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PubMed1995

Hering-Breüer reflexes in high-altitude infants.

1. Pulmonary ventilation was found to be similar in high-altitude and low-altitude newborn infants, but the breathing pattern was deeper and slower at high altitude (Mortola, J.P., Frappell, P.B., Frappell, D.E., Villena-Cabrera, N., Villena-Cabrera, M., Peña, F., Am Rev Respir Dis 1992, 46: 1206-9). We questioned the contribution of vagal reflexes to these differences in breathing pattern. 2. Measurements were performed on high-altitude (La Paz, Bolivia, 3600-4050 m, inspired O2 pressure approximately 92 mmHg, n = 34) and low-altitude infants (Santa Cruz, Bolivia, 400 m, PIO2 approximately 141 mmHg, n = 26). The strength of the Hering-Breüer inspiratory inhibitory reflex was estimated from the inspiratory time during a respiratory effort against airways closed at end-expiration (Tloccl). The strength of the Hering-Breüer expiratory facilitatory reflex was estimated from the expiratory duration when airways were occluded during expiration (TEoccl). 3. Tloccl was significantly longer than the open-airways TI at both low and high altitude, but significantly more so (approximately 14%) at high altitude. TEoccl was longer than open-airways TE in both groups of infants, but significantly less so at high altitude, whether TEoccl was compared between occlusions of similar tidal volume (on average, TEoccl at high altitude was 79% of that at low altitude) or similar airway pressure (87%). 4. The results suggest that at high altitude the contribution of the phasic volume-dependent vagal input to the inspiratory off-switch threshold is higher, and that the tonic vagal expiratory facilitation is lower, than at low altitude, presumably because of hypoxia.(ABSTRACT TRUNCATED AT 250 WORDS)

Altitude↗

PubMed1997

Increased left ventricular muscle mass after long-term altitude training in athletes.

The effects of long-term altitude training on altitude and sea-level physiological characteristics in elite endurance athletes were investigated. Seven Swedish elite cross-country skiers (five men, two women; mean age 27 years) spent 1 month training at 1900 m above sea level in Italy. Rollerski treadmill tests were performed before and 5 and 11 days after the altitude sojourn; three tests were also performed at altitude. Before and 1, 11 and 35 days after the altitude camp, echocardiographic and blood volume measurements were performed. The heart rates at both maximal (P < 0.05) and submaximal (P < 0.01) work loads were decreased by 5-9 beats min-1 at altitude. The haemoglobin concentration and haematocrit increased quickly at altitude with a corresponding decrease on return to sea level. The blood volume (7%) and total haemoglobin (3%) tended to be higher day 11 post-altitude (NS). There were no significant changes in diastolic internal diameter or wall thickness of the left ventricle, but the calculated cardiac left ventricular muscle mass was increased post-altitude (9-10%, P < 0.01). The maximal oxygen uptake increased in six of the seven skiers after the altitude training (day 11, mean 3%, NS). In conclusion, training at moderate altitude may cause a reduction in heart rates during exercise. Moreover, after long-term training at altitude, there may be an increase in the cardiac left ventricular muscle mass.

Adaptation, Physiological↗

PubMed1990

Blood gas transport properties in endurance-trained athletes living at different altitudes.

