Everest Summit Research Articles

Simulations of the human heat balance during Mount Everest summit attempts in spring and winter

The majority of research dealing with the impacts of the Himalayan climate on human physiology focuses on low air temperature, high wind speed, and low air pressure and oxygen content, potentially leading to hypothermia and hypoxia. Only a few studies describe the influence of the weather conditions in the Himalayas on the body’s ability to maintain thermal balance. The aim of the present research is to trace the heat exchange between humans and their surroundings during a typical, 6-day summit attempt of Mount Everest in the spring and winter seasons. Additionally, an emergency night outdoors without tent protection is considered. Daily variation of the heat balance components were calculated by the MENEX_HA model using meteorological data collected at automatic weather stations installed during a National Geographic expedition in 2019–2020. The data represent the hourly values of the measured meteorological parameters. The research shows that in spite of extreme environmental conditions in the sub-summit zone of Mount Everest during the spring weather window, it is possible to keep heat equilibrium of the climbers’ body. This can be achieved by the use of appropriate clothing and by regulating activity level. In winter, extreme environmental conditions in the sub-summit zone make it impossible to maintain heat equilibrium and lead to hypothermia. The emergency night in the sub-peak zone leads to gradual cooling of the body which in winter can cause severe hypothermia of the climber’s body. At altitudes < 7000 m, climbers should consider using clothing that allows variation of insulation and active regulation of their fit around the body.

Insights from the first winter weather observations near Mount Everest's summit

Insights from the first winter weather observations near Mount Everest's summit

The formation and composition of the Mount Everest plume in winter

Abstract. Mount Everest's summit pyramid is the highest obstacle on earth to the wintertime jet-stream winds. Downwind, in its wake, a visible plume can form. The meteorology and composition of the plume are unknown. Accordingly, daily from 1 November 2020 through 31 March 2021 (151 d), we observed real-time images from a geosynchronous meteorological satellite to identify the days plumes formed. The corresponding surface and upper-air meteorological data were collected. The massif was visible on 143 d (95 %), plumes formed on 63 d (44 %) and lasted an average of 12 h. We used the upper-air data with a basic meteorological model to show the plumes formed when sufficiently moist air was drawn into the wake. We conclude the plumes were composed initially of either cloud droplets or ice particles depending on the temperature. The plumes were not composed of resuspended snow. One plume was observed to glaciate downwind. We estimated snowfall from the plumes may be significant.

Mount Everest's photogenic weather during the post‐monsoon

Mount Everest's photogenic weather during the post‐monsoon

Reliability and validity of the Hypoxico Everest Summit II altitude generator

The Hypoxico Everest Summit II Altitude Generator produces normobaric hypoxic conditions, which are commonly used in altitude acclimation. Despite being used routinely within applied sport science, this system is yet to be independently validated. Thus, the aim of this study was to explore within- and between-day inter- and intra-machine reliability and validity. Two Hypoxico Everest Summit II Altitude Generators were investigated for six altitude settings in a randomised order (0.5, 3.0, 5.5, 8.0, 10.5, 12.0). Following institutional ethics approval, Hypoxico generated air was sequentially pumped into three Douglas bags, each with a 1-min collection period. Samples were collected on eight occasions, measuring inter- and intra-machine reliability, both within-day (9 AM–2 PM) and between-day (48-h) with samples analysed to determine FiO2 (%) and volume (L·min−1). Coefficient of variation (CV) was calculated for FiO2 and volume for each altitude setting. Mean CV for FiO2 did not exceed 0.42% within-day, 0.49% between-day and 0.81% inter-machine. Volume mean CV did not exceed 0.85% within-day, 0.91% between-day and 1.17% inter-machine. One-sampled t-tests were conducted comparing Hypoxico reference values with collected samples using equivalent FiO2 for each altitude setting with a Bonferroni corrected significance set at p &lt; 0.004. Settings 3.0, 5.5, 8.0, 10.5 and 12.0 all produced significantly different ( p &lt; 0.001) FiO2 concentrations than the reference values stated (−0.51, −0.97, −0.72, +0.41 and +0.40%, respectively). Altitude setting and 1-min volume had an inverse relationship. All settings produced a significantly lower ( p &lt; 0.001) volume by 21.80 to 35.40 L·min−1 as compared to the company’s claim of 126.6 L·min−1. The Hypoxico Everest Summit II produced a reliable and consistent air feed; however, the manufacturer’s reference values demonstrated poor agreement with machine produced FiO2 and volume. Therefore, it is recommended that athletes, practitioners and researchers self-validate the altitude generator post-warm-up using an accurate oxygen sensor for accuracy and safety purposes.

