Severe Acute Mountain Sickness Research Articles

Oral antioxidant supplementation does not prevent acute mountain sickness: double blind, randomized placebo-controlled trial

Acute mountain sickness may be caused by cerebrovascular fluid leakage due to oxidative damage to the endothelium. This may be reduced by oral antioxidant supplementation. To assess the effectiveness of antioxidant supplementation for the prevention of acute mountain sickness (AMS). A parallel-group double blind, randomized placebo-controlled trial. The study was conducted in a university clinical research facility and a high altitude research laboratory. Eighty-three healthy lowland volunteers ascended to 5200 m on the Apex 2 high altitude research expedition. The treatment group received a daily dose of 1 g l-ascorbic acid, 400 IU of alpha-tocopherol acetate and 600 mg of alpha-lipoic acid (Cultech Ltd., Wales, UK) in four divided doses. Prevalence of AMS was measured using the Lake Louise Consensus score sheet (LLS). Secondary outcomes were AMS severity measured using a novel visual analogue scale, arterial oxygen saturation and pulmonary artery systolic pressure (PASP). Forty-one subjects were allocated to the antioxidant group, and 42 to the placebo group. There was no difference in AMS incidence or severity between the antioxidant and placebo groups using the LLS at any time at high altitude. At the pre-determined comparison point at Day 2 at 5200 m, 69% of the antioxidant group (25/36) and 66% of the placebo group (23/35) had AMS using the LLS criteria (P = 0.74). No differences were observed between the groups for PASP, oxygen saturation, presence of a pericardial effusion or AMS assessed by VAS. This trial found no evidence of benefit from antioxidant supplementation at high altitude. NCT00664001.

Ginkgo biloba Does—and Does Not—Prevent Acute Mountain Sickness

To determine the efficacy of 2 different sources of Ginkgo biloba extract (GBE) in reducing the incidence and severity of acute mountain sickness (AMS) following rapid ascent to high altitude. Two randomized, double-blind, placebo-controlled cohort studies were conducted in which participants were treated with GBE (240 mg x d(-1)) or placebo prior to and including the day of ascent from 1600 m to 4300 m (ascent in 2 hours by car). Acute mountain sickness was diagnosed if the Environmental Symptom Questionnaire III acute mountain sickness-cerebral (AMS-C) score was > or =0.7 and the Lake Louise Symptom (LLS) score was > or =3 and the participant reported a headache. Symptom severity was also determined by these scores. Results were conflicting: Ginkgo biloba reduced the incidence and severity of AMS compared to placebo in the first but not the second study. In the first study, GBE reduced AMS incidence (7/21) vs placebo (13/19) (P = .027, number needed to treat = 3), and it also reduced severity (AMS-C = 0.77 +/- 0.26 vs 1.59 +/- 0.27, P = .029). In the second study, GBE did not reduce incidence or severity of AMS (GBE 4/15 vs placebo 10/22, P = .247; AMS-C = 0.48 +/- 0.13 vs 0.58 +/- 0.11, P = .272). The primary difference between the 2 studies was the source of GBE. The source and composition of GBE products may determine the effectiveness of GBE for prophylaxis of AMS.