Hemoglobin oxygen binding properties and acid-base status were investigated in Colombian athletes (A) and controls (C) from Cali (C-1000 m) and Bogotá (B-2600 m). [Hb] and Hct values were not influenced by altitude, but Hct was lower in the blood of athletes (in Cali 2.6%, in Bogotá 1.4%). Both training and altitude produced a right-shift of the standard oxygen dissociation curve (P50 in CC 28.5 +/- 0.9 mmHg, AC 31.0 +/- 1.4 mmHg, CB 29.6 +/- 1.5 mmHg) leading to highest P50 in blood of altitude athletes (32.3 +/- 1.1 mmHg). Opposite to the position of the ODC the slope "n" was only increased by altitude influence (delta "n" in controls 0.07, in athletes 0.28). The BCCO2 was increased in AC over the whole saturation range, whereas BCLac was neither significantly influenced by training nor by altitude. All altitude effects can be explained by higher [DPG] (delta[DPG] in controls 5.0 mumol/gHb, in athletes 3.9 mumol/gHb), but the cause for the training effects still remains unclear. The acid base status in altitude residents was characterized by low BE and pCO2, which was most pronounced in altitude athletes, the latter correcting the actual venous pH to normal values. No significant variations of the Hb-O2-binding properties could be detected in athletes one day after leaving high altitude when compared with blood samples of athletes taken at high altitude, whereas BE and venous pCO2 were already increased. It is concluded that high altitude athletes are favoured during aerobic and handicapped during anaerobic exercise after the rapid descent to low altitude.

Acid-Base Equilibrium↗

PubMed1996

Inhaled nitric oxide for high-altitude pulmonary edema.

BACKGROUND: Pulmonary hypertension is a hallmark of high-altitude pulmonary edema and may contribute to its pathogenesis. When administered by inhalation, nitric oxide, an endothelium-derived relaxing factor, attenuates the pulmonary vasoconstriction produced by short-term hypoxia. METHODS: We studied the effects of inhaled nitric oxide on pulmonary-artery pressure and arterial oxygenation in 18 mountaineers prone to high-altitude pulmonary edema and 18 mountaineers resistant to this condition in a high altitude laboratory (altitude, 4559 m). We also obtained lung-perfusion scans before and during nitric oxide inhalation to gain further insight into the mechanism of action of nitric oxide. RESULTS: In the high-altitude laboratory, subjects prone to high-altitude pulmonary edema had more pronounced pulmonary hypertension and hypoxemia than subjects resistant to high-altitude pulmonary edema. Arterial oxygen saturation was inversely related to the severity of pulmonary hypertension (r=-0.50, P=0.002). In subjects prone to high-altitude pulmonary edema, the inhalation of nitric oxide (40 ppm for 15 minutes) produced a decrease in mean (+/-SD) systolic pulmonary-artery pressure that was three times larger than the decrease in subjects resistant to such edema (25.9+/-8.9 vs. 8.7+/-4.8 mm Hg, P<0.001). Inhaled nitric oxide improved arterial oxygenation in the 10 subjects who had radiographic evidence of pulmonary edema (arterial oxygen saturation increased from 67+/-10 to 73+/-12 percent, P=0.047), whereas it worsened oxygenation in subjects resistant to high-altitude pulmonary edema. The nitric oxide-induced improvement in arterial oxygenation in subjects with high-altitude pulmonary edema was accompanied by a shift in blood flow in the lung away from edematous segments and toward nonedematous segments. CONCLUSIONS: The inhalation of nitric oxide improves arterial oxygenation in high-altitude pulmonary edema, and this beneficial effect may be related to its favorable action on the distribution of blood flow in the lungs. A defect in nitric nitric oxide synthesis may contribute to high-altitude pulmonary edema.

Administration, Inhalation↗

PubMed1995

Doppler assessment of hypoxic pulmonary vasoconstriction and susceptibility to high altitude pulmonary oedema.