INTEGRAL ASSESSMENT OF BODY RESERVES IN SKI RACERS DEVELOPING LOCAL REGIONAL MUSCLE ENDURANCE, STATOKINETIC AND HYPOXIA RESISTANCE

Aim. The article aims to assess the body reserves of ski racers who develop local-regional muscle endurance (LRME), statokinetic and hypoxia resistance. Materials and methods. 15–16-year-old highly skilled ski-racers (I, II category, candidates for master of sports) with sports experience of 5–7 years (n = 12) were examined. The following equipment was used to assess athletic fitness and sports performance: T 2100 GE treadmill system, CardioSoft diagnostic system (USA), HYPOXICO Everest Summit II altitude generator (USA), Angio Scan-01 P pulse oximeter sensor (Russia). Statistical analysis was performed using the SPSS information processing package. Results. The effect of techniques for developing LRME and hypoxia resistance on sports performance has been established. A generalized ranking of competitive performance is constructed and a regression model is described that establishes the dependence of sports performance on morphofunctional and metabolic statuses. The key indicators of morphofunctional and metabolic statuses were compared in athletes who used the methods for developing LRME and hypoxia resistance. Criteria are established for successful performance in sports reserve training, promising cross-country skiers, the modeling of status indicators with well-established technologies while maintaining the functional and metabolic potential and the level of health. Conclusion. The results of the study showed the effectiveness of combined technologies in sports training and allowed to identify markers of functional and metabolic statuses. The proposed technologies allowed to enhance adaptation and identify status markers. This made it possible to improve performance in the conditions of LRME and statokinetic and hypoxia resistance. Forecasting sports results allows regulating athletic fitness and making timely corrections to ensure successful sports performance.

INTEGRATED EFFECTS OF NORMOBARIC HYPOXIA AND METABOREFLEX ACTIVATION ON HEMODYNAMICS

IntroductionBoth metaboreflex activity and hypoxia affect hemodynamics. In particular, metaboreflex induces an augmentation in stroke volume (SV), systemic vascular resistance (SVR), and blood pressure (BP) by activating the sympathetic nervous system (SNS). In contrast, hypoxia produces a heart rate (HR)‐mediated increase in cardiac output (CO), while its effect on SVR is variable as it increases SNS activity but, at the same time, it triggers nitric oxide (NO) production in the endothelium, thus inducing venous and arteriolar dilation. Since studies on the possible interaction between metaboreflex and hypoxia are still lacking, our investigation aimed to study their combined effects on hemodynamics.Methods11 male subjects underwent a preliminary cardiopulmonary exercise test (CPET) on a cycle ergometer to assess their aerobic fitness. Then, a metaboreflex activation protocol in normoxia and normobaric hypoxia (fraction of inspired oxygen – FiO2 – of 13.5%) was conducted on separate days. Hypoxia was induced using a hypoxic gas generator (Everest Summit II Generator, Hypoxico, USA) connected to the subjects by a facemask. The metaboreflex activation protocol consisted of two randomly assigned sessions: one of post‐exercise muscle ischemia (PEMI) and one of control exercise recovery (CER). PEMI comprised a 3‐minute exercise bout pedaling at 30% of the maximum workload reached during the CPET followed by 3 minutes of vascular occlusion using an inflatable thigh cuff to stimulate the metaboreflex. CER was similar, but no occlusion was applied after the exercise session. SV, HR, CO, ventricular filling rate (VFR), and ventricular ejection rate (VER) were measured through impedance cardiography while mean blood pressure (MBP) was assessed using manual sphygmomanometer. SVR was calculated indirectly from CO and MBP according to Poiseuille’s law. Near‐infrared spectroscopy was employed to measure cerebral oxygenation (COX) and peripheral hemoglobin saturation (SPO2) to control the level of tissue hypoxia. Two‐way ANOVA and paired sample t‐test were utilized when appropriate.ResultsCO was increased during metaboreflex activation in normoxia (p= 0.013) but not in hypoxia. SV, CO, and VFR responses to metaboreflex (measured as the difference PEMI‐CER at the third minute after exercise) were reduced when the hypoxic stimulus was applied (p=0.02; p=0.02; p=0.003 respectively). Moreover, SVR response showed a nearly significant (p=0.07) increase in hypoxia, with MBP response being unchanged. COX and SPO2 confirmed that the hypoxic stimulus was effective.DiscussionResults demonstrated that hypoxia impaired the hemodynamic response to metaboreflex. Specifically, SV was reduced during metaboreflex in hypoxia because of a reduction in preload as a consequence of two mechanisms: 1) a reduction in venous return probably induced by NO‐mediated vasodilation of the venous bed; 2) an increase in right ventricle afterload likely produced by the pulmonary arterial system vasoconstriction. Of note, baroreflex successfully defended MBP response despite the reduced CO during hypoxia.