Pursed-lips breathing for improved oxygenation at altitude

Pursed-lips breathing (PLB) has repeatedly been shown to improve gas exchange with increased arterial oxygenation and saturation (SaO2) and decreased arterial carbon dioxide levels mainly by promoting slow and deep breathing pattern [1]. These effects were observed in healthy subjects at low and high altitude and in patients with many forms of pulmonary edema and those with obstructive lung diseases as well. Several mechanisms, e.g. deep breathing, recruitment of terminal airspaces, and changes regarding the work of breathing, the ventilation-perfusion matching, the alveolarcapillary pressure difference, or hemodynamic conditions, may be differently important for the improvement of oxygenation and the relieve of symptoms under various conditions. In their article in Sleep and Breathing, Tannheimer and colleagues present a case report on the successful therapy of severe acute mountain sickness (AMS) at 4,330 m by PLB [2], representing an interesting example of simple selftreatment of AMS. Nevertheless, this observation is not surprising because many years ago, Schoene et al. and Larson demonstrated similar results by the application of expiratory positive airway pressure in subjects with high altitude pulmonary edema (HAPE) [3, 4]. Due to the very low resting SaO2 (62%) at 4,330 m of the mountaineer studied by Tannheimer et al., I strongly suggest that this person actually suffered from HAPE. This assumption is also supported by the large SaO2 improvement during PLB. Schoene et al. and Larson also found much more impressive improvements of oxygen saturation in HAPE patients than healthy mountaineers. However, the increase in SaO2 and the expiratory pressure applied (∼10 cm H2O) in these patients were lower compared to the respective values reported by Tannheimer and colleagues. In fact, increasing expiratory pressures may cause increasing SaO2 values. But, which pressure levels are optimal? Biondi et al. showed that values above 15 cm H2O increased right ventricular afterload and decreased right ventricular contractility [5]. Tannheimer et al. report an extraordinary high expiratory pressure of about 55 cm H2O which could cause hemodynamic complications. Based on our recent observation when applying a continuous positive airway pressure helmet for HAPE treatment, I would suspect that much lower expiratory pressures (∼15 cm H2O) would have similar effects on the improvement of HAPE symptoms and the increase of arterial oxygenation and saturation as reported by Tannheimer et al. without potential risks arising from very high expiratory pressures [6]. Future studies are necessary to evaluate the effects of various expiratory pressures produced by PLB and to shed more light upon the impact of PLB methods on the complex and interactive physiology of normal and diseased respiratory apparatus. Although one cannot conclude on the basis of this case report that PLB represents a major treatment option for severe AMS or HAPE, the authors did a good job in conducting and reporting this study which addresses a “real world” medical question stimulating pursuing studies. Sleep Breath (2009) 13:119–120 DOI 10.1007/s11325-008-0241-3

Brain Natriuretic Peptide at Altitude: Relationship to Diuresis, Natriuresis, and Mountain Sickness

Acute mountain sickness (AMS) affects some new arrivals above an altitude of 2500 m. Hypobaric hypoxia is known to produce diuresis and has natriuretic effects due to the release of natriuretic peptides. We tested the hypothesis that increases in brain natriuretic peptide (BNP) at altitude correlates with increased urination and natriuresis as well as symptomatic AMS. Subjects were 14 mountaineers who undertook a Himalayan expedition that began at 100 m and passed through 3440 m en route to a final altitude of 5050 m. We measured the severity of AMS (Lake Louise Score), BNP values, nocturnal urine volume, and urine sodium concentration. Nocturnal urine volume increased from 490 +/- 90 mi at 3440 m to 1100 +/- 104 ml at 5050 m. BNP levels at the higher altitude were 10.6 +/- 4.7 pg x ml(-1) and were correlated with the severity of AMS in all mountaineers (Lake Louise Score 4 +/- 0.5 for AMS subjects). However, AMS severity did not correlate with urine volume or urine sodium concentration. Our results suggest that BNP secretion is not the cause of high-altitude diuresis. Further studies are needed to evaluate the possible role of BNP in individual responses to high altitude.

Optic nerve sheath diameter correlates with the presence and severity of acute mountain sickness: evidence for increased intracranial pressure

Increased intracranial pressure is suspected in the pathogenesis of acute mountain sickness (AMS), but no studies have correlated it with the presence or severity of AMS. We sought to determine whether increased optic nerve sheath diameter, a surrogate measure of intracranial pressure, is associated with the presence and severity of AMS. We performed a cross-sectional study of travelers ascending through Pheriche, Nepal (4,240 m), from March 3 to May 14, 2006. AMS was assessed using the Lake Louise score. Optic nerve sheath diameter was measured by ultrasound. Ultrasound exams were performed and read by separate blinded observers. Two-hundred eighty seven subjects were enrolled. Ten of these underwent repeat examination. Mean optic nerve sheath diameter was 5.34 mm [95% confidence interval (CI) 5.18-5.51 mm] in the 69 subjects with AMS vs. 4.46 mm (95% CI 4.39-4.54 mm) in the 218 other subjects (P < 0.0001). There was also a positive association between optic nerve sheath diameter and total Lake Louise score (P for trend < 0.0001). In a multivariate logistic regression model of factors associated with AMS, optic nerve sheath diameter was strongly associated with AMS (odds ratio 6.3; 95% CI, 3.7-10.8; P < 0.001). In 10 subjects with repeat examinations, change in Lake Louise score had a strong positive correlation with change in optic nerve sheath diameter (R(2) = 0.84, P < 0.001). Optic nerve sheath diameter, a proxy for intracranial pressure, is associated with the presence and severity of AMS.