BACKGROUND: Subjects with previous high altitude pulmonary oedema may have stronger than normal hypoxic pulmonary vasoconstriction. Susceptibility to high altitude pulmonary oedema may be detectable by echo Doppler assessment of the pulmonary vascular reactivity to breathing a hypoxic gas mixture at sea level. METHODS: The study included 20 healthy controls, seven subjects with a previous episode of high altitude pulmonary oedema, and nine who had successfully climbed to altitudes of 6000-8842 m during the 40th anniversary British expedition to Mount Everest. Echo Doppler measurements of pulmonary blood flow acceleration time (AT) and ejection time (ET), and of the peak velocity of the tricuspid regurgitation jet (TR), were obtained under normobaric conditions of normoxia (fraction of inspired oxygen, FIO2, 0.21), of hyperoxia (FIO2 1.0), and of hypoxia (FIO2 0.125). RESULTS: Hypoxia decreased AT/ET by mean (SE) 0.06 (0.01) in the control subjects, by 0.11 (0.01) in those susceptible to high altitude pulmonary oedema, and by 0.02 (0.02) in the successful high altitude climbers. Hypoxia increased TR in the three groups by 0.22 (0.06) (n = 14), 0.56 (0.13) (n = 5), and 0.18 (0.1) (n = 7) m/s, respectively. However, AT/ET and/or TR measurements outside the normal range, defined as mean +/- 2 SD of measurements obtained in the controls under hypoxia, were observed in only two of the subjects susceptible to high altitude pulmonary oedema and in five of the successful high altitude climbers. CONCLUSIONS: Pulmonary vascular reactivity to hypoxia is enhanced in subjects with previous high altitude pulmonary oedema and decreased in successful high altitude climbers. However, echo Doppler estimates of hypoxic pulmonary vaso-constriction at sea level cannot reliably identify subjects susceptible to high altitude pulmonary oedema or successful high altitude climbers from a normal control population.

Adult↗

PubMed1996

Effect of altitude and socioeconomic status on VO2max and anaerobic power in prepubertal Bolivian girls.

The aim of this work was to evaluate the effects of high altitude and low socioeconomic status (SES) on aerobic and anaerobic power in 11-yr-old Bolivian girls. At both high (3,600 m) and low (420 m) altitudes, low-SES groups of girls were compared to similarly aged, high-SES girls. At low altitude, low-SES girls were also compared with younger high-SES girls with the same anthropometric characteristics. Anthropometric data were similar between high-SES and low-SES girls at both altitudes, but low-SES girls showed a 9-mo growth delay. Maximal O2 uptake was significantly lower for low-SES girls at both altitudes. Values did not differ when expressed relative to body weight at high altitude for high-SES vs. low-SES girls (37.6 +/- 1.2 vs. 39.3 +/- 1.0 ml.min-1.kg body wt-1), but a difference persisted at low altitude between high- and low-SES girls (37.5 +/- 1.0 vs. 34.7 +/- 0.7 ml.min-1.kg body wt-1). Anaerobic power (Pmax, force-velocity test; Pwing, Wingate test) was reduced for low-SES girls at both altitudes, whatever the mode of expression. For a given SES, the relative anaerobic performances were lower at low altitude. At low altitude, low-SES girls developed lower anaerobic power than did younger high-SES girls with similar anthropometric characteristics. In conclusion, at both altitudes, the reduction of anaerobic performances observed in girls of low SES could not be totally explained by anthropometric factors. Structural and/or functional muscle alterations are suggested. Moreover, at low altitude, tropical and other factors may have contributed to differences in performance between low- and high-SES girls.

Altitude↗

PubMed2006

Alterations in cerebral dynamics at high altitude following partial acclimatization in humans: wakefulness and sleep.

We tested the hypothesis that, following exposure to high altitude, cerebrovascular reactivity to CO2 and cerebral autoregulation would be attenuated. Such alterations may predispose to central sleep apnea at high altitude by promoting changes in brain PCO2 and thus breathing stability. We measured middle cerebral artery blood flow velocity (MCAv; transcranial Doppler ultrasound) and arterial blood pressure during wakefulness in conditions of eucapnia (room air), hypocapnia (voluntary hyperventilation), and hypercapnia (isooxic rebeathing), and also during non-rapid eye movement (stage 2) sleep at low altitude (1,400 m) and at high altitude (3,840 m) in five individuals. At each altitude, sleep was studied using full polysomnography, and resting arterial blood gases were obtained. During wakefulness and polysomnographic-monitored sleep, dynamic cerebral autoregulation and steady-state changes in MCAv in relation to changes in blood pressure were evaluated using transfer function analysis. High altitude was associated with an increase in central sleep apnea index (0.2 +/- 0.4 to 20.7 +/- 23.2 per hour) and an increase in mean blood pressure and cerebrovascular resistance during wakefulness and sleep. MCAv was unchanged during wakefulness, whereas there was a greater decrease during sleep at high altitude compared with low altitude (-9.1 +/- 1.7 vs. -4.8 +/- 0.7 cm/s; P < 0.05). At high altitude, compared with low altitude, the cerebrovascular reactivity to CO2 in the hypercapnic range was unchanged (5.5 +/- 0.7 vs. 5.3 +/- 0.7%/mmHg; P = 0.06), while it was lowered in the hypocapnic range (3.1 +/- 0.7 vs. 1.9 +/- 0.6%/mmHg; P < 0.05). Dynamic cerebral autoregulation was further reduced during sleep (P < 0.05 vs. low altitude). Lowered cerebrovascular reactivity to CO2 and reduction in both dynamic cerebral autoregulation and MCAv during sleep at high altitude may be factors in the pathogenesis of breathing instability.