Polyphase deformation, dynamic metamorphism, and metasomatism of Mount Everest’s summit limestone, east central Himalaya, Nepal/Tibet

New samples collected from a transect across the summit limestone of Mount Everest (Qomolangma Formation) show that multiple distinct deformational events are discretely partitioned across this formation. Samples from the highest exposures of the Qomolangma Formation (Everest summit) preserve a well-developed mylonitic foliation and microstructures consistent with deformation temperatures of ≥250 °C. Thermochronologic and microstructural results indicate these fabrics were ingrained during initial contractile phases of Himalayan orogenesis, when crustal thickening was accommodated by folding and thrusting of the Tethyan Sedimentary Sequence. In contrast, samples from near the base of the Qomolangma Formation (South Summit) preserve extensional shear deformation, indicate metasomatism at temperatures of ∼500 °C, and contain a synkinematic secondary mineral assemblage of muscovite + chlorite + biotite + tourmaline + rutile. Shear fabrics preserved in South Summit samples are associated with activity on the Qomolangma detachment, while the crystallization of secondary phases was the result of reactions between the limestone protolith and a volatile, boron-rich fluid that infiltrated the base of the Qomolangma Formation, resulting in metasomatism. The 40 Ar/ 39 Ar dating of synkinematic muscovite indicates the secondary assemblage crystallized at ca. 28 Ma and that shear fabrics were ingrained at ≥18 Ma. This paper presents the first evidence that Everest’s summit limestone records multiple phases of deformation associated with discrete stages in Himalayan orogenesis, and that the structurally highest strand of the South Tibetan detachment on Everest was initially active as a distributed shear zone before it manifested as a discrete brittle detachment at the base of the Qomolangma Formation.

Real-Time Electrocardiogram Transmission from Mount Everest during Continued Ascent

The feasibility of a real-time electrocardiogram (ECG) transmission via satellite phone from Mount Everest to determine a climber’s suitability for continued ascent was examined. Four Taiwanese climbers were enrolled in the 2009 Mount Everest summit program. Physiological measurements were taken at base camp (5300 m), camp 2 (6400 m), camp 3 (7100 m), and camp 4 (7950 m) 1 hour after arrival and following a 10 minute rest period. A total of 3 out of 4 climbers were able to summit Mount Everest successfully. Overall, ECG and global positioning system (GPS) coordinates of climbers were transmitted in real-time via satellite phone successfully from base camp, camp 2, camp 3, and camp 4. At each camp, Resting Heart Rate (RHR) was transmitted and recorded: base camp (54–113 bpm), camp 2 (94–130 bpm), camp 3 (98–115 bpm), and camp 4 (93–111 bpm). Real-time ECG and GPS coordinate transmission via satellite phone is feasible for climbers on Mount Everest. Real-time RHR data can be used to evaluate a climber’s physiological capacity to continue an ascent and to summit.

Career perspective: John B West.

I have been fortunate to work in two areas of extreme physiology and medicine: very high altitude and the microgravity of spaceflight. My introduction to high altitude medicine was as a member of Sir Edmund Hillary's Silver Hut Expedition in 1960–1961 when a small group of physiologists spent the winter and spring at an altitude of 5,800 m just south of Mt. Everest. The physiological objective was to obtain a better understanding of the acclimatization process of lowlanders during exposure to a very high altitude for several months. As far as we knew, no one had ever spent so long at such a high altitude before. The success of this expedition prompted me to organize the 1981 American Medical Research Expedition to Everest where the scientific objective was to determine the physiological changes that allow humans to survive in the extreme hypoxia of the highest point on earth. There is good evidence that this altitude is very near the limit of human tolerance to oxygen deprivation. Much novel information was obtained including an extraordinary degree of hyperventilation which reduced the alveolar partial pressure of carbon dioxide (Pco2) to about 8 mmHg (1.1 kPa) on the summit, and this in turn allowed the alveolar partial pressure of oxygen, PO2, to be maintained at a viable level of about 35 mmHg (4.7 kPa). The low Pco2 caused a severe degree of respiratory alkalosis with an arterial pH exceeding 7.7. These were the first physiological measurements to be made on the Everest summit, and essentially, none has been made since. The second extreme environment is microgravity. We carried out an extensive series of measurements on astronauts in the orbiting laboratory known as SpaceLab in the 1990s. Many aspects of pulmonary function are affected by gravity, so it was not surprising that many changes were found. However, overall gas exchange remained efficient. Some of the findings such as an anomalous behavior of inhaled helium and sulfur hexafluoride have still not been explained. Measurements made after astronauts were exposed to 6 months of microgravity in the International Space Station indicate that the function of the lung returns to its preexposure state within a few days.

