Operation Everest III (Comex'97): the effect of simulated sever hypobaric hypoxia on lipid peroxidation and antioxidant defence systems in human blood at rest and after maximal exercise.

Eight subjects were placed in a decompression chamber for 31 days at pressures from sea level (SL) to 8848 m altitude equivalent. Whole blood lipid peroxidation (LP) was increased at 6000 m by a mean of 23% (P<0.05), at 8000 m by 79% (P<0.01) and at 8848 m by 94% (P<0.01). (All figures are means.) Two days after return to sea level (RSL), it remained high, by 81% (P<0.01), while corresponding erythrocyte GSH/GSSG ratios decreased by 31, 46, 49, 48%, respectively (each P<0.01). Erythrocyte SOD and plasma ascorbate did not change significantly. At sea level, maximal exercise induced a 49% increase in LP (P<0.01), and a 27% decrease in erythrocyte GSH/GSSG ratio relative to resting values (P<0.05). At 6000 m, the LP was enhanced further from 23 (P<0.05) to 66% (P<0.01), and after RSL from 81 (P<0.01) to 232% (P<0.01), while pre-exercise GSH/GSSG ratios did not change significantly. Exercise did not change plasma ascorbate relative to sea level or to 6000 m, but decreased after RSL by 32% (P<0.01). These findings suggest that oxidative stress is induced by prolonged hypobaric hypoxia, and is maintained by rapid return to sea level, similar to the post-hypoxic re-oxygenation process. It is increased by physical exercise.

Doppler study of middle cerebral artery blood flow velocity and cerebral autoregulation during a simulated ascent of Mount Everest.

OBJECTIVE: To explore cerebral hemodynamics in 8 healthy volunteers in a hypobaric chamber up to the altitude of Mount Everest after a progressive stepwise decompression to 8,848 m. METHODS: Physiological, clinical, and transcranial Doppler data were collected after at least 3 days at 5,000, 6,000, and 7,000 m and within 4 hours of reaching 8,000 m and returning to sea level. RESULTS: Three subjects were excluded at 8,000 and 8,848 m because of acute neurological deficits. Heart rate increased; mean arterial pressure remained stable; PaO2 and PaCO2 decreased with altitude; hemoglobin (Hb) and hematocrit (Ht) increased; arterial O2 content decreased over 6,000 m; middle cerebral artery blood flow velocity (MCAv) increased only during acute exposure to 8,000 m; and the corresponding pulsatility (PI) and resistivity indices (RI) decreased over 5,000 m. PI and RI correlated with heart rate. The transient hyperemic response (THR) of MCAv to common carotid compression was depressed at 8,000 m. CONCLUSIONS: At 8,000 m, the increase in MCAv seemed to reflect the normal hemodynamic response to acute hypoxia. The decrease of THR at this altitude could be an indication of impaired cerebral autoregulation. The role of impaired cerebral autoregulation in the genesis of acute neurologic deficits, observed at 8,000 m and above in 3 subjects, remains speculative.

A study of mood changes and personality during a 31-day period of chronic hypoxia in a hypobaric chamber (Everest-Comex 97).

High altitudes of more than 3,000 meters produce physiological disorders and adverse changes in mood states. In the present study, we report analyses of mood states and personality traits in eight experienced climbers participating in a 31-day period of confinement in hypobaric chamber and gradual decompression from sea level to 8,848 m (Experiment 'Everest-Comex 97'). The subjects were tested at 5,500 m and 6,500 m on Day 13, 5,000 m and 6,500 m on Day 24, and 8,000 m and 8,848 m altitude on Days 27 and 31. Adverse changes in mood states, such as Vigor and Fatigue, occurred at 8,000 m and 8,848 m, which were significantly correlated with cerebral altitude symptomatology. In addition, a significant negative correlation was found between Fatigue and Factor C, which is a personality measure of emotional stability. We suggest that individuals with low emotional stability could be more sensitive to environmental stressors than more emotionally stable subjects who face reality.

Color discrimination under chronic hypoxic conditions (simulated climb "Everest-Comex 97").

Hypoxia is known to alter visual functions. In the present study, the effects of chronic hypobaric hypoxia upon visual color discrimination were studied in 8 subjects participating in a simulated climb from sea level (PO2 = 210 hPa) to 8,848 m (PO2 = 70 hPa) over a 31-day period of confinement in a decompression chamber ('Everst-Comex 97'). During these investigations, the subjects were required to discriminate between colors of different hue in the red, blue, and green ranges. Alterations in color discrimination increased slightly but significantly as altitude increased. Impairments occurred mainly in the red and blue ranges. In addition, our results further indicate that color discrimination would be affected only when a minimum threshold of difference between color stimuli is not present. Methodological and physiological implications are discussed.

