Electrocardiographic aspects of deep dives in elite breath-hold divers.

The cardiac diving response, 12-lead electrocardiogram (ECG) and the prevalence, time of onset, and possible associations of cardiac arrhythmias were examined during deep breath-hold (BH) dives. Nine elite BH divers (33.2 +/- 3.6 years; mean +/- SD) performed one constant-weight dive of at least 75% of their best personal performance (70 +/- 7 meters for 141 +/- 22 seconds) wearing a 12-lead ECG Holter monitor. Diving parameters (depth and time), oxygen saturation (SaO2), blood lactate concentration and ventilatory parameters were also recorded. Bradycardia during these dives was pronounced (52.2 +/- 12.2%), with heart rates dropping to 46 +/- 10 beats/minute. The diving reflex was strong, overriding the stimulus of muscular exercise during the ascent phase of the dive for all divers. Classical arrhythmias occurred, mainly after surfacing, and some conduction alterations were detected at the bottom of the dives. The BH divers did not show any right shift of the QRS electrical axis during their dives.

A new biophysical decompression model for estimating the risk of articular bends during and after decompression.

The biophysical models that intend to predict the risk of decompression sickness after a change of pressure are not numerous. Few approaches focus in particular on joints as target tissues, with the aim to describe properly the mechanisms inducing pain. Nevertheless, for this type of decompression incidents, called articular bends, no model proved to fit the empirical results for a broad range of exposures and decompression procedures. We present here an original biophysical decompression model for describing the occurrence of articular bends. A target joint is broken down into two parts that exchange inert gases with the blood by perfusion and with each other by diffusion over distances of a few millimetres. This diffusion pathway allows the slow amplification of microbubbles growing during and after decompression, consistent with the possible delayed occurrence of bends. The diffusion coefficients introduced into this model are larger than those introduced into most modern decompression models. Their value remains physical (#10(-9)m(2)/s). Inert gas exchanges and the formation, amplification and resorption of microbubbles during and after decompression were simulated. We used a critical gas volume criterion for predicting the occurrence of bends. A risk database extracted from COMEX experience and other published studies were used for the correlation of model parameters not known a priori. We considered a large range of exposure, and the commonly used inert gases nitrogen and helium. This correlation phase identified the worst biophysical conformations most likely to lead to the formation, in tissues such as tendons, of a large number of microbubbles recruited from pre-existing gas nuclei during decompression. The risk of bends occurrence was found to be linked to the total separated gas volume generated during and after decompression. A clamping phenomenon occurs soon after the start of decompression, greatly slowing the gas exchanges controlled especially by the oxygen window. This model, which reproduces many empirical findings, may be considered both descriptive and predictive.

The pathway to drive decompression microbubbles from the tissues to the blood and the lymphatic system as a part of this transfer.

The formation sites of the microbubbles that are routinely detected in the bloodstream at precordial level by Doppler after a decompression are reviewed and discussed here. First, microbubbles could form on the endothelium lumen wall of the capillaries, at specific nanometric sites, but the release mechanism of such small emerging entities remains puzzling. They could be also formed from pre-existing gas nuclei present in the blood when favorable local hydrodynamic/supersaturation conditions generate microcavitation and tribonucleation phenomena. Finally, tissues could represent large pools for microbubble formation and amplification. Nevertheless, it remains to explain what the potential pathways are to drive them to the blood. Knowing that the permeability of most of the blood capillary network is quite low, an alternative is proposed for such transport. The lymphatic system, which drains the interstitial fluid to guarantee the fluid balance of tissues, could allow the transfer of micrometric elements like stabilized microbubbles formed in tissues on long distances. A final rejection in the bloodstream at the termination of both right lymphatic and thoracic ducts can be expected. The characteristics of this slow transport, activated by the muscular pump, could explain the detection on long periods of massive venous gas emboli.

Effects of hyperbaric exposures on cardiac pacemakers.