Acclimatization↗

PubMed2003

Cardiopulmonary hemodynamics of blue-sheep, Pseudois nayaur, as high-altitude adapted mammals.

The blue-sheep, pika, and yak live in the Tibetan highlands at an altitude of 6,100 m and are typical mammals adapted to high-altitudes. These animals have a long history of habitation at high-altitudes and are considered to be "animals completely adapted to high-altitudes" because of their physiological and morphological traits that are well adapted to high-altitude environments. To evaluate the physiological characteristics of high-altitude adaptation in the blue-sheep, changes in the pulmonary hemodynamics during exposure to simulated-altitudes at 0, 2,300, and 4,500 m were examined by means of a climatic chamber in Qinghai Province, China (altitude 2,300 m). Seven blue-sheep inhabiting the mountains (3,000 m) of Qinghai Province, China, were compared with 5 pigs raised in the same area as controls. The primary items of measurement were the body weight (BW), systemic arterial pressure (Psa), pulmonary artery pressure (Ppa), hematocrit (Ht), left ventricular weight (LVW), right ventricular weight (RVW), and blood gas profile. The principal findings of this study are: (1) Ht, an index of right ventricular hypertrophy (RVW/LVW), and oxygen consumption (Vdot;O(2)) were significantly lower in the blue sheep compared with the pigs; (2) When the animals were exposed to simulated-altitudes at 0, 2,300, and 4,500 m, Ppa increased significantly in tandem with altitude elevation in both species, but the increases were significantly smaller in the blue-sheep; and (3) Ppa/Psa, an index of the right ventricular load, increased with the altitude in both species, but the increases were smaller in the blue sheep. From these observations, low Ht and RVW/LVW and significant attenuation of hypoxic pulmonary vasoconstriction (HPV) in the blue-sheep is considered to be characteristics of animals completely adapted to high-altitudes, such as the pika.

Altitude↗

PubMedDate not supplied

[Estimation of gasometric values at different altitudes above sea level in Mexico].

We calculated reference values for arterial blood gases at different altitudes in Mexico assuming that sea level PaCO2 is 40 Torr, and in Mexico City (2.24 km. above the sea level) is 31.13 Torr, average of reported reference values. With the previous two points, it is possible to calculate a linear regression: PaCO2 = 40-3.96(altitude in km.). The equation is very similar to that calculated from reports in alveolar gas in North-Americans (Fitzgerald < 5 km): PACO2 = 39.3-3.11(altitude in km), and from subjects acclimatized to acute altitude exposure (< 5 km): PACO2 = 38.3-2.5 (altitude in km). It is also similar to a alinear equation that can be calculated assuming that hyperventilation in permanent habitants of moderate altitudes is inversely proportional to inspired molar concentration of O2: PaCO2 = PIO2/3.74. On the other hand, the equation is very different than that obtained from Andean natives (Hurtado): PaCO2 = 40.4-1.35(altitude in km). The proposed linear equation for Mexico gives very similar results (< 2 Torr difference) than a complex curvilinear equation by Morris et al. appropriate only up to 2.3 km. Evidence from acute exposure to altitude (acclimatized) and in North-Americans (alveolar gas) supports a reasonably accurate linear relationship up to 4 km. and also that the increase in ventilation in response to moderate altitudes in adult permanent residents is inversely proportional to molar concentration of O2. PAO2 was calculated with alveolar gas equation and resting the P(A-a)O2 we obtained PaO2. In conclusion, according to reference values in Mexico City, PaCO2 decreases about 4 Torr per km of altitude above the sea level. The decrease is similar to that reported in North-Americans and in acute exposure to altitude (acclimatized), but much less than that reported in native Peruvians. Ventilation is inversely proportional to the molar concentration of O2 at least up to an altitude where SaO2 is at or above 90%.