Prophylactic Low-Dose Acetazolamide Reduces the Incidence and Severity of Acute Mountain Sickness

Previous studies have shown low-dose acetazolamide to be effective in preventing AMS in persons already at high altitude and then moving higher, a relatively low risk situation. We wished to evaluate prophylactic administration of low-dose acetazolamide for reducing the incidence and severity of AMS in a high-risk setting: rapid ascent from 1600 to 4300 m. We performed a double-blind, randomized, placebo-controlled study with human subjects (n=44) exposed to 4300 m for 24 h. Subjects were treated for 3 days prior to ascent to 4300 m and during day 1 at altitude with placebo (n=22) or acetazolamide 250 mg/day (125 mg bid, n=22). AMS diagnosis required both an AMS-C score from the Environmental Symptom Questionnaire-III>or=0.7 and a Lake Louise Symptom (LLS) questionnaire score>or=3 plus headache. Acetazolamide reduced the incidence of AMS compared to placebo-treated subjects (14% vs. 45%, respectively, p=0.02), and the number needed to treat was 3. The AMS-C and LLS scores were lower in acetazolamide-treated subjects, indicating less severe AMS. Low-dose acetazolamide administered prior to ascent and on day 1 at 4300 m effectively reduced the incidence and severity of AMS in a high-risk setting.

Severe Acute Mountain Sickness and Suspected High Altitude Cerebral Edema Related to Nitroglycerin Use

An elite mountaineer reported severe acute mountain sickness and ataxia during an 8000-m expedition and concomitant use of transdermal nitroglycerin patches aimed to prevent frostbites. Use of nitroglycerin for this purpose is off-label, and its safety has not been assessed. Moreover, a relation between nitrate-induced cerebral vasodilation and high altitude cerebral edema is theoretically possible on a pathophysiological basis. It is our opinion that nitroglycerin use at high altitude should be discouraged, as efficacy in the prevention of frostbites is questionable and safety has not been assessed.

DPOAEs in High Altitude Disease at Mount Everest

Objective The aim of this study was to measure DPOAEs in climbers on Mount Everest as a criterion for differential diagnosis of high altitude disease. The levels of distortion product otoacoustic emissions (DPOAEs) change at frequencies between 0,75 kHz and 1,5 kH along with intracranial pressure (ICP). DPOAEs are suggested for monitoring ICP changes. Methods In order to determine the etiology of DPOAE-level changes obtained in 6 climbers with severe acute mountain sickness, blood oxygen saturation was measured simultaneously, and a standard request form of Lake-Louis symptoms of high altitude disease was filled in with every DPOAE measurement. Data are presented from DPOAE measurements at frequencies of 1, 1.5, 2, 3 and 4 kHz during an ascent to Mount Everest (8848 m) up to an altitude of 7800 m. Results In all climbers, DPOA levels decreased at 4 kHz and 3 kHz with declining oxygen saturation (SaO2) at high altitude. That has been described in many prior animal studies. On the other hand, DPOAE at 1 kHz showed decreasing levels only with symptoms of high altitude disease (AMS). In one climber with severe symptoms of intracranial hypertension after the ascent to the high camp at 7800 m, decreasing DPOAE levels at 1 kHz were measured in the absence of declining blood oxygen saturation. The most pronounced decline of DPOAEs at 1 kHz was also seen on that occasion. Conclusions DPOAEs are suggested for detection of intracranial hypertension and early detection of high-altitude cerebral edema.

Microhemorrhages in Nonfatal High-Altitude Cerebral Edema

Vasogenic edema in the corpus callosum is a characteristic finding in high-altitude cerebral edema (HACE). Furthermore, microhemorrhages have been found at autopsies in brains of HACE victims. The objective of this study was to determine if microhemorrhages also occur in nonlethal HACE. Consequently, magnetic resonance imaging (MRI) was performed in patients who had suffered from HACE and in patients who had suffered from severe acute mountain sickness (AMS) by applying imaging techniques highly susceptible to blood or blood remnants. Two experienced neuroradiologists independently evaluated the exams blinded to clinical data. The MRI was performed 2 to 31 months after the event. The MRI of the HACE patients revealed multiple hemosiderin depositions in the brain--predominantly found in the corpus callosum--indicative of microhemorrhages. These changes were not present in the three AMS patients. In summary, hemosiderin deposits detectable by MRI predominantly in the corpus callosum indicate that microhemorrhages occur in nonlethal HACE, which may serve as a novel diagnostic MRI sign for HACE even many months after the event.