Data on tolerance of cardiac pacemakers during diving are very scarce. The aim of this study was to test electronic and mechanical tolerances of pacemakers exposed to experimental reproductions of pressures encountered during diving. Two samples each of 20 different models of cardiac pacemakers were exposed to compression during continuous telemetric monitoring. The first sample of each model was exposed to a pressure of 60 metres of sea water (msw). Each second sample was first exposed to a pressure of 30 msw then to 60 msw hyperbaric testing, with a period of 1 month between the two tests. Electronic function and structural integrity of the cans were evaluated. No electronic dysfunction was noted. We merely observed in some devices a transient increase of the pacing rate during pressurisation. No significant deformation of the can (< or =0.2 mm) was observed after the 30 msw hyperbaric test. However, after the 60 msw test, more than half of the devices tested were significantly and definitively deformed. These results show that tested pacemakers preserved a normal electronic function up to 60 msw but most of the tested devices demonstrated significant deformations of the pacemaker can for the hyperbaric exposure observed deeper than 30 msw. Without prejudging diving aptitude for implanted pacemaker patients, it therefore seems prudent to advise them against diving beyond 30 msw because of the potential for electronic dysfunction beyond that depth.

Heart rate responses during a breath-holding competition in well-trained divers.

The diving response elicited by breath-holding (BH) and immersion mainly consists of bradycardia, decreased cardiac output, and peripheral vasoconstriction. These responses reduce oxygen consumption and thereby prolong the duration of the dive. They may also lead to cardiac arrhythmias or hypoxia, however, which in turn may play a role in the occurrence of syncope during BH. The aim of the present study was to analyze the cardiac responses to prolonged breath-holding in elite divers during a competition. Heart rate behaviour and the incidence of arrhythmia were recorded in 16 well-trained breath-hold divers (BHD) using a cardio-frequency meter (for 15 divers) and a Holter (for one diver) during maximal static breath-holding. Anthropometric, spirometric, and training characteristics such as percentage of body fat, pulmonary volumes and years of BH training were also determined. Forced vital capacity (FVC) and forced expiratory volume in one second (FEV (1)) were higher than the predicted values (+7.7%, p<0.05 and+6.6%, p<0.05, respectively). During the static BH, divers presented apneic bradycardia (-44%) correlated with static BH times (p<0.05); this was associated with cardiac arrhythmias (supraventricular extrasystoles and ventricular extrasystoles) in the Holter-equipped subject. These results are in agreement with those obtained in laboratory conditions and confirm the existence of cardiac arrhythmias in well-trained BHD.

Ascent rate, age, maximal oxygen uptake, adiposity, and circulating venous bubbles after diving.

Decompression sickness in diving is recognized as a multifactorial phenomenon, depending on several factors, such as decompression rate and individual susceptibility. The Doppler ultrasonic detection of circulating venous bubbles after diving is considered a useful index for the safety of decompression because of the relationship between bubbles and decompression sickness risk. The aim of this study was to assess the effects of ascent rate, age, maximal oxygen uptake (VO(2 max)), and percent body fat on the production of bubbles after diving. Fifty male recreational divers performed two dives at 35 m during 25 min and then ascended in one case at 9 m/min and in the other case at 17 m/min. They performed the same decompression stops in the two cases. Twenty-eight divers were Doppler monitored at 10-min intervals, until 60 min after surfacing, and the data were analyzed by Wilcoxon signed-rank test to compare the effect of ascent rate on the kinetics of bubbles. Twenty-two divers were monitored 60 min after surfacing. The effect on bubble production 60 min after surfacing of the four variables was studied in 47 divers. The data were analyzed by multinomial log-linear model. The analysis showed that the 17 m/min ascent produced more elevated grades of bubbles than the 9 m/min ascent (P < 0.05), except at the 40-min interval, and showed relationships between grades of bubbles and ascent rate and age and interaction terms between VO(2 max) and age, as well as VO(2 max) and percent body fat. Younger, slimmer, or aerobically fitter divers produced fewer bubbles compared with older, fatter, or poorly physically fit divers. These findings and the conclusions of previous studies performed on animals and humans led us to support that ascent rate, age, aerobic fitness, and adiposity are factors of susceptibility for bubble formation after diving.

