scholarly journals Association between ACTN3 and acute mountain sickness

2019 ◽  
Vol 41 (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.

scholarly journals Acclimatization at High Altitudes using Machine Learning

2020 ◽  
Vol 8 (6) ◽  
pp. 5618-5621
Keyword(s):  
Heart Rate ◽  
Acute Mountain Sickness ◽  
Support Vector ◽  
High Altitudes ◽  
Fitness Level ◽  
Vector Machines ◽  
Rapid Ascent ◽  
Mountain Sickness ◽  
Partial Oxygen

The objective is to classify the fitness level of individuals at high altitudes and their susceptibility to acute mountain sickness (AMS). AMS is caused due to rapid ascent to hypobaric and hypoxic environments the physical variables taken into consideration are the heart rate (HR) and the saturated volume of partial oxygen level (SPO2). HR and SPO2 levels were chosen as they are the factors most affected by hypobaric and hypoxic environments. We aim to build an index of acclimatization that classifies the level of acclimatization based on the values of Heart Rate and SPO2 levels using support vector machines. The model is trained using HR and SPO2 values of 100 individuals over seven days, with six days at high altitude and first day at seas level. Adaptability at higher altitudes varies from one individual to another based on their lifestyle, fitness levels and different factors, so classification may help identify individuals who have adapted inadequately so steps may be taken to acclimatize efficiently. The index classifies individuals into four categories: Highly Acclimatized, Normally Acclimatized, Partially Acclimatized and Susceptible. Classification of acclimatization levels can be used by military personnel training at high altitudes and medical applications.

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

2001 ◽  
Vol 2 (4) ◽  
pp. 509-514 ◽  
Author(s):  
Allen Cymerman ◽  
Stephen R. Muza ◽  
Beth A. Beidleman ◽  
Dan T. Ditzler ◽  
Charles S. Fulco
Keyword(s):  
Acute Mountain Sickness ◽  
Postural Instability ◽  
Simulated Altitude ◽  
Mountain Sickness

scholarly journals Heart rate variability changes at 2400 m altitude predicts acute mountain sickness on further ascent at 3000–4300 m altitudes

2012 ◽  
Vol 3 ◽  
Author(s):  
Heikki M. Karinen ◽  
Arja Uusitalo ◽  
Henri Vähä-Ypyä ◽  
Mika Kähönen ◽  
Juha E. Peltonen ◽  
...  
Keyword(s):  
Heart Rate ◽  
Heart Rate Variability ◽  
Acute Mountain Sickness ◽  
Mountain Sickness

Effect of repeated normobaric hypoxia exposures during sleep on acute mountain sickness, exercise performance, and sleep during exposure to terrestrial altitude

2011 ◽  
Vol 300 (2) ◽  
pp. R428-R436 ◽  
Author(s):  
Charles S. Fulco ◽  
Stephen R. Muza ◽  
Beth A. Beidleman ◽  
Robby Demes ◽  
Janet E. Staab ◽  
...  
Keyword(s):  
Heart Rate ◽  
Exercise Performance ◽  
Hypobaric Hypoxia ◽  
Sham Group ◽  
Acute Mountain Sickness ◽  
Time Trial ◽  
Normobaric Hypoxia ◽  
Performance Decrement ◽  
Mountain Sickness ◽  
End Tidal

There is an expectation that repeated daily exposures to normobaric hypoxia (NH) will induce ventilatory acclimatization and lessen acute mountain sickness (AMS) and the exercise performance decrement during subsequent hypobaric hypoxia (HH) exposure. However, this notion has not been tested objectively. Healthy, unacclimatized sea-level (SL) residents slept for 7.5 h each night for 7 consecutive nights in hypoxia rooms under NH [ n = 14, 24 ± 5 (SD) yr] or “sham” ( n = 9, 25 ± 6 yr) conditions. The ambient percent O2 for the NH group was progressively reduced by 0.3% [150 m equivalent (equiv)] each night from 16.2% (2,200 m equiv) on night 1 to 14.4% (3,100 m equiv) on night 7, while that for the ventilatory- and exercise-matched sham group remained at 20.9%. Beginning at 25 h after sham or NH treatment, all subjects ascended and lived for 5 days at HH (4,300 m). End-tidal Pco2, O2 saturation (SaO2), AMS, and heart rate were measured repeatedly during daytime rest, sleep, or exercise (11.3-km treadmill time trial). From pre- to posttreatment at SL, resting end-tidal Pco2 decreased ( P < 0.01) for the NH (from 39 ± 3 to 35 ± 3 mmHg), but not for the sham (from 39 ± 2 to 38 ± 3 mmHg), group. Throughout HH, only sleep SaO2 was higher (80 ± 1 vs. 76 ± 1%, P < 0.05) and only AMS upon awakening was lower (0.34 ± 0.12 vs. 0.83 ± 0.14, P < 0.02) in the NH than the sham group; no other between-group rest, sleep, or exercise differences were observed at HH. These results indicate that the ventilatory acclimatization induced by NH sleep was primarily expressed during HH sleep. Under HH conditions, the higher sleep SaO2 may have contributed to a lessening of AMS upon awakening but had no impact on AMS or exercise performance for the remainder of each day.

High altitude deterioration

1954 ◽  
Vol 143 (910) ◽  
pp. 40-42 ◽  
Keyword(s):  
High Altitude ◽  
Individual Variation ◽  
Acute Mountain Sickness ◽  
Hard Work ◽  
High Altitudes ◽  
Appetite Loss ◽  
Prolonged Stay ◽  
Loss Of Weight ◽  
The Subject ◽  
Mountain Sickness

High altitude deterioration means a gradual diminution in man’s capacity to do work at great heights. This is associated with insomnia, lack of appetite, loss of weight and increasing lethargy. These symptoms appear after a prolonged stay above 18000 ft. and there is great individual variation. Man would deteriorate after a time at these heights even under the best con­ditions: if he is doing hard work and is subjected to many strains, mental and physical, other factors are brought to bear which will aggravate this basic state. Such factors are illness, exhaustion, starvation and dehydration. Symptoms similar to those of deterioration, but more acute in onset, appear if man goes too quickly to high altitudes without first acclimatizing. These symptoms of acute mountain sickness disappear if the subject returns to lower levels for some time. If he goes to moderate heights when acclimatizing he will be able to stay for reasonably long periods without undue trouble. Exhaustion at high altitudes is often only cured by coming down to lower levels, as above a certain height there seems to be little or no recovery.

scholarly journals Acute mountain sickness: increased severity during simulated altitude compared with normobaric hypoxia

1996 ◽  
Vol 81 (5) ◽  
pp. 1908-1910 ◽  
Author(s):  
Robert C. Roach ◽  
Jack A. Loeppky ◽  
Milton V. Icenogle
Keyword(s):  
Significant Contribution ◽  
Acute Mountain Sickness ◽  
Barometric Pressure ◽  
Normal Pressure ◽  
Normobaric Hypoxia ◽  
Simulated Altitude ◽  
Healthy Men ◽  
Altitude Exposure ◽  
Symptom Scores ◽  
Mountain Sickness

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.

scholarly journals Effects of acetazolamide and dexamethasone on cerebral hemodynamics in hypoxia

2011 ◽  
Vol 110 (5) ◽  
pp. 1219-1225 ◽  
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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