Postural Instability and Acute Mountain Sickness During Exposure to 24 Hours of Simulated Altitude (4300 m)

Roach, Robert C., Jack A. Loeppky, and Milton V. Icenogle.Acute mountain sickness: increased severity during simulated altitude compared with normobaric hypoxia. J. Appl. Physiol. 81(5): 1908–1910, 1996.—Acute mountain sickness (AMS) strikes those in the mountains who go too high too fast. Although AMS has been long assumed to be due solely to the hypoxia of high altitude, recent evidence suggests that hypobaria may also make a significant contribution to the pathophysiology of AMS. We studied nine healthy men exposed to simulated altitude, normobaric hypoxia, and normoxic hypobaria in an environmental chamber for 9 h on separate occasions. To simulate altitude, the barometric pressure was lowered to 432 ± 2 (SE) mmHg (simulated terrestrial altitude 4,564 m). Normobaric hypoxia resulted from adding nitrogen to the chamber (maintained near normobaric conditions) to match the inspired[Formula: see text] of the altitude exposure. By lowering the barometric pressure and adding oxygen, we achieved normoxic hypobaria with the same inspired[Formula: see text] as in our laboratory at normal pressure. AMS symptom scores (average scores from 6 and 9 h of exposure) were higher during simulated altitude (3.7 ± 0.8) compared with either normobaric hypoxia (2.0 ± 0.8; P < 0.01) or normoxic hypobaria (0.4 ± 0.2; P < 0.01). In conclusion, simulated altitude induces AMS to a greater extent than does either normobaric hypoxia or normoxic hypobaria, although normobaric hypoxia induced some AMS.

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Effects of acetazolamide and dexamethasone on cerebral hemodynamics in hypoxia

Journal of Applied Physiology ◽

10.1152/japplphysiol.01393.2010 ◽

2011 ◽

Vol 110 (5) ◽

pp. 1219-1225 ◽

Cited By ~ 31

Author(s):

Andrew W. Subudhi ◽

Andrew C. Dimmen ◽

Colleen G. Julian ◽

Megan J. Wilson ◽

Ronney B. Panerai ◽

...

Keyword(s):

Cerebral Autoregulation ◽

Acute Mountain Sickness ◽

Artery Blood Flow ◽

Hemodynamic Parameters ◽

Simulated Altitude ◽

Hemodynamic Changes ◽

Double Blind ◽

Cerebral Hemodynamic ◽

Mountain Sickness ◽

Dynamic Cerebral Autoregulation

Previous attempts to detect global cerebral hemodynamic differences between those who develop headache, nausea, and fatigue following rapid exposure to hypoxia [acute mountain sickness (AMS)] and those who remain healthy have been inconclusive. In this study, we investigated the effects of two drugs known to reduce symptoms of AMS to determine if a common cerebral hemodynamic mechanism could explain the prophylactic effect within individuals. With the use of randomized, placebo-controlled, double-blind, crossover design, 20 healthy volunteers were given oral acetazolamide (250 mg), dexamethasone (4 mg), or placebo every 8 h for 24 h prior to and during a 10-h exposure to a simulated altitude of 4,875 m in a hypobaric chamber, which included 2 h of exercise at 50% of altitude-specific V̇o2max. Cerebral hemodynamic parameters derived from ultrasound assessments of dynamic cerebral autoregulation and vasomotor reactivity were recorded 15 h prior to and after 9 h of hypoxia. AMS symptoms were scored using the Lake Louise Questionnaire (LLQ). It was found that both drugs prevented AMS in those who became ill on placebo (∼70% decrease in LLQ), yet a common cerebral hemodynamic mechanism was not identified. Compared with placebo, acetazolamide reduced middle cerebral artery blood flow velocity (11%) and improved dynamic cerebral autoregulation after 9 h of hypoxia, but these effects appeared independent of AMS. Dexamethasone had no measureable cerebral hemodynamic effects in hypoxia. In conclusion, global cerebral hemodynamic changes resulting from hypoxia may not explain the development of AMS.

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Simulated Altitude During The Night Reduces Severity Of Acute Mountain Sickness

Medicine & Science in Sports & Exercise ◽

10.1249/01.mss.0000354183.90450.67 ◽

2009 ◽

Vol 41 ◽

pp. 175 ◽

Cited By ~ 6

Author(s):

Christoph Dehnert ◽

Astrid Böhm ◽

Elmar Menold ◽

Igor Grigoriev ◽

Peter Bärtsch

Keyword(s):

Acute Mountain Sickness ◽

Simulated Altitude ◽

Mountain Sickness

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Association between ACTN3 and acute mountain sickness

Genes and Environment ◽

10.1186/s41021-019-0133-8 ◽

2019 ◽

Vol 41 (1) ◽

Cited By ~ 1

Author(s):

Ricardo Muller Bottura ◽

Giscard Humberto Oliveira Lima ◽

Debora Cristina Hipolide ◽

João Bosco Pesquero

Keyword(s):

