◽  
R. Prasad ◽  
R. C. Sawhney
Keyword(s):  
Thyroid Hormones ◽  
Extreme Altitude

Oxygen transport during exercise at extreme altitude: Operation everest II

1987 ◽  
Vol 16 (9) ◽  
pp. 993-998 ◽  
Author(s):  
John T Reeves ◽  
Bertron M Groves ◽  
John R Sutton ◽  
Peter D Wagner ◽  
Allen Cymerman ◽  
...  
Keyword(s):  
Oxygen Transport ◽  
Extreme Altitude
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