American Medical Research Expedition to Everest

The primary objective of the American Medical Research Expedition to Everest was to obtain information on human physiology at the highest possible altitude, including the Everest summit. An important data point was the barometric pressure on the summit, because this determines the inspired P(O(2)). The first measurement ever taken was 253.0 mmHg. Because modeling studies had shown that extreme hyperventilation was essential to reach these great altitudes, 34 alveolar gas samples were collected above an altitude of 8000 m, including 4 on the summit. These showed that hyperventilation reduced the alveolar P(CO(2)) to between 7 and 8 mmHg in one climber. An important finding was that alveolar P(O(2)) was defended at a value of about 35 mmHg by the increasing hyperventilation as the climbers ascended higher. Venous blood samples collected on two summiters gave a mean base excess of -7.2 meq.L(-1). Using the alveolar P(CO(2)) value, this gave an arterial pH of over 7.7, indicating an extreme degree of respiratory alkalosis. While climbing at an altitude of 8300 m, one summiter showed a respiratory frequency of 86 breaths.min(-1) and tidal volume of 1.26 L, indicating very rapid shallow breathing. Maximal oxygen consumption for the summit was derived by having well-acclimatized subjects exercise maximally at an altitude of 6300 m while breathing 14% oxygen. The V(O(2)) was just over 1 L.min(-1), which is sufficient to explain how exceptional humans can reach the summit without supplementary oxygen. In addition to the measurements at altitudes over 8000 m, data were obtained at two camps at 5400- and 6300-m altitude. These gave information on the control of ventilation, periodic breathing, blood physiology, cerebral function, and metabolism.

Operation Everest II

In October 1985, 25 years ago, 8 subjects and 27 investigators met at the United States Army Research Institute for Environmental Medicine (USARIEM) altitude chambers in Natick, Massachusetts, to study human responses to a simulated 40-day ascent of Mt. Everest, termed Operation Everest II (OE II). Led by Charlie Houston, John Sutton, and Allen Cymerman, these investigators conducted a large number of investigations across several organ systems as the subjects were gradually decompressed over 40 days to the Everest summit equivalent. There the subjects reached a V(O)(2)max of 15.3 mL/kg/min (28% of initial sea-level values) at 100 W and arterial P(O(2)) and P(CO(2)) of approximately 28 and approximately 10 mm Hg, respectively. Cardiac function resisted hypoxia, but the lungs could not: ventilation-perfusion inequality and O(2) diffusion limitation reduced arterial oxygenation considerably. Pulmonary vascular resistance was increased, was not reversible after short-term hyperoxia, but was reduced during exercise. Skeletal muscle atrophy occurred, but muscle structure and function were otherwise remarkably unaffected. Neurological deficits (cognition and memory) persisted after return to sea level, more so in those with high hypoxic ventilatory responsiveness, with motor function essentially spared. Nine percent body weight loss (despite an unrestricted diet) was mainly (67%) from muscle and exceeded the 2% predicted from energy intake-expenditure balance. Some immunological and lipid metabolic changes occurred, of uncertain mechanism or significance. OE II was unique in the diversity and complexity of studies carried out on a single, courageous cohort of subjects. These studies could never have been carried out in the field, and thus complement studies such as the American Medical Research Expedition to Everest (AMREE) that, although more limited in scope, serve as benchmarks and reality checks for chamber studies like OE II.

The Impact of Global Warming on Mount Everest

Global warming impacts a wide range of human activities and ecosystems. One unanticipated consequence of the warming is an increase in barometric pressure throughout the troposphere. Mount Everest's extreme height and resulting low barometric pressure places humans near its summit in an extreme state of hypoxia. Here we quantify the degree with which this warming is increasing the barometric pressure near Everest's summit and argue that it is of such a magnitude as to make the mountain, over time, easier to climb.