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.

Anti-inflammatory properties of molecular hydrogen: investigation on parasite-induced liver inflammation.

Molecular hydrogen reacts with the hydroxyl radical, a highly cytotoxic species produced in inflamed tissues. It has been suggested therefore to use gaseous hydrogen in a new anti-inflammatory strategy. We tested this idea, with the aid of the equipment and skills of COMEX SA in Marseille, a group who experiments with oxygen-hydrogen breathing mixtures for professional deep-sea diving. The model used was schistosomiasis-associated chronic liver inflammation. Infected animals stayed 2 weeks in an hyperbaric chamber in a normal atmosphere supplemented with 0.7 MPa hydrogen. The treatment had significant protective effects towards liver injury, namely decreased fibrosis, improvement of hemodynamics, increased NOSII activity, increased antioxidant enzyme activity, decreased lipid peroxide levels and decreased circulating TNF-alpha levels. Under the same conditions, helium exerted also some protective effects, indicating that hydroxyl radical scavenging is not the only protective mechanism. These findings indicate that the proposed anti-inflammatory strategy deserves further attention.

Ascent rate and circulating venous bubbles in recreational diving.

The aim of this study was to assess the effect of the ascent rate on the production of venous circulating bubbles during the decompression following a recreational dive. Twenty-eight recreational divers performed two open water dives at 35 m during 25 minutes. Ascent rate up to the decompression stop was in one case 9 meter per minute (m/min) and in the other case 17 m/min. Circulating venous bubbles were screened using continuous wave Doppler every 10 minutes during one hour after surfacing. Bubbles Doppler signals were graded according to the Spencer scale (from 0 to IV), and the Kisman integrated severity score (KISS) was calculated. Statistical analysis demonstrated a significantly higher bubbles grade and a significantly higher KISS following the rapid decompression compared to the slow one (respectively p = 0.001 and p = 0.0001). In conclusion, these results demonstrate that a 9 m/min ascent rate is safer than a 17 m/min one.

Operation Everest III: role of plasma volume expansion on VO(2)(max) during prolonged high-altitude exposure.

We hypothesize that plasma volume decrease (DeltaPV) induced by high-altitude (HA) exposure and intense exercise is involved in the limitation of maximal O(2) uptake (VO(2)(max)) at HA. Eight male subjects were decompressed for 31 days in a hypobaric chamber to the barometric equivalent of Mt. Everest (8,848 m). Maximal exercise was performed with and without plasma volume expansion (PVX, 219-292 ml) during exercise, at sea level (SL), at HA (370 mmHg, equivalent to 6, 000 m after 10-12 days) and after return to SL (RSL, 1-3 days). Plasma volume (PV) was determined at rest at SL, HA, and RSL by Evans blue dilution. PV was decreased by 26% (P < 0.01) at HA and was 10% higher at RSL than at SL. Exercise-induced DeltaPV was reduced both by PVX and HA (P < 0.05). Compared with SL, VO(2)(max) was decreased by 58 and 11% at HA and RSL, respectively. VO(2)(max) was enhanced by PVX at HA (+9%, P < 0.05) but not at SL or RSL. The more PV was decreased at HA, the more VO(2)(max) was improved by PVX (P < 0.05). At exhaustion, plasma renin and aldosterone were not modified at HA compared with SL but were higher at RSL, whereas plasma atrial natriuretic factor was lower at HA. The present results suggest that PV contributes to the limitation of VO(2)(max) during acclimatization to HA. RSL-induced PVX, which may be due to increased activity of the renin-aldosterone system, could also influence the recovery of VO(2)(max).

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.