Altitude↗

PubMed1989

Cardiovascular effects of chronic carbon monoxide and high-altitude exposure.

At higher altitudes, ambient carbon monoxide levels are increasing with the number of residents and tourists and their use of motor vehicles and heating devices (such as fireplaces, furnaces, and stoves). Although chronic exposure to carbon monoxide or high altitude causes pronounced cardiovascular changes in humans as well as in animals, there is little information on the effects elicited by these stressors combined. Data from acute studies and theoretical considerations suggest that carbon monoxide inhaled at altitude may be more detrimental than carbon monoxide inhaled at sea level. It is not known, however, if the cardiovascular system adapts or deteriorates with continuous, concurrent exposure to carbon monoxide and high altitude. Male laboratory rats were exposed for six weeks in steel barometric chambers to altitudes ranging from 3,300 ft (ambient) to 18,000 ft and to concentrations ranging from 0 to 500 parts per million (ppm)2. Carbon monoxide had no effect on body weight at any altitude. There was a tendency for hematocrit to increase even at the lowest concentration of carbon monoxide (9 ppm), but the increase did not become significant until 100 ppm. At 10,000 ft, there was a tendency for total heart weight to increase in rats inhaling 100 ppm carbon monoxide. Although its effects on the heart at altitude are complex, carbon monoxide, in concentrations of 500 ppm or less, had little effect on the right ventricle; it did not exacerbate any effects due to altitude. There was a tendency for the left ventricle weight to increase with exposure to 35 ppm carbon monoxide at altitude, but the increase was not significant until 100 ppm carbon monoxide. Heart rate, blood pressure, cardiac output, and peripheral resistance were unaffected by exposure to 35 ppm carbon monoxide or 10,000-ft altitude singly or in combination. I conclude that six weeks of exposure to 35 ppm carbon monoxide does not produce measurable effects in the healthy laboratory rat, nor does it exacerbate the effects produced by exposure to 10,000-ft altitude. Basal carboxyhemoglobin (COHb) level (due to endogenous carbon monoxide production) was increased from 0.7 to 1.0 percent at 10,000 ft, and to 1.7 percent at 15,000 ft. This suggests that the high-altitude resident has a greater initial body burden of COHb and will attain the COHb level associated with the National Ambient Air Quality Standard for carbon monoxide more quickly than the sea-level resident.

Altitude↗

PubMed1998

Maximal and submaximal exercise performance at altitude.

BACKGROUND: Exercise performance data of numerous altitude research studies and competitive sporting events of the last four decades are reviewed. METHODS: The primary focus is on the wide interindividual variation associated with maximal and submaximal exercise performance that occurs at different altitudes and for different periods of time at altitude. RESULTS: Fitness level, pre-exposure resident altitude, gender, and duration of altitude exposure are qualitatively assessed to determine their contribution to the overall variability. Of these, pre-altitude exposure fitness level difference contributes the most variability and gender difference contributes the least. It is also determined that beginning at an altitude of 580 m, maximal aerobic power (VO2max reduced and does not improve with extended exposure as long as the individual's level of fitness level is not altered significantly by increases in activity, exercise training or by altitude-induced physical deterioration. Submaximal exercise performance is also impaired at altitude. CONCLUSION: By assessing the performance of elite athletes, who are performing at an "all-out" effort in precisely timed events for which they are trained, it is determined that: a) the magnitude of submaximal exercise impairment is proportional to both the elevation and exercise duration at a given altitude; and b) submaximal exercise performance at altitude can improve with continued exposure without an increase in VO2max. Muscle strength, maximal muscle power, and anaerobic performance at altitude are not affected as long as muscle mass is maintained. In addition, performance is not impaired in athletic activities that have a minimal aerobic component and can be performed at high velocity (e.g., sprints).