Exercise-induced VEGF transcriptional activation in brain, lung and skeletal muscle

Muscle VEGF expression is upregulated by exercise. Whether this VEGF response is regulated by transcription and/or post-transcriptional mechanisms is unknown. Hypoxia may be responsible: myocyte P(O2) falls greatly during exercise and VEGF is a hypoxia-responsive gene. Whether exercise induces VEGF expression in other organs important to acute physical activity is also unknown. To address these questions, we created a VEGF-Luciferase reporter mouse and measured VEGF transcription, mRNA and protein responses to (a) acute exercise and (b) short-term hypoxia (FI(O2) = 0.06) in brain (brainstem, cerebellum, cortex, hippocampus and striatum), muscle, lung, heart and liver. Exercise increased VEGF transcription, mRNA and protein in brain (hippocampus only), lungs and skeletal muscles, but not liver or heart. Hypoxia increased VEGF expression only in brain (cortex, hippocampus and striatum). New transcription appears to be a major exercise-induced regulatory step for increasing VEGF expression in muscle, lung and brain. Hippocampal VEGF expression was the only component of the exercise response recapitulated by hypoxia equivalent to the Everest summit.

Hemoglobin P50 during A Simulated Ascent of Mt. Everest, Operation Everest II

The amount of O(2) available to tissues is essentially the product of cardiac output, [Hb], and O(2) saturation. Saturation depends on P(O2) and the O(2)Hb dissociation curve. With altitude, increased [2,3-DPG] shifts the dissociation curve rightward, but hypocapnia and alkalosis move it leftward. We determined both standard and in vivo P(50) in 5 fit subjects decompressed over 42 days in an altitude chamber to the equivalent of the Mt. Everest summit (Operation Everest II). Arterial and venous blood was sampled at five "altitudes " (P(B) = 760, 429, 347, 282, 253 mmHg), and P(O2), P(CO2), pH, O(2) saturation, [Hb] and [2,3-DPG] were measured. As reported previously, 2,3-DPG levels increased from 1.7 (P(B) = 760) to 3.8 mmol/L (P(B) = 282). Standard P(50) also increased (from 28.2 mmHg at sea level to 33.1 on the summit, p<0.001). Alone, this would have lowered saturation by 12 percentage points at a summit arterial P(O2) of approximately 30 mmHg. However, in vivo P(50) remained between 26 and 27 mmHg throughout due to progressive hypocapnia and alkalosis. Calculations suggest that the increase in standard P(50) did not affect summit V(O2 MAX)), alveolar, arterial and venous P(O2)'s, but reduced arterial and venous O(2) saturations by 8.4 and 17.4 points, respectively, and increased O(2) extraction by 7.9 percentage points. Reduced saturation was balanced by increased extraction, resulting in no significant overall O(2) transport benefit, thus leaving unanswered the question of the purpose of increased [2,3-DPG] concentrations at altitude.

Human responses to extreme altitudes

It is a strange coincidence that the highest point on Earth is very close to the limit of human tolerance to hypoxia. The physiological changes that allow humans to reach these extreme altitudes involve enormous alterations of their normal state. It is useful to contrast this response with two others to high altitude. One is acclimatization that allows lowlanders to ascend to altitudes of up to 5000 m and remain there for an indefinite period. The other is evolutionary adaptation which allows highlanders to live continuously over generations at altitudes up to 5000 m. These two responses enable humans to survive for an indefinite period at high altitude. By contrast, the changes that allow ascent to extreme altitudes are not compatible with an extended stay because of a poorly-understood process called high-altitude deterioration. The most important physiological response to extreme altitude is extreme hyperventilation which, on the summit of Mt. Everest, drives the alveolar P(CO(2)) down to 7-8 mmHg. This is associated with a marked respiratory alkalosis with an arterial pH exceeding 7.7. Interestingly this alkalosis increases the oxygen affinity of hemoglobin, a response which the successful climber shares with many other animals in oxygen-deprived environments. The arterial P(O(2)) on the Everest summit is only about 30 mmHg and falls on exercise because of diffusion limitation of oxygen across the blood-gas barrier. Maximal oxygen consumption on the summit is just over 1 liter.min(-1). Anaerobic metabolism as measured by blood lactate levels is paradoxically reduced at extreme altitudes.