Respiratory rate within the first hour of ascent predicts subsequent acute mountain sickness severity.

Altitude illness results from hypobaric hypoxia at altitudes higher than 2500 meters above sea level. To determine whether vital signs can be used as predictors for severe acute mountain sickness, we carried out a prospective observational study. A cohort of 90 individuals (male/female ratio: 2; age: 13 - 65 years) in a mountain hotel's clinic at 3450 meters in Iran were studied from September through October 2006. Demographics and vital signs were measured during the first hour of ascent. The individuals were followed for acute mountain sickness symptoms including headache, dizziness, nausea or vomiting, insomnia, and fatigue. Lake Louise criteria were used to diagnose acute mountain sickness. Severe acute mountain sickness was considered if a score of equal or more than 5 was present. Significance was assigned to values of P<0.05. Acute mountain sickness was diagnosed in 34 (37.8%) participants after 24 hours of ascent. Severe acute mountain sickness was detected in 14 (15.6%) participants. A respiratory rate of 20 or more during the first hour of ascent was recorded for nine (64.3%) patients with severe acute mountain sickness and 15 (19.7%) individuals in the negative/mild acute mountain sickness group. This suggests an association between early high respiratory rates and risk of subsequent severe acute mountain sickness (P=0.001). There is an association between a rise in the respiratory rate and susceptibility to acute mountain sickness. This can enable us to predict severe acute mountain sickness and prevent it. Furthermore, Tochal Mountain Hotel guests should be aware of the risk of acute mountain sickness and should be recommended to use prophylactic acetazolamide or dexamethasone before ascent.

Distortion product otoacoustic emissions for assessment of intracranial hypertension at extreme altitude?

The levels of distortion product otoacoustic emissions (DPOAEs) change at frequencies between 0.75 and 1.5 kHz along with intracranial pressure (ICP) and DPOAEs are suggested for monitoring ICP changes. Elevated ICP plays a major role in high-altitude disease, but direct measurement is unlikely to be feasible at high altitudes. The aim of the presented study was to measure DPOAEs at extreme altitudes in order to determine whether information about elevated ICP can be obtained. Data are presented from DPOAE measurements at the frequencies 1, 1.5, 2, 3 and 4 kHz in 13 climbers during an ascent to Gasherbrum II (8,035 m) up to an altitude of 7,400 m. Valid DPOAE measurements could be obtained in all climbers. DPOAE levels exhibited great variability concerning both the affected frequency range and the change. As expected due to elevated ICP, DPOAE levels decreased in some of the climbers at 1 kHz. However, an even more pronounced decline of DPOAE levels was observed at 3 and 4 kHz, which cannot be explained by intracranial hypertension. Possible other reasons for DPOAE level changes at extreme altitude are hypoxia, increased serum osmolarity and unbalanced middle ear pressure. Only one climber developed severe acute mountain sickness with clinical signs of intracranial hypertension. The most pronounced decline of DPOAEs at 1 kHz was seen on that occasion, which suggests a possible use of DPOAEs for detection of intracranial hypertension and early detection of high-altitude cerebral edema.

High hopes at high altitudes: pharmacotherapy for acute mountain sickness and high-altitude cerebral and pulmonary oedema

The pharmacotherapy of prevention and treatment of acute altitude- related problems – acute mountain sickness, high-altitude cerebral oedema and high-altitude pulmonary oedema – is reviewed. Drug therapy is only part of the answer to the medical problems of high altitude; prevention should include slow ascent and treatment of the more severe illnesses should include appropriate descent. Carbonic anhydrase inhibitors, in particular acetazolamide, remain the most effective drugs in preventing, to a large extent, the symptoms of acute mountain sickness, and can be used in the immediate management of the more severe forms of altitude-related illnesses. Glucocorticoids in relatively large doses are also effective preventative drugs, but at present are largely reserved for the treatment of the more severe acute mountain sickness and acute cerebral oedema. Calcium channel blockers and PDE-5 inhibitors are effective in the management of acute pulmonary oedema. Further work is required to establish the role of antioxidants and anticytokines in these syndromes.