Heart Rate ◽

Statistical Analysis ◽

Acute Mountain Sickness ◽

Muscle Fibers ◽

Genetic Differences ◽

Type I ◽

Simulated Altitude ◽

High Altitudes ◽

Metabolic Processes ◽

Mountain Sickness

Abstract Background During the process of acclimatization, when our organism needs to adjust several metabolic processes in the attempt of establishing a better oxygenation, it is normal that individuals present some symptoms that can lead to the disease of the mountain. However, not everyone presents such symptoms and individuals native of high altitudes regions present genetic differences compared to natives of low altitudes which can generate a better acute adaptation. One of these differences is the higher proportion of type I muscle fibers, which may originate from the R577X polymorphism of the ACTN3 gene. The aim of this study was to compare the response of individuals with different ACTN3 genotypes at simulated 4500 m altitude on the presence of Acute Mountain Sickness (AMS) symptoms. Twenty-three volunteers (RR = 7, RX = 8, XX = 8) spent 4 hours exposed to a simulated altitude of 4500 m inside a normobaric hypoxia chamber. Lactate and glucose concentrations, SpO2, heart rate and the symptoms of AMS were analyzed immediately before entering the chamber and at each hour of exposure. Statistical analysis was performed using IBM SPSS Statistics 21 software. Results Our results point to an association between AMS symptoms and the presence of R allele from R577X polymorphism. Conclusion We conclude that individuals with at least one R allele of the R577X polymorphism seems to be more susceptible to the effects of hypoxia during the acclimatization process and may develop AMS symptoms.

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Acute mountain sickness is not related to cerebral blood flow: a decompression chamber study

Journal of Applied Physiology ◽

10.1152/jappl.1999.86.5.1578 ◽

1999 ◽

Vol 86 (5) ◽

pp. 1578-1582 ◽

Cited By ~ 28

Author(s):

Ralf W. Baumgartner ◽

Ioakim Spyridopoulos ◽

Peter Bärtsch ◽

Marco Maggiorini ◽

Oswald Oelz

Keyword(s):

Blood Flow ◽

Cerebral Blood Flow ◽

Acute Mountain Sickness ◽

Transcranial Doppler Sonography ◽

Simulated Altitude ◽

Chamber Study ◽

Mountain Sickness ◽

Low Altitude ◽

Artery Flow

To evaluate the pathogenetic role of cerebral blood flow (CBF) changes occurring before and during the development of acute mountain sickness (AMS), peak mean middle cerebral artery flow velocities ([Formula: see text]) were assessed by transcranial Doppler sonography in 10 subjects at 490-m altitude, and during three 12-min periods immediately (SA1), 3 (SA2), and 6 (SA3) h after decompression to a simulated altitude of 4,559 m. AMS cerebral scores increased from 0.16 ± 0.14 at baseline to 0.44 ± 0.31 at SA1, 1.11 ± 0.88 at SA2( P < 0.05), and 1.43 ± 1.03 at SA3( P < 0.01); correspondingly, three, seven, and eight subjects had AMS. Absolute and relative[Formula: see text] at simulated altitude, expressed as percentages of low-altitude values (%[Formula: see text]), did not correlate with AMS cerebral scores. Average %[Formula: see text] remained unchanged, because %[Formula: see text]increased in three and remained unchanged or decreased in seven subjects at SA2 and SA3. These results suggest that CBF is not important in the pathogenesis of AMS and shows substantial interindividual differences during the first hours at simulated altitude.

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Influence of Acute Normobaric Hypoxia on Hemostasis in Volunteers with and without Acute Mountain Sickness

BioMed Research International ◽

10.1155/2015/593938 ◽

2015 ◽

Vol 2015 ◽

pp. 1-9 ◽

Cited By ~ 7

Author(s):

Marc Schaber ◽

Veronika Leichtfried ◽

Dietmar Fries ◽

Maria Wille ◽

Hannes Gatterer ◽

...

Keyword(s):

Acute Mountain Sickness ◽

Activated Partial Thromboplastin Time ◽

Reference Ranges ◽

Simulated Altitude ◽

Coagulation Time ◽

Hemostatic System ◽

Mountain Sickness ◽

Healthy Participants ◽

Generation Test ◽

Maximum Clot Firmness

Introduction. The aim of the present study was to investigate whether a 12-hour exposure in a normobaric hypoxic chamber would induce changes in the hemostatic system and a procoagulant state in volunteers suffering from acute mountain sickness (AMS) and healthy controls.Materials and Methods. 37 healthy participants were passively exposed to 12.6% FiO2(simulated altitude hypoxia of 4,500 m). AMS development was investigated by the Lake Louise Score (LLS). Prothrombin time, activated partial thromboplastin time, fibrinogen, and platelet count were measured and specific methods (i.e., thromboelastometry and a thrombin generation test) were used.Results. AMS prevalence was 62.2% (LLS cut off of 3). For the whole group, paired samplet-tests showed significant increase in the maximal concentration of generated thrombin. ROTEM measurements revealed a significant shortening of coagulation time and an increase of maximal clot firmness (InTEM test). A significant increase in maximum clot firmness could be shown (FibTEM test).Conclusions. All significant changes in coagulation parameters after exposure remained within normal reference ranges. No differences with regard to measured parameters of the hemostatic system between AMS-positive and -negative subjects were observed. Therefore, the hypothesis of the acute activation of coagulation by hypoxia can be rejected.

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