Changes in maximal performance of inspiratory and skeletal muscles during and after the 7.1-MPa Hydra 10 record human dive.

During the 7.1-MPa hydrogen-helium-oxygen record human dive, we tested the hypothesis that the increased ambient pressure would alter the maximal muscle performance, specifically that breathing dense gas would lead to fatigue of the respiratory muscle. A group of hand muscles (adductor pollicis, AP) and the inspiratory muscles (IM) were studied in three professional divers. Maximal voluntary contractions (MVC) of AP and maximal inspiratory pressure (P(i(max))) generated by IM were measured prior to the dive, during compression and decompression, and then 1 and 2 months after the dive. The decrease in MVC (-22%) was significant at 3.1 MPa, i.e. at the beginning of the introduction of hydrogen into the breathing mixture, whereas P(i(max)) fell progressively during the dive and decompression (maximal DeltaP(i(max)) = -55%), a significant reduction still being measured 1 month after the dive. The altered IM function was attributed to the consequences of long-term ventilatory loading, a condition associated with breathing a dense gas. The transient decrease in MVC of the skeletal muscle would indicate a possible effect of the hyperbaric environment, possibly the high partial pressure of hydrogen, on neuromuscular drive.

Operation Everest III (Comex '97): modifications of cardiac function secondary to altitude-induced hypoxia. An echocardiographic and Doppler study.

During Operation Everest III (Comex '97), to assess the consequences of altitude-induced hypoxia, eight volunteers were decompressed in a hypobaric chamber, with a decompression profile simulating the climb of Mount Everest. Cardiac function was assessed using a combination of M-mode and two-dimensional echocardiography, with continuous and pulsed Doppler at 5,000, 7,000, and 8,000 m as well as 2 d after return to sea level (RSL). On simulated ascent to altitude, aortic and left atrial diameters, left ventricular (LV) diameters, and right ventricular (RV) end-systolic diameter fell regularly. Heart rate (HR) increased at all altitudes accompanied by a decrease in stroke volume; in total, cardiac output (Q) remained unchanged. LV filling was assessed on transmitral and pulmonary venous flow profiles. Mitral peak E velocity decreased, peak A velocity increased, and E/A ratio decreased. Pulmonary venous flow velocities showed a decreased peak D velocity, a decreased peak S velocity, and a reduction of the D/S ratio. Systolic pulmonary arterial pressure (Ppa) showed a progressive and constant increase, as seen on the elevation of the right ventricular/right atrial (RV/RA) gradient pressure from 19.0 +/- 2.4 mm Hg at sea level up to 40.1 +/- 3.3 mm Hg at 8,000 m (p < 0.05), and remained elevated 2 d after recompression to sea level (SL) (not significant). In conclusion, this study confirmed the elevation of pulmonary pressures and the preservation of LV contractility secondary to altitude-induced hypoxia. It demonstrated a modification of the LV filling pattern, with a decreased early filling and a greater contribution of the atrial contraction, without elevation of LV end-diastolic pressure.

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.

Circulating venous bubbles in recreational diving: relationships with age, weight, maximal oxygen uptake and body fat percentage.

Decompression sickness (DCS) is recognized as a multifactorial phenomenon depending on several individual factors, such as age, adiposity, and level of fitness. The detection of circulating venous bubbles is considered as a useful index for the safety of a decompression, because of the relationship between bubbles and DCS probability. The aim of this work was to study the effects of individual variables which can be assessed non invasively, on the grades of bubbles detected 60 min, after diving by means of Doppler monitoring, in a sample of 40 male recreational scuba divers. The variables investigated were: age, weight, maximal oxygen uptake (VO2max) and percentage of body fat (%BF). Bubble signals were graded according to the code of Spencer. The relationships between the bubble grades (BG) and the variables investigated were studied using two methods: the differences between the average values of each variable at each BG were analyzed by the Scheffe test. Then we performed the non-parametric Spearman correlation analysis. Significant differences (P < 0.05) were found (Scheffe test) between average values of the variables at grade 0 and 3 (age: P = 0.0323; weight: P = 0.0420; VO2max: P = 0.0484), except for %BF (P = 0.1697). Relationships with P < 0.01 were found (Spearman correlation) between BG and the variables: age: p = 0.486, P = 0.0024; weight: p = 0.463, P = 0.0039; VO2max: p = -0.481, P = 0.0027; except for %BF: p = 0.362, P = 0.0237. This work showed that bubble production after hyperbaric exposures depends on several individual factors. The effects of age, weight and VO2max are more significant than the effect of %BF. We concluded that to take into account such variables in decompression tables and diving computer programs should allow to adapt the decompression procedures to individual risk factors and reduce the DCS probability.