Acclimatization↗

PubMed2026

Sex modifies the association of high-altitude hypoxia with poor sleep quality and depression in school-age children and adolescents.

BACKGROUND: While chronic exposure to high-altitude hypoxia is known to impair sleep and mental health, whether these effects are sex-dependent remains unclear. This study addresses a critical gap by investigating how sex modifies the association between high-altitude hypoxia and risks of poor sleep quality, depressive symptoms, and their co-occurrence in children and adolescents. METHODS: In this cross-sectional study (March-May 2024), we enrolled 1,345 long-term residents of the Shannan Tibet Autonomous Prefecture (altitude: 3,650-4,800 m) and 2,909 age-matched controls from low-altitude plains (Anhui Province, China). Sleep quality and depression were assessed using the Pittsburgh Sleep Quality Index (PSQI) and Montgomery-Asberg Depression Rating Scale (MADRS), respectively. Sex-stratified analyses and interaction metrics (RERI/AP/SI) were employed to evaluate additive and multiplicative effects. RESULTS: High-altitude residents exhibited significantly higher prevalence of poor sleep (24.2% vs. 18.7%, P < 0.001), depression (23.6% vs. 15.3%, P < 0.001), and their co-occurrence (12.6% vs. 8.6%, P < 0.001) compared to low-altitude controls. A significant negative additive interaction (RERI = - 0.78, 95% CI: -1.35 to - 0.3; P < 0.001) indicated that sex modifies the altitude-outcome association. Specifically: (1) high-altitude residence significantly increased poor sleep risk in males (OR = 1.60, 95% CI: 1.26-2.03) but not in females (OR = 1.39, 95% CI: 1.07-1.79); and (2) the expected female predominance in poor sleep observed in the plain region (OR = 1.452, 95% CI: 1.191-1.769) disappeared in the plateau region (OR = 0.865, 95% CI: 0.667-1.121). Similar patterns were independently replicated for depressive symptoms. These findings confirm that high-altitude exposure differentially increases risk in males rather than protecting females. CONCLUSION: Males show marked vulnerability to high-altitude-associated sleep and mood impairments, while females demonstrate resilience. Sex-tailored interventions for high-altitude populations, particularly targeting male adolescents, are urgently needed.

Humans↗

PubMed2003

Cardio-pulmonary interactions at high altitude. Pulmonary hypertension as a common denominator.

The purpose of this review is to find the evidence that a disproportionate pulmonary vasoconstriction persisting for days, weeks and years during residence at high altitude is the common pathophysiologic mechanism of high altitude pulmonary edema (HAPE), subacute mountain sickness and chronic mountain sickness. A recent finding in early HAPE suggests that transmission of excessively elevated pulmonary artery pressure to the pulmonary capillaries leading to alveolar hemorrhage as the pathophysiologic mechanism of HAPE. The elevated incidence of HAPE in Indian soldiers led the Indian Army to extend the acclimatization period from a few days to 5 weeks. Using this protocol, HAPE was prevented, but after several weeks of residence at an altitude of 6000m dyspnea, anasarca and pleuro-pericardial effusion developed. Clinical examination revealed severe congestive right heart failure. This condition has been previously described in long-term high altitude residents of the Himalaya and the Andes. In rats, smooth muscle cells appear in normally non-muscular arterioles within days of simulated altitude. Rapid remodeling of the small precapillary arteries may prevent HAPE but increase pulmonary vascular resistance leading to pulmonary hypertension in long-term high altitude residents. Symptoms and signs of HAPE, subacute mountain sickness and chronic mountain sickness reverse completely after residents are transfered to low altitude. In conclusion, these findings strongly suggest that pulmonary hypertension at high altitude, which could be named "high altitude pulmonary hypertension", is the principal and common pathogenic factor of all three cardio-pulmonary manifestations of high altitude illness. Accordingly, subacute mountain sickness and chronic mountain sickness could be renamed in "acute-" and "chronic right heart failure of high altitude", respectively.