Psychomotor skills learning under chronic hypoxia.

Psychomotor deficits are a prominent feature in subjects exposed to hypoxia. Eight subjects exposed to chronic hypoxia during a simulated climb to 8848 m (Everest-Comex 97) were investigated using both a simple psychomotor task (Purdue pegboard) and two complex psychomotor tasks including a recognition task of either a color stimulus (high semantic level) or an abstract sign (low semantic level). Exposure to hypoxic stress mainly produced psychomotor skills learning deficits compared to control study, with greater deficits in the complex psychomotor task. The pattern of results suggests disruptions of motor strategic process. Our data further suggest that the relative strength of implicit or automatic memory processes associated with semantic information processing may increase when disturbances occur in brain functions.

Operation Everest III (COMEX '97). Effects of prolonged and progressive hypoxia on humans during a simulated ascent to 8,848 M in a hypobaric chamber.

Exposure to high altitude induces physiological or pathological modifications that are not always clearly attributable to a specific environmental factor: hypoxia, cold, stress, inadequate food. The principal goal of hypobaric chamber studies is to determine the specific effect of hypoxia. Eight male volunteers ("altinauts"), aged 23 to 37 were selected. They were first preacclimatized in the Observatoire Vallot (4,350 m) before entering the chamber. The chamber was progressively decompressed down to 253 mmHg barometric pressure, with a recovery period of 3 days at 5,000 m in the middle of the decompression period. They spent a total of 31 days in the chamber. Eighteen protocols were organized by 14 European teams, exploring the limiting factors of physical and psychological performance, and the pathophysiology of acute mountain sickness (AMS). All subjects reached 8,000 m and 7 of them reached the simulated altitude of 8,848 m. Three altinauts complained of transient neurological symptoms which resolved rapidly with reoxygenation. Body weight decreased by 5.4 kg through a negative caloric balance. Only four days after the return to sea-level, subjects had recovered 3.4 kg, i.e. 63% of the total loss. At 8,848 m (n = 5), PaO2 was 30.6 +/- 1.4 mmHg, PCO2 11.9 +/- 1.4 mmHg, pH 7.58 +/- 0.02 (arterialized capillary blood). Hemoglobin concentration increased from 14.8 +/- 1.4 to 18.4 +/- 1.5 g/dl at 8,000 m and recovered within 4 days at sea-level. AMS score increased rapidly at 6,000 m and was maximal at 7,000 m, especially for sleep. AMS was related to alteration in color vision and elevation of body temperature. VO2MAX decreased by 59% at 7,000 m. The purpose of this paper is to give a general description of the study and the time course of the main clinical and physiological parameters. The altinauts reached the "summit" (for some of them three consecutive times) in better physiological conditions than it would have been possible in the mountains, probably because acclimatization and other environmental factors such as cold and nutrition were controlled.

An anxiety, personality and altitude symptomatology study during a 31-day period of hypoxia in a hypobaric chamber (experiment 'Everest-Comex 1997').

Extreme environmental situations are useful tools for the investigation of the general processes of adaptation. Among such situations, high altitude of more than 3000 m produces a set of pathological disorders that includes both cerebral (cAS) and respiratory (RAS) altitude symptoms. High altitude exposure further induces anxiety responses and behavioural disturbances. The authors report an investigation on anxiety responses, personality traits, and altitude symptoms (AS) in climbers participating in a 31-day period of confinement and gradual decompression in a hypobaric chamber equivalent to a climb from sea-level to Mount Everest (8848 m altitude). Personality traits, state-trait anxiety, and AS were assessed, using the Cattell 16 Personality Factor questionnaire (16PF), the Spielberger's State-Trait Anxiety Inventory (STAI), and the Lake Louise concensus questionnaire. Results show significant group effect for state-anxiety and AS; state-anxiety and AS increased as altitude increased. They also show that state-type anxiety shows a similar time-course to cAS, but not RAS. Alternatively, our results demonstrate a significant negative correlation between Factor M of the 16PF questionnaire, which is a personality trait that ranges from praxernia to autia. In contrast, no significant correlation was found between personality traits and AS. This suggests that AS could not be predicted using personality traits and further support that personality traits, such as praxernia (happening sensitivity), could play a major role in the occurrence of state-type anxiety responses in extreme environments. In addition, the general processes of coping and adaptation in individuals participating in extreme environmental experiments are discussed.