Appetite at "high altitude" [Operation Everest III (Comex-'97)]: a simulated ascent of Mount Everest.

We hypothesized that progressive loss of body mass during high-altitude sojourns is largely caused by decreased food intake, possibly due to hypobaric hypoxia. Therefore we assessed the effect of long-term hypobaric hypoxia per se on appetite in eight men who were exposed to a 31-day simulated stay at several altitudes up to the peak of Mt. Everest (8,848 m). Palatable food was provided ad libitum, and stresses such as cold exposure and exercise were avoided. At each altitude, body mass, energy, and macronutrient intake were measured; attitude toward eating and appetite profiles during and between meals were assessed by using questionnaires. Body mass reduction of an average of 5 +/- 2 kg was mainly due to a reduction in energy intake of 4.2 +/- 2 MJ/day (P < 0.01). At 5,000- and 6,000-m altitudes, subjects had hardly any acute mountain sickness symptoms and meal size reductions (P < 0.01) were related to a more rapid increase in satiety (P < 0.01). Meal frequency was increased from 4 +/- 1 to 7 +/- 1 eating occasions per day (P < 0. 01). At 7,000 m, when acute mountain sickness symptoms were present, uncoupling between hunger and desire to eat occurred and prevented a food intake necessary to meet energy balance requirements. On recovery, body mass was restored up to 63% after 4 days; this suggests physiological fluid retention with the return to sea level. We conclude that exposure to hypobaric hypoxia per se appears to be associated with a change in the attitude toward eating and with a decreased appetite and food intake.

Cough frequency and cough receptor sensitivity to citric acid challenge during a simulated ascent to extreme altitude.

The aim of this study was to determine the frequency of cough and the citric acid cough threshold during hypobaric hypoxia under controlled environmental conditions. Subjects were studied during Operation Everest 3. Eight subjects ascended to a simulated altitude of 8,848 m over 31 days in a hypobaric chamber. Frequency of nocturnal cough was measured using voice-activated tape recorders, and cough threshold by inhalation of increasing concentrations of citric acid aerosol. Spirometry was performed before and after each test. Subjects recorded symptoms of acute mountain sickness and arterial oxygen saturation daily. Air temperature and humidity were controlled during the operation. Cough frequency increased with increasing altitude, from a median of 0 coughs (range 0-4) at sea level to 15 coughs (range 3-32) at a simulated altitude of 8,000 m. Cough threshold was unchanged on arrival at 5,000 m compared to sea level (geometric mean difference (GMD) 1.0, 95% confidence intervals (CI) 0.5-2.1, p=0.5), but fell on arrival at 8,000 m compared to sea level (GMD 3.3, 95% CI 1.1-10.3, p=0.043). There was no relationship between cough threshold and symptoms of acute mountain sickness, oxygen saturation or forced expiratory volume in one second. Temperature and humidity in the chamber were controlled between 18-24 degrees C and 30-60%, respectively. These results confirm an increase in cough frequency and cough receptor sensitivity associated with hypobaric hypoxia, and refute the hypothesis that high altitude cough is due to the inhalation of cold, dry air. The small sample size makes further conclusions difficult, and the cause of altitude-related cough remains unclear.

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.