scholarly journals Respiratory alkalinization and posterior cerebral artery dilatation predict acute mountain sickness severity during 10 h normobaric hypoxia

2020 ◽  
Vol 106 (1) ◽  
pp. 175-190
Author(s):  
Holly Barclay ◽  
Saptarshi Mukerji ◽  
Bengt Kayser ◽  
Terrence O'Donnell ◽  
Yu‐Chieh Tzeng ◽  
...  
Keyword(s):  
Cerebral Artery ◽  
Posterior Cerebral Artery ◽  
Acute Mountain Sickness ◽  
Normobaric Hypoxia ◽  
Mountain Sickness

No effect of patent foramen ovale on acute mountain sickness and pulmonary pressure in normobaric hypoxia

2021 ◽  
Author(s):  
Kaitlyn G. DiMarco ◽  
Kara M. Beasley ◽  
Karina Shah ◽  
Julia P. Speros ◽  
Jonathan E. Elliott ◽  
...  
Keyword(s):  
Patent Foramen Ovale ◽  
Acute Mountain Sickness ◽  
Normobaric Hypoxia ◽  
Foramen Ovale ◽  
Pulmonary Pressure ◽  
Mountain Sickness

The Effect of an Expiratory Resistance Mask with Dead Space on Sleep, Acute Mountain Sickness, Cognition, and Ventilatory Acclimatization in Normobaric Hypoxia

2019 ◽  
Vol 20 (1) ◽  
pp. 61-70 ◽  
Author(s):  
Alexander Patrician ◽  
Michael M. Tymko ◽  
Hannah G. Caldwell ◽  
Connor A. Howe ◽  
Geoff B. Coombs ◽  
...  
Keyword(s):  
Dead Space ◽  
Acute Mountain Sickness ◽  
Normobaric Hypoxia ◽  
Expiratory Resistance ◽  
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.

scholarly journals Remote ischemic preconditioning delays the onset of acute mountain sickness in normobaric hypoxia

2015 ◽  
Vol 3 (3) ◽  
pp. e12325 ◽  
Author(s):  
Marc M. Berger ◽  
Hannah Köhne ◽  
Lorenz Hotz ◽  
Moritz Hammer ◽  
Kai Schommer ◽  
...  
Keyword(s):  
Ischemic Preconditioning ◽  
Acute Mountain Sickness ◽  
Normobaric Hypoxia ◽  
Remote Ischemic Preconditioning ◽  
Mountain Sickness

Normobaric hypoxia and symptoms of acute mountain sickness: Elevated brain volume and intracranial hypertension

2014 ◽  
Vol 75 (6) ◽  
pp. 890-898 ◽  
Author(s):  
Justin S. Lawley ◽  
Noam Alperin ◽  
Ahmet M. Bagci ◽  
Sang H. Lee ◽  
Paul G. Mullins ◽  
...  
Keyword(s):  
Intracranial Hypertension ◽  
Brain Volume ◽  
Acute Mountain Sickness ◽  
Normobaric Hypoxia ◽  
Mountain Sickness

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 Neutrophil Gelatinase-Associated Lipocalin: Its Response to Hypoxia and Association with Acute Mountain Sickness

2013 ◽  
Vol 35 ◽  
pp. 537-542 ◽  
Author(s):  
Adrian Mellor ◽  
Christopher Boos ◽  
Mike Stacey ◽  
Tim Hooper ◽  
Chris Smith ◽  
...  
Keyword(s):  
Biochemical Marker ◽  
Point Of Care ◽  
Acute Mountain Sickness ◽  
Normobaric Hypoxia ◽  
Neutrophil Gelatinase Associated Lipocalin ◽  
Clinical Challenge ◽  
Significant Difference ◽  
Mountain Sickness ◽  
Neutrophil Gelatinase ◽  
And Oxidative Stress

