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PubMed2000

[Physical exercise impairs the acute stage of adaptation to moderate altitude].

UNLABELLED: A recent study has reported the impairment of high altitude adaptation capacity by physical exercise in a decompression chamber. The aim of our protocol was to evaluate if physical exercise at moderate altitude in the Alps would show a similar effect. 8 alpinists were examined in a randomised cross-over trial at 171 m and at 3000 m altitude under sedentary and under exercise condition (50% maximal workload on the bicycle ergometer four times 30 minutes during the first 6 hours of an 8 hour observation period at each altitude). At the beginning and at the end of each observation period AMS scores and arterial oxygen saturation SaO2 were measured. The differences of the AMS scores and the differences of SaO2 at both test conditions were compared at both altitudes. RESULTS: In comparison to sedentary condition, the differences between initial and final AMS scores at 3000 m altitude were significantly higher (-0.38 +/- 0.52 vs. -1.25 +/- 0.46, diff 0.88, 95% CI 0.58 to 1.17, p < 0.01), as well as the difference between initial and final SaO2 (-0.25 +/- 0.71% vs. 2.25 +/- 1.04%, diff. -2.5%, 95% CI for the diff. -3.59 to -1.41, p < 0.01). AMS score and SaO2 did not change after exercise at 171 m altitude. CONCLUSION: Physical exercise impairs the acute stage of adaptation to moderate altitude. This is mainly due to the exercise-induced exaggeration of arterial hypoxaemia.

Acute Disease↗
PubMed2003

[Physical activity and training at high altitude].

In recent years there has been a growing interest in the effects of high altitudes on the human body. High altitudes are being frequented by more and more people for sport and leisure pursuits, and are increasingly being used both as a training environment and for investigating the healthy body in hypoxic conditions. During the ascent from sea level, atmospheric pressure and partial oxygen pressure decrease, humidity and temperature decrease, and radiation is elevated. The altitudes at which physiological changes and clinical symptoms occur are not constant, but variations may usually appear above 2300-2800 meters. There is a wide variability of reactions to low oxygen in the air inhaled. The physiological parameters during both rest and physical activity at high altitudes are different from those at sea level, and the differences are reflected in concomitant changes in attitude and behavior. Research into altitude as a training environment that could improve athletic endurance and performance has grown in the last decade, with the development of a number of new training methods, such as "Living High--Training Low" and "Training High--Living Low". These have contributed to an improvement of performance in a significant number of athletes. This article will demonstrate the impact and possible dangers of physical activity at high altitude, and will present the current knowledge and methods of altitude training. This article reviews the influence of low air and oxygen pressure on athletic performance. Recommendations are presented regarding physical activity at high altitude and nutritional support.

Acclimatization↗
PubMed1988

Acute high-altitude illness.

Acute high-altitude illness usually occurs at elevations of 8,000 ft or more, is more common than is generally appreciated and is often confused with other disorders. The acute forms of high-altitude illness include acute mountain sickness, high-altitude pulmonary edema, high-altitude cerebral edema and high-altitude retinal hemorrhage. These illnesses often occur simultaneously and in severe forms can be fatal. Gradual ascent and acetazolamide help prevent acute mountain sickness and high-altitude pulmonary edema. The definitive treatment for all forms of high-altitude illness is descent to a lower altitude.

Acute Disease↗
PubMed2000

Lung volume, chest size, and hematological variation in low-, medium-, and high-altitude central Asian populations.

To evaluate adaptive responses to high-altitude environment, we examined three groups of healthy adult males from Central Asia: 94 high-altitude (HA) Kirghiz subjects (3,200 m above sea level); 114 middle-altitude (MA) Kazakh subjects (2,100 m), and 90 low-altitude (LA) Kirghiz subjects (900 m). Data on chest size (chest perimeter and chest diameter), lung volume (forced expiratory volume (FEV) and forced expiratory volume in 1 sec (FEV1)), and hematological parameters (hemoglobin, erythrocytes, hematocrit, and SaO(2)) are discussed. The results show that 1) chest shape is less flat in the samples living at higher altitude. In the HA sample, chest perimeter is lower but chest excursion is high. 2) In the highlanders, forced vital capacity (FVC) and FEV1 are no higher than in the other samples, even when corrected for stature and body weight. The negative correlation between FVC-FEV1 and age decreases with increasing altitude. 3) The HA and MA samples have higher values of hemoglobin, erythrocytes, and hematocrit. The HA sample has lower SaO(2) and higher arterial oxygen content than the LA sample. No association between hematocrit and age was detected in the four samples. The results indicate that the high-altitude Kirghiz present features of developmental acclimatization to hypobaric hypoxia which are also strongly influenced by other major high-altitude environmental stresses.