Hypoxia-Induced Acute Mountain Sickness is Associated with Intracellular Cerebral Edema: A 3 T Magnetic Resonance Imaging Study

Acute mountain sickness is common among not acclimatized persons ascending to high altitude; the underlying mechanism is unknown, but may be related to cerebral edema. Nine healthy male students were studied before and after 6-h exposure to isobaric hypoxia. Subjects inhaled room air enriched with N(2) to obtain arterial O(2) saturation values of 75 to 80%. Acute mountain sickness was assessed with the environmental symptom questionnaire, and cerebral edema with 3 T magnetic resonance imaging in 18 regions of interest in the cerebral white matter. The main outcome measures were development of intra- and extracellular cerebral white matter edema assessed by visual inspection and quantitative analysis of apparent diffusion coefficients derived from diffusion-weighted imaging, and B0 signal intensities derived from T2-weighted imaging. Seven of nine subjects developed acute mountain sickness. Mean apparent diffusion coefficient increased 2.12% (baseline, 0.80+/-0.09; 6 h hypoxia, 0.81+/-0.09; P=0.034), and mean B0 signal intensity increased 4.56% (baseline, 432.1+/-98.2; 6 h hypoxia, 450.7+/-102.5; P<0.001). Visual inspection of magnetic resonance images failed to reveal cerebral edema. Cerebral acute mountain sickness scores showed a negative correlation with relative changes of apparent diffusion coefficients (r=-0.83, P=0.006); there was no correlation with relative changes of B0 signal intensities. In conclusion, isobaric hypoxia is associated with mild extracellular (vasogenic) cerebral edema irrespective of the presence of acute mountain sickness in most subjects, and severe acute mountain sickness with additional mild intracellular (cytotoxic) cerebral edema.

Completion of the Railroad to Lhasa

High Altitude Medicine & BiologyVol. 7, No. 4 EditorialCompletion of the Railroad to LhasaJohn B. WestJohn B. WestSearch for more papers by this authorPublished Online:18 Dec 2006https://doi.org/10.1089/ham.2006.7.263AboutSectionsPDF/EPUB ToolsPermissionsDownload CitationsTrack CitationsAdd to favorites Back To Publication ShareShare onFacebookTwitterLinked InRedditEmail "Completion of the Railroad to Lhasa." , 7(4), pp. 263–264FiguresReferencesRelatedDetailsCited byDistribution characteristics of indoor oxygen concentration under natural ventilation in oxygen-enriched buildings at high altitudes15 April 2021 | Building Simulation, Vol. 14, No. 6Mosquitoes established in Lhasa city, Tibet, China6 August 2013 | Parasites & Vectors, Vol. 6, No. 1Altitude Illness in Qinghai–Tibet Railroad Passengers Tian Yi Wu, Shou Quan Ding, Sheng Lin Zhang, Jin Qing Duan, Bao Yu Li, Zhong Yan Zhan, Qin Li Wu, Suolung Baomu, Bao Zhu Liang, Shu Rang Han, Yu Ling Jie, Gang Li, Lin Sun, and Bengt Kayser4 October 2010 | High Altitude Medicine & Biology, Vol. 11, No. 3Reduced Incidence and Severity of Acute Mountain Sickness in Qinghai–Tibet Railroad Construction Workers after Repeated 7-Month Exposures despite 5-Month Low Altitude Periods Tian Yi Wu, Shou Quan Ding, Jin Liang Liu, Man Tang Yu, Jian Hou Jia, Jun Qing Duan, Zuo Chuan Chai, Rui Chen Dai, Sheng Lin Zhang, Bao Zhu Liang, Ji Zhui Zhao, De Tang Qi, Yong Fu Sun, and Bengt Kayser23 September 2009 | High Altitude Medicine & Biology, Vol. 10, No. 3 Volume 7Issue 4Dec 2006 InformationCopyright 2006, Mary Ann Liebert, Inc.To cite this article:John B. West.Completion of the Railroad to Lhasa.High Altitude Medicine & Biology.Dec 2006.263-264.http://doi.org/10.1089/ham.2006.7.263Published in Volume: 7 Issue 4: December 18, 2006PDF download