Introduction to a previously unpublished paper by A. M. Kellas.

the Possibility of Ascending Mount Everest,” by A. M. Kellas, which was written in 1920, is a previously unpublished landmark for people who have a historical interest in the physiology of extreme altitude and, in particular, the challenge of climbing Mt. Everest. The circumstances of the manuscript have been discussed in detail elsewhere (West, 1987), but a brief summary is appropriate here. Alexander Mitchell Kellas (1868–1921) (Fig. 1) was exceptional in that he combined pioneering contributions to the exploration of the Everest area with a great deal of insight into the physiological problems of its immense altitude. Between 1907 and 1921 he took part in eight expeditions to the Himalayas, mainly on his own or with a few Sherpa companions (West, 1989), and when permission was given by the Tibetan authorities for the first official expedition to Everest in 1921, he probably knew more about the approaches to the mountain than anybody else. At the same time, he probably had as much experience as anybody of the difficulties of climbing to altitudes over 6000 m, and he had developed a keen interest in the physiological problems of extreme altitudes. The present paper is an exact printed version of an unpublished typescript that has been languishing in the archives of the Alpine Club in London for some 80 years (Fig. 2). Another almost identical manuscript is in the archives of the Royal Geographical Society in London. The original typescript is not easy to read and includes a number of longhand additions made by Kellas in elegant but very small writing, but careful scrutiny has resulted in an authoritative version. It is very rewarding to finally be able to publish this manuscript on the 80th anniversary of Kellas’s death. As in the case of all historical manuscripts, some parts are more useful than others. For example, the long section on mountain sickness and the physiology of acclimatization (printed here in a smaller typeface), while containing some points of historical interest and a snapshot of knowledge around 1920, may be tedious to some people. However, because the opportunity has finally arrived to let the manuscript see the light of day, it seemed best to print it in its entirety. The most interesting parts of the manuscript deal with Kellas’s predictions for physiological variables on the Everest summit, including barometric pressure, alveolar PO2, arterial oxygen saturation, maximal oxygen consumption, and maximal climbing rate. In addition, there HIGH ALTITUDE MEDICINE & BIOLOGY Volume 2, Number 3, 2001 Mary Ann Liebert, Inc.

Tolerance to severe hypoxia: lessons from Mt. Everest

Human tolerance to chronic severe hypoxia has been elucidated by two recent high altitude studies: the 1981 American Medical Research Expedition to Everest, and Operation Everest II, a 40-day low pressure chamber-simulated ascent of Everest. The severe oxygen deprivation of extreme altitudes can only be tolerated because of an enormous increase in ventilation which defends the alveolar Po2 against the reduced inspired value. Nevertheless the arterial Po2 on the Everest summit is less than 30 mmHg. The hyperventilation results in a very low arterial Pco2 which causes severe respiratory alkalosis. This has the advantage of increasing the oxygen affinity of hemoglobin and accelerating the oxygen loading by the pulmonary capillary under diffusion-limited conditions. Cardiac function is astonishingly well maintained up to extreme altitudes. The relationship between cardiac output and work rate is the same as at sea level, and there is evidence that myocardial contractility is well preserved in spite of the extreme hypoxemia. However, there is impairment of central nervous system function at high altitude which persists following return to sea level. Significant abnormalities of motor coordination persisted for more than 12 months in most members of the Everest expedition. There is evidence that the climbers who ventilate most at high altitude have the most central nervous system impairment, presumably because of the more severe cerebral vasoconstriction.

The 1988 Stevenson Memorial lecture. Physiological responses to severe hypoxia in man.

Recent measurements at extreme altitude and in low pressure chamber simulations have clarified the human responses to extreme hypoxia. Man can only tolerate the severe oxygen deprivation of great altitudes by an enormous increase in ventilation which has the advantage of defending the alveolar PO2 against the reduced inspired PO2. Nevertheless the arterial PO2 on the Everest summit is less than 30 Torr (1 Torr = 133.3 Pa). An interesting consequence of the hyperventilation is that the respiratory alkalosis greatly increases the oxygen affinity of the hemoglobin and assists in oxygen loading by the pulmonary capillary. The severe hypoxemia impairs the function of many organ systems including the central nervous system, and there is evidence of residual impairment of memory and manipulative skill in climbers returning from great altitudes. At the altitude of Mt. Everest, maximal oxygen uptake is reduced to 20-25% of its sea level value, and it is exquisitely sensitive to barometric pressure. It is likely that the seasonal variation of barometric pressure affects the ability of man to reach the summit without supplementary oxygen.