Adaptation, Physiological↗
PubMed2002

Plasma melatonin, pinealocyte morphology, and surface receptors/antigen expression on macrophages/microglia in the pineal gland following a high-altitude exposure.

The present study examined the effects of high-altitude exposure on the pineal gland, the main source of production of melatonin. It was surmised that hypoxia experienced at high altitude, caused by decreased oxygen tension in the ambient air, might lead to some structural alterations in the pineal gland and, hence, affect its melatonin production. Adult Wistar rats were exposed to an altitude of 8,000 m for 2 hr in an altitude chamber and then sacrificed at various time intervals after the exposure. Normal rats kept at ground level were used as controls. Blood samples were collected at various time intervals for measurement of plasma melatonin level, and the pineal glands from both groups were processed for electron microscopy and immunohistochemistry. The plasma melatonin level showed a steady increase following altitude exposure peaking at 7 days and returned to control levels thereafter. Between 1 and 4 days after altitude exposure, the mitochondrial number and lipid droplets in the pinealocytes appeared to be reduced compared with those in control rats. At 7 days, however, the mitochondrial numbers and lipid droplets were noticeably increased. At the same time interval, the expression of complement type 3 receptors and major histocompatibility class II antigens as detected with the antibodies OX-42 and OX-6, respectively, in macrophages/microglia was up-regulated compared with that in the control rats and those killed at earlier times. This was attributed to the increased serum melatonin after the altitude exposure. By 14 and 21 days, the ultrastructure of pinealocytes and immunoreactivity of macrophages/microglia were comparable with those in the control rats. We conclude from this study that an altitude exposure in rats leads to an increase in melatonin production, which returned to control levels with passage of time.

Altitude Sickness↗
PubMed1986

Beneficial effects of exercising at moderate altitude on red cell oxygen transport and on exercise performance.

The effect of a ascent to moderate altitude (2,300 m) and altitude training on the O2-transport properties of Hb and their possible consequences on tissue oxygenation during exercise were studied on six control and six training subjects. A rapid increase in P-50 values (+2.4 mm Hg, 0.32 kPa) was measured within one day after ascent. At the end of the stay at altitude (13th day) P-50 values were higher in subjects performing training than in controls. At altitude a slow but constant increase in 2,3-DPG, pyruvate kinase activity and reticulocyte count was found, which was more pronounced in training subjects as compared to controls. Ascent to altitude resulted in a decreased maximal performance capacity (-9%), but both groups recovered during the stay. In training subjects maximal exercise performance was increased after descent. Exercise at altitude was performed at a lower heart rate (controls: -10/min; training: -18/min) and at a lower lactate concentration (-4 mmol/l). These data indicate a positive effect of adaptation to altitude on exercise performance. Training itself shifts the ODC to the right and adds this effect to the effects of passive altitude adaptation on the O2-binding properties of hemoglobin.

Acclimatization↗
PubMed1996

Benefits of training at moderate altitude versus sea level training in amateur runners.

After more than 25 years of research of altitude training (AT) there is no consensus regarding either the training programme at altitude or the effects of AT on performance at sea level. Based on a review of the research work on AT, we investigated combined base training and interval training at moderate altitude and compared immediate and delayed effects on sea level performance with those following similar sea level training (SLT). The altitude group (AG, 10 male amateur runners) trained at 2315 m (natural altitude) and the sea level group (SLG, 12 male amateur runners) at 187 m. Both groups performed 7 days of base training (running on a trail) lasting between 60 and 90 min a day and 5 days of interval training (speed and hill runs) for between 10 and 45 min a day. Incremental exercise tests were performed 1 week before (t1), 3 days after (t2) and 16 days after (t3) the 12-day main training period. Within AG, exercise performance improved from t1 to t2 by 8% (P < 0.05) and from t2 to t3 by 8% (P < 0.05). Maximum oxygen uptake (VO2max) increased from t2 to t3 by 10% (P < 0.05). Within SLG exercise performance increased from t2 to t3 by 8% (P < 0.05). At t3, relative and absolute VO2max in AG were significantly higher in comparison with SLG (P = 0.005 and P = 0.046 respectively). The improved performance 3 days after AT may be explained in part by an increased oxygen uptake at submaximal exercise intensities without a change in VO2max. Further enhancement in performance 2 weeks after AT, however, seems to have been due to the clearly enhanced VO2max. Progressive cardiovascular adjustments might have contributed primarily to the time-dependent improvements observed after AT, possibly by an enhanced stroke volume overcompensating the reduced heart rates during submaximal exercise. In conclusion, our findings would suggest that training at a moderate natural altitude improves performance at sea level more than SLT. Combining base and interval training with regulation of intensity by training at constant heart rates during acclimatization at altitude would seem to be a successful training regimen for amateur runners. Most beneficial effects became apparent during the subsequent SLT around 2 weeks after return from altitude. Therefore, we are convinced that AT should be reconsidered as a potent tool for enhancing aerobic capacity, at least in non-elite athletes.