Acute Mountain Sickness: Influence of Fluid Intake

High altitude and exposure to cold are associated with significant levels of dehydration because of cold-altitude urine output, high energy expenditures, and poor access to water. The aims of the present study were to measure the fluid intake and urine output among military mountaineers during their stay at high altitude and to study the level of fluid intake and decrease in urine output in relation with acute mountain sickness (AMS). This study used an analytic prospective follow-up design of hydration-dehydration conditions of a group of mountaineers with similar characteristics (military group). Data collected each day included quantity and type of fluid intake, urine output in 24 hours, other fluid output (as diarrhea or vomiting), and symptoms or signs of AMS according to the Lake Louise consensus score. Values are given as mean +/- SE. A 1-factor analysis of variance procedure and t test were used to compare variables. The mountaineers consumed a variety of fluids, including water, tea, coffee, soup, Isostar, and milk. Daily fluid intake was 2800 +/- 979 mL, with a maximum intake of 4700 mL. Daily urine output was 1557 +/- 758 mL. When we stratify our sample at the median by fluid intake, a significant correlation is detected with mean balance and mean urine output. Mountaineers developing AMS demonstrated reduced urine output (mean 1336 mL) when compared with those without AMS (mean 1655 mL). We found that fluid intake was associated but insignificantly correlated with incidence and degree of AMS. Past research suggests that vigorous hydration decreases incidence and severity of AMS and other altitude illnesses. Our results also imply that aggressive fluid intake is protective, but our limited sample size yielded insufficient power to demonstrate a statistically significant difference.

Successful Treatment of Severe Acute Mountain Sickness and Excessive Pulmonary Hypertension with Dexamethasone in a Prepubertal Girl

Successful Treatment of Severe Acute Mountain Sickness and Excessive Pulmonary Hypertension with Dexamethasone in a Prepubertal Girl

Acute Mountain Sickness and SaO2 in Moderate Altitude Versus Sea-level Residents Ascending to 4300 m

When sea-level residents (SLR) rapidly ascend to ∼4300 m, arterial oxygen saturation (SaO2) is low, and the incidence and severity of acute mountain sickness (AMS) is typically high, especially following heavy exertion in the early hours of altitude exposure. On the other hand, moderate-altitude residents (MAR) have a higher initial SaO2 upon arrival at 4300 m (Muza 2004) compared to SLR, but it is unknown whether they also exhibit a lower incidence and severity of AMS. PURPOSE: To determine in MAR, compared to SLR, whether ventilatory acclimatization, obtained during residence at 1800–2200 m (21 ±3 mo, ± SD), reduces the incidence and severity of AMS for up to 72 h of exposure to 4300 m with heavy exertion in the early hours of altitude exposure. METHODS: Sixteen MAR (9 men, 7 women; 30±3 yr, 69±9 kg) and eighteen male SLR (25±5 yr, 78±9 kg;) completed an Environmental Symptoms Questionnaire (ESQ) and resting SaO (pulse oximeter) measurement in the morning at their residence altitude (Colorado Springs, CO (CS), and Palo Alto, CA (PA), respectively) and after ∼10, 24, 48, and 72 h residence on Pikes Peak (PP, 4300 m, 458 mmHg). AMS was assessed using the validated “AMS-Cerebral” (AMS-C) factor score in which a score of > 0.7 is indicative of AMS. Each subject completed a 2–4 h cycle exercise bout (50–60% VO2peak) within the first 5 h of altitude exposure. RESULTS: The incidence of AMS was lower (P < 0.05) in MAR compared to SLR, respectively, at PP10 (13% vs. 72%), PP24 (0% vs. 61 %), PP48 (0% vs. 56%), and PP72 (0% vs. 44%). The severity of AMS was also lower (P < 0.05) in MAR compared to SLR, respectively at PP10 (0.4 ± 0.2 vs. 1.5±1.3), PP24 (0.2 ± 0.2 vs. 1.4±1.2), PP48 (0.1 ± 0.2 vs. 1.4±1.5), andPP72 (0.1 ± 0.1 vs. 0.7 ± 0.7). The PP3 exercise SaO2 was higher (P < 0.01) in MAR compared to SLR (80±3% vs.74±6%). Resting SaO2 was similar in MAR and SLR at PP24 (86±2% vs. 83±6%), but higher (P < 0.05) in MAR at PP48 (89±3% vs. 83±6%) and PP72 (89±3% vs. 84±4%). CONCLUSION:These results show that compared to residence at sea level, residence at moderate altitude is very effective in decreasing the incidence and severity of AMS upon exposure to a higher altitude (4300 m) due, in part, to a greater degree of ventilatory acclimatization.