Altitude↗

PubMed2006

Altitude-related cough.

Cough is a troublesome condition which affects many visitors to high altitude. Traditionally it has been attributed to the inspiration of the cold, dry air which characterizes the high altitude environment. This aetiology was brought into question by observations and experiments in long duration hypobaric chamber studies in which cough still occurred despite controlled temperature and humidity. Anecdotally however, exercise, possibly via the associated increase in ventilation, does appear to precipitate cough at altitude. It is likely that the term, altitude-related cough, covers a number of conditions and aetiologies. These aetiologies are discussed and include water loss from the respiratory tract; high altitude pulmonary oedema; acute mountain sickness; bronchoconstriction; respiratory tract infections; vasomotor rhinitis and post-nasal drip; and alterations in the central control of respiration. We hypothesize that there are two forms of altitude-related cough: a cough which may occur at relatively low altitudes and which is related to exercise and persists despite descent and a cough which does not occur at altitudes below 5000-6000 m and which improves rapidly with descent to lower altitude. The treatment of altitude-related cough is symptomatic and frequently ineffective. Further work is required to understand the nature and aetiology of the cough which occurs at high altitude before effective therapies can be developed.

Acute Disease↗

PubMed1997

Ventilation during simulated altitude, normobaric hypoxia and normoxic hypobaria.

To investigate the possible effect of hypobaria on ventilation (VE) at high altitude, we exposed nine men to three conditions for 10 h in a chamber on separate occasions at least 1 week apart. These three conditions were: altitude (PB = 432, FIO2 = 0.207), normobaric hypoxia (PB = 614, FIO2 = 0.142) and normoxic hypobaria (PB = 434, FIO2 = 0.296). In addition, post-test measurements were made 2 h after returning to ambient conditions at normobaric normoxia (PB = 636, FIO2 = 0.204). In the first hour of exposure VE was increased similarly by altitude and normobaric hypoxia. The was 38% above post-test values and end-tidal CO2 (PET(CO2) was lower by 4 mmHg. After 3, 6 and 9 h, the average VE in normobaric hypoxia was 26% higher than at altitude (p < 0.01), resulting primarily from a decline in VE at altitude. The difference between altitude and normobaric hypoxia was greatest at 3 h (+ 39%). In spite of the higher VE during normobaric hypoxia, the PET(CO2) was higher than at altitude. Changes in VE and PET(CO2) in normoxic hypobaria were minimal relative to normobaric normoxia post-test measurements. One possible explanation for the lower VE at altitude is that CO2 elimination is relatively less at altitude because of a reduction in inspired gas density compared to normobaric hypoxia; this may reduce the work of breathing or alveolar deadspace. The greater VE during the first hour at altitude, relative to subsequent measurements, may be related to the appearance of microbubbles in the pulmonary circulation acting to transiently worsen matching. Results indicate that hypobaria per se effects ventilation under altitude conditions.

Adult↗

PubMed2006

High altitude adaptation in Tibetans.