Adult↗
PubMed1999

Cerebral blood flow velocity responses to hypoxia in subjects who are susceptible to high-altitude pulmonary oedema.

Cerebral blood flow increases on exposure to high altitude, and perhaps more so in subjects who develop acute mountain sickness. We determined cerebral blood flow by transcranial Doppler ultrasound of the middle cerebral artery at sea level, in normoxia (fraction of inspired O2, F(I)O2 0.21), and during 15-min periods of either hypoxic (F(I)O2 0.125) or hyperoxic (F(I)O2 1.0) breathing, in 7 subjects with previous high-altitude pulmonary oedema, 6 climbers who had previously tolerated altitudes between 6000 m and 8150 m, and in 20 unselected controls. Hypoxia increased mean middle cerebral artery flow velocity from 69 (3) to 83 (4) cm x s(-1) (P<0.001) in the controls, from 63 (3) to 75 (3) cm x s(-1) (P<0.001) in the high-altitude pulmonary-oedema-susceptible subjects, and from 58 (4) to 70 (4) cm x s(-1) (P<0.001) in the successful high-altitude climbers. Hyperoxia decreased mean middle cerebral flow velocity to 60 (3) cm x s(-1) (P<0.001), 53 (3) cm x s(-1) (P<0.01), and 49 (3) cm x s(-1) (P<0.01) in the controls, high-altitude pulmonary-oedema-susceptible, and high-altitude climbers, respectively. We conclude that a transcranial Doppler-based estimate of cerebral blood flow is affected by hypoxic and hyperoxic breathing, and that it is not predictive of tolerance to high altitude.

Adult↗
PubMed1991

Echocardiographic assessment of left ventricular function and wall motion at high altitude in normal subjects.

To understand the effects of high-altitude hypoxia on cardiac function and the change in cardiac function during high-altitude acclimatization, precise studies were first performed at greater than 5,000 m of altitude in Himalaya by 2-dimensional echocardiography. In addition to examining well-known indexes of cardiac function, the centerline method was used to assess regional wall motion, which has not been examined under conditions of high-altitude hypoxia. The subjects were 11 climbing members (aged 21 to 43 years) of the Kyoto University Medical Research Expedition of Xixabangma (8,027 m) in 1990. Examinations were performed at sea level, at the base camp (5,020 m), and twice at the advanced base camp (5,650 m). Heart rate, left ventricular (LV) end-diastolic volume, cardiac output, mean rate of circumferential fiber shortening, ejection fraction, % fractional shortening, and regional LV wall motion were measured. At high altitude, heart rate increased to 136% of the sea level value, but gradually decreased in the degree of increment at the early and late advanced base camp measurements. LV end-diastolic volume decreased significantly by 70%. At base camp there were significant increases in ejection fraction, mean rate of circumferential fiber shortening, and % fractional shortening, which showed little change during the long-term stay at high altitude. Regional wall motion at high altitude (measured by the center-line method) decreased at the septal wall and increased at the posterolateral wall. These results demonstrate that: (1) LV cardiac performance at high altitude is enhanced significantly in spite of reduced preload. After good acclimatization, cardiac performance remains augmented, but there is a tendency to decrease the degree of augmentation. (2) In regional LV wall motion, septal wall motion is impaired, but LV posterolateral wall motion shows a compensatory increase.