Acute Mountain Sickness (AMS) is a common clinical challenge at high altitude (HA). A point-of-care biochemical marker for AMS could have widespread utility. Neutrophil gelatinase-associated lipocalin (NGAL) rises in response to renal injury, inflammation and oxidative stress. We investigated whether NGAL rises with HA and if this rise was related to AMS, hypoxia or exercise. NGAL was assayed in a cohort (n=22) undertaking 6 hours exercise at near sea-level (SL); a cohort (n=14) during 3 hours of normobaric hypoxia (FiO2 11.6%) and on two trekking expeditions (n=52) to over 5000 m. NGAL did not change with exercise at SL or following normobaric hypoxia. During the trekking expeditions NGAL levels (ng/ml, mean ± sd, range) rose significantly (P<0.001) from 68 ± 14 (60–102) at 1300 m to 183 ± 107 (65–519); 143 ± 66 (60–315) and 150 ± 71 (60–357) at 3400 m, 4270 m and 5150 m respectively. At 5150 m there was a significant difference in NGAL between those with severe AMS (n=7), mild AMS (n=16) or no AMS (n=23): 201 ± 34 versus 171 ± 19 versus 124 ± 12 respectively (P=0.009for severe versus no AMS;P=0.026for mild versus no AMS). In summary, NGAL rises in response to prolonged hypobaric hypoxia and demonstrates a relationship to the presence and severity of AMS.

Symptom Progression in Acute Mountain Sickness During a 12-Hour Exposure to Normobaric Hypoxia Equivalent to 4500 M

2014 ◽  
Vol 15 (4) ◽  
pp. 446-451 ◽  
Author(s):  
Martin Burtscher ◽  
Maria Wille ◽  
Verena Menz ◽  
Martin Faulhaber ◽  
Hannes Gatterer
Keyword(s):  
Acute Mountain Sickness ◽  
Normobaric Hypoxia ◽  
Mountain Sickness ◽  
Symptom Progression

Acute mountain sickness, chemosensitivity, and cardiorespiratory responses in humans exposed to hypobaric and normobaric hypoxia

2014 ◽  
Vol 116 (7) ◽  
pp. 945-952 ◽  
Author(s):  
Normand A. Richard ◽  
Inderjeet S. Sahota ◽  
Nadia Widmer ◽  
Sherri Ferguson ◽  
A. William Sheel ◽  
...  
Keyword(s):  
Ventilatory Response ◽  
Minute Ventilation ◽  
Acute Mountain Sickness ◽  
Blood Oxygenation ◽  
Normobaric Hypoxia ◽  
Hypoxic Exposure ◽  
Hypoxic Ventilatory Response ◽  
Before And After ◽  
Mountain Sickness ◽  
Normobaric Normoxia

We examined the control of breathing, cardiorespiratory effects, and the incidence of acute mountain sickness (AMS) in humans exposed to hypobaric hypoxia (HH) and normobaric hypoxia (NH), and under two control conditions [hypobaric normoxia (HN) and normobaric normoxia (NN)]. Exposures were 6 h in duration, and separated by 2 wk between hypoxic exposures and 1 wk between normoxic exposures. Before and after exposures, subjects ( n = 11) underwent hyperoxic and hypoxic Duffin CO2 rebreathing tests and a hypoxic ventilatory response test (HVR). Inside the environmental chamber, minute ventilation (V̇e), tidal volume (Vt), frequency of breathing ( fB), blood oxygenation, heart rate, and blood pressure were measured at 5 and 30 min and hourly until exit. Symptoms of AMS were evaluated using the Lake Louise score (LLS). Both the hyperoxic and hypoxic CO2 thresholds were lower after HH and NH, whereas CO2 sensitivity was increased after HH and NH in the hypoxic test and after NH in the hyperoxic test. Values for HVR were similar across the four exposures. No major differences were observed for V̇e or any other cardiorespiratory variables between NH and HH. The LLS was greater in AMS-susceptible than in AMS-resistant subjects; however, LLS was alike between HH and NH. In AMS-susceptible subjects, fB correlated positively and Vt negatively with the LLS. We conclude that 6 h of hypoxic exposure is sufficient to lower the peripheral and central CO2 threshold but does not induce differences in cardiorespiratory variables or AMS incidence between HH and NH.

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