Since the beginning of the Himalayan climbing era, the anecdotal extraordinary physical performance at high altitude of Sherpas and Tibetans has intrigued scientists interested in altitude adaptation. These ethnic groups may have been living at high altitude for longer than any other population, and the hypothesis of a possible evolutionary genetic adaptation to altitude makes sense. Reviewed here is the evidence as to whether Tibetans are indeed better adapted for life and work at high altitude as compared to other populations and, if so, whether this better adaptation might be inborn. Tibetans, compared to lowlanders, maintain higher arterial oxygen saturation at rest and during exercise and show less loss of aerobic performance with increasing altitude. Tibetans have greater hypoxic and hypercapnic ventilatory responsiveness, larger lungs, better lung function, and greater lung diffusing capacity than lowlanders. Blood hemoglobin concentration is lower in Tibetans than in lowlanders or Andeans living at similar altitudes. Tibetans develop only minimal hypoxic pulmonary hypertension and have higher levels of exhaled nitric oxide than lowlanders or Andeans. Tibetans' sleep quality at altitude is better and they desaturate less at night. Several of these findings are also found in Tibetans born at low altitude when exposed for the first time to high altitude once adult. In conclusion, Tibetans indeed seem better adapted to life and work at high altitude, and this superior adaptation may very well be inborn, even though its exact genetic basis remains to be elucidated.

Acclimatization↗

PubMed2006

Symptoms of acute mountain sickness in Sherpas exposed to extremely high altitude.

Droma, Yunden, Masayuki Hanaoka, Buddha Basnyat, Amit Arjyal, Pritam Neupane, Anil Pandit, Dependra Sharma, and Keishi Kubo. Symptoms of acute mountain sickness in Sherpas exposed to extremely high altitude. High Alt. Med. Biol. 7:312-314, 2006.--The aim of this field interview was to investigate the current state of affairs concerning acute mountain sickness (AMS) in high-altitude residents, specifically the Sherpas at 3440 m above sea level, when they are exposed rapidly to altitudes significantly higher than their residing altitudes. Out of 105 Sherpas (44 men and 61 women, 31.2 +/- 0.8 yr), 104 had mountain-climbing experiences to 5701.4 +/- 119.1-m altitude in average 3.5 times each year. On the other hand, only 68 out of 111 non-Sherpas (29.9 +/- 0.8 yr) had experience of 1.4 +/- 1.5 climbs to an average 2688.6 +/- 150.4-m altitude in their mountaineering histories (p < 0.0001). Among the 104 Sherpas, 45 (43.3%) complained of at least one AMS symptom (headache, gastrointestinal symptoms, weakness, dizziness, and difficulty sleeping) in their experiences of mountaineering at an average 5518.9 +/- 195.9-m altitude. And 16 out of the 68 non-Sherpas (23.5%) reported the AMS symptoms at a mean altitude of 2750.0 +/- 288.8 m. Moreover, we also noticed that the Sherpa women showed a significantly higher Sa(O(2) ) (93.9 +/- 0.2%) than did Sherpa men (92.4 +/- 0.3%, p = 0.0001) at an altitude of 3440 m. The brief field interview evidenced that Sherpas might suffer from AMS when exposed to altitudes significantly higher than their residing altitude.

Acclimatization↗

PubMed2006

Risk of impaired coagulation in warfarin patients ascending to altitude (>2400 m).

Approximately 476,000 people on warfarin therapy visit a resort at altitude (>2400 m) annually in Colorado. Clinicians practicing at altitude have expressed concern that ascent to altitude adversely affects coagulation in patients taking warfarin in both high altitude residents and visitors. We sought to determine the effect of ascent to and descent from altitude on coagulation in warfarin patients, as assessed by the international normalized ratio (INR). A retrospective medical chart review was conducted on all warfarin patients treated between August 1998 and October 2003 at a cardiology clinic in which travel to and from altitude was documented in association with each INR measurement in high altitude residents. Of the 1139 INR measurements in 49 patients, 143 were associated with changes in altitude (in 32 of 49 patients). The odds of an INR measurement being below the prescribed range were 2.7 times (95% CI: 1.2-5.8) higher among warfarin patients with recent ascent to altitude, 2.1 times (95% CI: 1.4-3.2) higher among warfarin patients with atrial fibrillation, and 5.6 (95% CI: 2.3-13.7) times higher among warfarin patients with both atrial fibrillation and recent ascent to altitude. Increasing altitude is a risk factor for subtherapeutic INR in warfarin patients and this risk is doubled in atrial fibrillation patients.

Altitude↗