Acclimatization↗
PubMed1981

Reduced physical work capacity at high altitude--a role for left ventricular dysfunction.

Physical work capacity is reduced in sea level residents--lowlanders (LL) as compared to high altitude residents--highlanders (HL). To determine possible etiologies, cardiac performance was studied in two groups of healthy male volunteers (13 LL and 11 HL) utilizing systolic time intervals during rest, submaximal and maximal exercise. The LL were studied at sea level and subsequently during 10 days of residence at an altitude of 3658 m. The HL were studied at high altitude alone. The LL were restudied 30-45 min after administration of intravenous furosemide at high altitude. Mean maximal oxygen uptake (VO2max) was reduced by 26% in the LL group at high altitude in comparison to sea level values and by 20% in relation to the HL group. Cardiac performance was estimated by the pre-ejection period/left ventricular ejection time ratio. This index was significantly increased in the LL group at high altitude in comparison to sea level values during submaximal and maximal exercise (P less than 0.01). Intravenous furosemide in the LL group increased the heart rate (P less than 0.05) at rest and during exercise but VO2max and cardiac performance were unchanged. It is hypothesized that reduced physical work capacity at high altitude in the LL group may be related to depression of cardiac performance in these subjects. Administration of intravenous furosemide did not influence cardiac performance in the LL group at high altitude.

Adult↗
PubMed1984

A comparative study on the effect of training at altitude and at sea level on endurance and certain biochemical variables.

The aim of this study was to ascertain the effects of training at altitude (1750 m. PB = 630mmHg) and at sea level (10m, PB = 760mmHg) as well as that of a period of adaptation of originally sea level-trained rats at altitude on endurance capacity. The average run time to exhaustion was 185.3 +/- 3.7 min for rats trained at altitude in comparison with 150.0 +/- 10.3 min for sea level-trained rats. After 14 days of adaptation at altitude, no significant difference in running time to exhaustion between rats trained at altitude (189.0 +/- 16.4 min) and those trained at sea level (177.2 +/- 11.6 min) was apparent. The improved endurance capacity of rats trained at altitude (when tested at altitude) is probably attributable to an increased respiratory capacity as is evident from the significantly increased levels of the citric acid cycle marker enzyme, citrate synthase (citrate oxaloacetate-lyase, EC 4.1.3.7) in the liver and gastrocnemius muscle of rats trained at altitude as compared to those trained at sea level.

Altitude↗
PubMed2005

Transient impairment of flow-mediated vasodilation in patients with metabolic syndrome at moderate altitude (1,700 m).

BACKGROUND: The influence of moderate altitude on the cardiovascular system in patients with metabolic syndrome has not been investigated sufficiently, yet. The aim of this study was to assess the effect of acute and mid-term exposure to moderate altitude (1,700 m) on endothelial function in patients with metabolic syndrome. METHODS: Flow-mediated (FMD) and nitroglycerin-mediated vasodilation (NMD) were assessed in 18 patients with coronary risk factors on 5 occasions: (1) at location A (576 m), (2) on the first day at moderate altitude (location B, 1,700 m), (3) after 3 weeks at moderate altitude, (4) and (5) again at location A (6 and 16 weeks after the stay at moderate altitude, respectively). In addition, markers of lipid metabolism, serum erythropoietin and endothelin were measured. RESULTS: FMD on the first day at moderate altitude was similar compared to baseline FMD at location A (7.0 +/- 3.3 vs. 7.4 +/- 4.6%; NS). A 3-week stay at moderate altitude was associated with a significant reduction in FMD (7.4 +/- 4.6 vs. 3.8 +/- 2.5%; p < 0.05) despite a decrease in baseline diameter (4.5 +/- 0.3 vs. 4.3 +/- 0.4 mm; p < 0.05). Six weeks after returning to location A, FMD was still reduced compared to baseline (4.3 +/- 2.8%; p < 0.05) and after further 16 weeks, FMD returned to baseline values (5.5 +/- 3.5%). However, metabolic parameters improved significantly. In contrast, NMD and endothelin levels remained unchanged. CONCLUSION: In patients with metabolic syndrome, a sojourn of 3 weeks at moderate altitude leads to a prolonged, but reversible impairment of FMD. The discrepancy to improvement of other cardiovascular and metabolic parameters requires further investigation.

Adult↗
PubMed1990

Cognition and metacognition at extreme altitudes on Mount Everest.