Physiological Responses of Ultraendurance Athletes and Nonathletes During an Attempt to Summit Denali

To compare altitude responses of 2 ultraendurance athletes and 2 nonathletes during a 2-week expedition on Denali (Mount McKinley). The severity of acute mountain sickness (AMS) symptoms (Lake Louise AMS guidelines) and pulmonary function parameters (forced vital capacity, forced expiratory volume in 1 second, peak expiratory flow) as well as resting heart rate and arterial oxygen saturation measurements were taken during the climb. Baseline measurements were made at 375 m, and field tests were performed at altitudes of 2200 m, 2400 m, 3000 m, 3400 m, 4100 m, 4300 m, and 10 m. Nonathletes reported moderate AMS symptoms at altitudes up to and including 3000 m, whereas ultraendurance athletes reported moderate AMS symptoms at altitudes above 3000 m. Considerable daily variation existed in pulmonary function measures within and between groups; however, the largest shift from baseline and between groups occurred at 3000 m where ultraendurance athletes had increased and nonathletes had decreased peak expiratory flow and forced vital capacity. Resting heart rate increased and arterial oxygen saturation decreased with altitude. Highly aerobically fit individuals may be more susceptible to delayed and more prolonged onset of AMS than are moderately fit individuals. Pulmonary function, although highly variable, also may be dissimilar between these groups.

Ginkgo Biloba Extract Prevents High Altitude Pulmonary Edema in Rats

Ginkgo biloba reduces the severity of acute mountain sickness in humans, but protection against high altitude pulmonary edema (HAPE) has not been reported. This study was conducted to determine if G. biloba would prevent early HAPE in rats. Six rats (ginkgo group) received G. biloba (200 mg/kg body weight in drinking water and an equal amount in peanut butter) for 2 days before and during high altitude exposure (380 mmHg pressure for 24 h). Six other rats (control group) received water and peanut butter alone. Protein concentrations in bronchoalveolar lavage fluid (BALF) were increased in control rats (19.8 +/- 2.6 mg/dL) compared to ginkgo rats (11.6 +/- 0.9 mg/dL; p = 0.014), demonstrating that untreated (control) rats developed mild HAPE following high altitude exposure. For comparison, BALF protein concentrations in sea-level rats (air group) given peanut butter were 12.6 +/- 0.8 mg/dL (n = 6). Although pleural effusions did not develop in any rats, the protein concentrations of pleural fluid were also increased in control rats (4.9 +/- 0.16 g/dL) compared to ginkgo rats (4.0 +/- 0.13; p = 0.001); air group: 3.5 +/- 0.08 g/dL. There were no differences in wet/dry lung weight ratios between groups, but wet left lung weights/preexposure body weight were increased in control rats (1.26 +/- 0.02 g/kg) compared to the ginkgo group (1.17 +/- 0.01 g/kg; p = 0.002); air group: 1.11 +/- 0.03 g/kg. In conclusion, the data show that G. biloba prevents the development of early HAPE in rats.

Early fluid retention and severe acute mountain sickness

Field studies of acute mountain sickness (AMS) usually include variations in exercise, diet, and environmental conditions over days and development of clinically apparent edemas. The purpose of this study was to clarify fluid status in persons developing AMS vs. those remaining without symptoms during simulated altitude with controlled fluid intake, diet, temperature, and without exercise. Ninety-nine exposures of 51 men and women to reduced barometric pressure (426 mmHg = 16,000 ft. = 4,880 m) were carried out for 8-12 h. AMS was evaluated by Lake Louise (LL) and AMS-C scores near the end of exposure. Serial measurements included fluid balance, electrolyte excretions, and plasma concentrations, regulating hormones, and free water clearance. Comparison between 16 subjects with the lowest AMS scores near the end of exposure ("non-AMS": mean LL = 1.0, range = 0-2.5) and 16 others with the highest AMS scores ("AMS": mean LL = 7.4, range = 5-11) demonstrated significant fluid retention in AMS beginning within the first 3 h, resulting from reduced urine flow. Plasma Na+ decreased significantly after 6 h, indicating dilution throughout the total body water. Excretion of Na+ and K+ trended downward with time in both groups, being lower in AMS after 6 h, and the urine Na+-to-K+ ratio was significantly higher for AMS after 6 h. Renal compensation for respiratory alkalosis, plasma renin activity, aldosterone, and atrial natriuretic peptide were not different between groups, with the latter tending to rise and aldosterone falling with time of exposure. Antidiuretic hormone fell in non-AMS and rose in AMS within 90 min of exposure and continued to rise in AMS, closely associated with severity of symptoms and fluid retention.