The FACTRETRIEVAL2 test battery, which assesses both retrieval of general information from memory and metacognition about that retrieval, was administered to people before and after a recent expedition to Mount Everest and at extreme altitudes above 6,400 m (higher than any mountain in North America or Europe). The major findings were as follows: First, the same extreme altitudes already known to impair learning did not affect either accuracy or latency of retrieval, and this robustness of retrieval occurred for both recall and forced-choice recognition. Second, extreme altitude did affect metacognition: The climbers showed a decline in their feeling of knowing both while at extreme altitude and after returning to Kathmandu (i.e., both an effect and an aftereffect of extreme altitude). Third, extreme altitude had different effects than alcohol intoxication (previously assessed by Nelson. McSpadden, Fromme, & Marlatt, 1986). Alcohol intoxication affected retrieval without affecting metacognition, whereas extreme altitude affected metacognition without affecting retrieval; this different pattern for extreme altitude versus alcohol intoxication implies that (a) hypoxia does not always yield the same outcome as alcohol intoxication and (b) neither retrieval nor metacognition is strictly more sensitive than the other for detecting changes in independent variables.

Adult↗
PubMed2006

Effect of acetazolamide on leg endurance exercise at sea level and simulated altitude.

Acetazolamide can be taken at sea level to prevent acute mountain sickness during subsequent altitude exposure. Acetazolamide causes metabolic acidosis at sea level and altitude, and increases SaO2 (arterial oxygen saturation) at altitude. The aim of the present study was to determine whether acetazolamide impairs muscle endurance at sea level but not simulated altitude (4300 m for <3 h). Six subjects (20+/-1 years of age; mean+/-S.E.M.) performed exhaustive constant work rate one-leg knee-extension exercise (25+/-2 W) once a week for 4 weeks, twice at sea level and twice at altitude. Each week, subjects took either acetazolamide (250 mg) or placebo orally in a double-blind fashion (three times a day) for 2 days. On day 2, all exercise bouts began approx. 2.5 h after the last dose of acetazolamide or placebo. Acetazolamide caused similar acidosis (pH) in all subjects at sea level (7.43+/-0.01 with placebo compared with 7.34+/-0.01 with acetazolamide; P<0.05) and altitude (7.48+/-0.03 with placebo compared with 7.37+/-0.01 with acetazolamide; P<0.05). However, endurance performance was impaired with acetazolamide only at sea level (48+/-4 min with placebo compared with 36+/-5 min with acetazolamide; P<0.05), but not altitude (17+/-2 min with placebo compared with 20+/-3 min with acetazolamide; P = not significant). In conclusion, lack of impairment of endurance performance by acetazolamide compared with placebo at altitude was probably due to off-setting secondary effects resulting from acidosis, e.g. ventilatory induced increase in SaO2 for acetazolamide compared with placebo (89+/-1 compared with 86+/-1% respectively; P<0.05), which resulted in an increased oxygen pressure gradient from capillary to exercising muscle.

Acetazolamide↗
PubMed1997

The cGMP pathway is not responsible for the blunted hypoxic vasoconstriction in rat lungs after altitude exposure.

To examine the contribution of the cyclic guanosine monophosphate (cGMP) pathway in changes in pulmonary vasoconstriction during the initial days of altitude exposure, we tested the effects of LY83583 (an inhibitor of guanylate cyclase activation) and those of N(G)-monomethyl-L-arginine (an inhibitor of nitric oxide synthesis) on airway hypoxia- (3% O2) and angiotensin II- (AII, 0.2 microg) induced vasoconstrictions in lungs from the rats exposed to either moderate altitude (MA, 570 torr) or high altitude (HA, 430 torr) At 2 days' exposure, hypoxic response was significantly blunted compared with the response in low-altitude (LA, 710 torr) lungs in an altitude-dependent manner. At 7 days' exposure, the response was recovered fully in MA lungs but partially in HA lungs. AII response was not significantly blunted at 2 days' exposure, but was significantly augmented in an altitude-dependent manner at 7 days' exposure. LY83583 (10 micromol L(-1)) potentiated both responses in LA lungs but did not significantly potentiate either response in any altitude-exposed lungs. N(G)-monomethyl-L-arginine (10 micromol L(-1)) potentiated both responses in LA lungs but did not significantly potentiate either response in HA lungs at 2 days' and 7 days' exposure. Thus the cGMP pathway is not responsible for either the change in hypoxic vasoconstriction or the change in AII vasoconstriction in rat lungs during the initial 7 days of altitude exposure.

Altitude↗
PubMed2006

High-altitude exposure reduces inspiratory muscle strength.

It was the aim of the study to assess the maximal pressure generated by the inspiratory muscles (MIP) during exposure to different levels of altitude (i.e., hypobaric hypoxia). Eight lowlanders (2 females and 6 males), aged 27 - 46 years, participated in the study. After being evaluated at sea level, the subjects spent seven days at altitudes of more than 3000 metres. On the first day, they rode in a cable car from 1200 to 3200 metres and performed the first test after 45 - 60 minutes rest; they then walked for two hours to a mountain refuge at 3600 metres, where they spent three nights (days 2 - 3); on day 4, they walked for four hours over a glacier to reach Capanna Regina Margherita (4559 m), where they spent days 5 - 7. MIP, flow-volume curve and SpO (2) % were measured at each altitude, and acute mountain sickness (Lake Louise score) was recorded. Increasing altitude led to a significant decrease in resting SpO (2) % (from 98 % to 80 %) and MIP (from 134 to 111 cmH (2)O) (baseline to day 4: p < 0.05); there was an improvement in SpO (2) % and a slight increase in MIP during the subsequent days at the same altitude. Expiratory (but not inspiratory) flows increased, and forced vital capacity and FEF (75) decreased at higher altitudes. We conclude that exposure to high altitude hypoxia reduces the strength of the respiratory muscles, as demonstrated by the reduction in MIP and the lack of an increase in peak inspiratory flows. This reduction is more marked during the first days of exposure to the same altitude, and tends to recover during the acclimatisation process.

Adult↗
PubMed1992

Training at altitude in practice.

There can be little doubt that training at altitude is fundamental to preparing an athlete for competition at altitude. However the value of training at altitude for competition at sea level appears on the one hand to lack total acceptance amongst sports scientists; and on the other to hold some cloak of mystery for coaches who have yet to enjoy first hand experience. The fact is that very few endurance athletes will ignore the critical edge which altitude training affords. Each fraction of a percentage of performance advantage gained through methods which are within the rules of fair play in sport, may shift the balance between failure and achievement. Moreover, there is growing support for application of training at altitude for speed-related disciplines. This paper aims to demystify the subject by dealing with practical aspects of training at altitude. Such aspects include a checklist of what should and should not be done at altitude, when to use altitude relative to target competitions, and specific training examples.

Acclimatization↗
PubMed2002

Salmeterol for the prevention of high-altitude pulmonary edema.

BACKGROUND: Pulmonary edema results from a persistent imbalance between forces that drive water into the air space and the physiologic mechanisms that remove it. Among the latter, the absorption of liquid driven by active alveolar transepithelial sodium transport has an important role; a defect of this mechanism may predispose patients to pulmonary edema. Beta-adrenergic agonists up-regulate the clearance of alveolar fluid and attenuate pulmonary edema in animal models. METHODS: In a double-blind, randomized, placebo-controlled study, we assessed the effects of prophylactic inhalation of the beta-adrenergic agonist salmeterol on the incidence of pulmonary edema during exposure to high altitudes (4559 m, reached in less than 22 hours) in 37 subjects who were susceptible to high-altitude pulmonary edema. We also measured the nasal transepithelial potential difference, a marker of the transepithelial sodium and water transport in the distal airways, in 33 mountaineers who were prone to high-altitude pulmonary edema and 33 mountaineers who were resistant to this condition. RESULTS: Prophylactic inhalation of salmeterol decreased the incidence of high-altitude pulmonary edema in susceptible subjects by more than 50 percent, from 74 percent with placebo to 33 percent (P=0.02). The nasal potential-difference value under low-altitude conditions was more than 30 percent lower in the subjects who were susceptible to high-altitude pulmonary edema than in those who were not susceptible (P<0.001). CONCLUSIONS: Prophylactic inhalation of a beta-adrenergic agonist reduces the risk of high-altitude pulmonary edema. Sodium-dependent absorption of liquid from the airways may be defective in patients who are susceptible to high-altitude pulmonary edema. These findings support the concept that sodium-driven clearance of alveolar fluid may have a pathogenic role in pulmonary edema in humans and therefore represent an appropriate target for therapy.

Administration, Inhalation↗