scholarly journals Appetite at “high altitude” [Operation Everest III (Comex-’97)]: a simulated ascent of Mount Everest

1999 ◽  
Vol 87 (1) ◽  
pp. 391-399 ◽  
Author(s):  
Margriet S. Westerterp-Plantenga ◽  
Klaas R. Westerterp ◽  
Mira Rubbens ◽  
Christianne R. T. Verwegen ◽  
Jean-Paul Richelet ◽  
...  
Keyword(s):  
Food Intake ◽  
High Altitude ◽  
Body Mass ◽  
Hypobaric Hypoxia ◽  
Acute Mountain Sickness ◽  
Mount Everest ◽  
Physiological Fluid ◽  
Per Se ◽  
Mountain Sickness ◽  
Desire To Eat

We hypothesized that progressive loss of body mass during high-altitude sojourns is largely caused by decreased food intake, possibly due to hypobaric hypoxia. Therefore we assessed the effect of long-term hypobaric hypoxia per se on appetite in eight men who were exposed to a 31-day simulated stay at several altitudes up to the peak of Mt. Everest (8,848 m). Palatable food was provided ad libitum, and stresses such as cold exposure and exercise were avoided. At each altitude, body mass, energy, and macronutrient intake were measured; attitude toward eating and appetite profiles during and between meals were assessed by using questionnaires. Body mass reduction of an average of 5 ± 2 kg was mainly due to a reduction in energy intake of 4.2 ± 2 MJ/day ( P < 0.01). At 5,000- and 6,000-m altitudes, subjects had hardly any acute mountain sickness symptoms and meal size reductions ( P < 0.01) were related to a more rapid increase in satiety ( P < 0.01). Meal frequency was increased from 4 ± 1 to 7 ± 1 eating occasions per day ( P < 0.01). At 7,000 m, when acute mountain sickness symptoms were present, uncoupling between hunger and desire to eat occurred and prevented a food intake necessary to meet energy balance requirements. On recovery, body mass was restored up to 63% after 4 days; this suggests physiological fluid retention with the return to sea level. We conclude that exposure to hypobaric hypoxia per se appears to be associated with a change in the attitude toward eating and with a decreased appetite and food intake.

Elevated plasma S100B levels in high altitude hypobaric hypoxia do not correlate with acute mountain sickness

2014 ◽  
Vol 36 (9) ◽  
pp. 779-785 ◽  
Author(s):  
Craig D. Winter ◽  
Timothy R. Whyte ◽  
John Cardinal ◽  
Stephen E. Rose ◽  
Peter K. O’Rourke ◽  
...  
Keyword(s):  
High Altitude ◽  
Hypobaric Hypoxia ◽  
Acute Mountain Sickness ◽  
Elevated Plasma ◽  
Mountain Sickness

scholarly journals Energy and Water Balance at High Altitude

Physiology ◽  
2001 ◽  
Vol 16 (3) ◽  
pp. 134-137 ◽  
Author(s):  
Klaas R. Westerterp
Keyword(s):  
Weight Loss ◽  
Water Balance ◽  
High Altitude ◽  
Body Mass ◽  
Fat Mass ◽  
Acute Mountain Sickness ◽  
Fat Free Mass ◽  
Mountain Sickness

Many studies have shown that subjects lose significant amounts of body mass, fat mass as well as fat-free mass, during a climb to and/or a stay at high altitude. Altitude-induced weight loss is mainly caused by malnutrition due to hypoxia-related satiety, independent of acute mountain sickness.

Flying, altitude, and diving

2021 ◽  
pp. 593-608
Author(s):  
Terry Robinson ◽  
Jane Scullion
Keyword(s):  
Lung Disease ◽  
High Altitude ◽  
Atmospheric Pressure ◽  
Hypobaric Hypoxia ◽  
Acute Mountain Sickness ◽  
Gas Composition ◽  
Gaseous Exchange ◽  
High Altitudes ◽  
Mountain Sickness

Up to an altitude of approximately 30,000 feet, the composition of the gas in the air we breathe remains almost constant. Atmospheric pressure decreases exponentially with altitude. This means that although the gas composition at high altitude remains the same, the air is less dense, resulting in less available oxygen for gaseous exchange. Hypobaric hypoxia therefore develops as a result of low atmospheric atmosphere. This chapter discusses the effects of flying, high altitudes, and diving on respiration. It starts by describing atmospheric pressure and altitude, the then-acute mountain sickness (AMS) and its management. Flying with lung disease is covered, alongside fitness to fly, the use of in-flight oxygen, and general precautions to take. Diving, diving-related illnesses, and practising the sport with pre-existing lung conditions are also included.

Optic nerve sheath diameter changes at high altitude and in acute mountain sickness: meta-regression analyses

2020 ◽  
pp. bjophthalmol-2020-317717
Author(s):  
Tou-Yuan Tsai ◽  
George Gozari ◽  
Yung-Cheng Su ◽  
Yi-Kung Lee ◽  
Yu-Kang Tu
Keyword(s):  
Optic Nerve ◽  
High Altitude ◽  
Acute Mountain Sickness ◽  
Optic Nerve Sheath Diameter ◽  
Optic Nerve Sheath ◽  
Cochrane Library ◽  
Regression Analyses ◽  
Spline Regression ◽  
Nerve Sheath ◽  
Mountain Sickness

Background/aimsTo assess changes in optic nerve sheath diameter (ONSD) at high altitude and in acute mountain sickness (AMS).MethodsCochrane Library, EMBASE, Google Scholar and PubMed were searched for articles published from their inception to 31st of July 2020. Outcome measures were mean changes of ONSD at high altitude and difference in ONSD change between subjects with and without AMS. Meta-regressions were conducted to investigate the relation of ONSD change to altitude and time spent at that altitude.ResultsEight studies with 248 participants comparing ONSD from sea level to high altitude, and five studies with 454 participants comparing subjects with or without AMS, were included. ONSD increased by 0.14 mm per 1000 m after adjustment for time (95% CI: 0.10 to 0.18; p<0.01). Restricted cubic spline regression revealed an almost linear relation between ONSD change and time within 2 days. ONSD was greater in subjects with AMS (mean difference=0.47; 95% CI: 0.14 to 0.80; p=0.01; I2=89.4%).ConclusionOur analysis shows that ONSD changes correlate with altitude and tend to increase in subjects with AMS. Small study number and high heterogeneity are the limitations of our study. Further large prospective studies are required to verify our findings.

scholarly journals A Prospective Epidemiological Study of Acute Mountain Sickness in Nepalese Pilgrims Ascending to High Altitude (4380 m)

PLoS ONE ◽  
2013 ◽  
Vol 8 (10) ◽  
pp. e75644 ◽  
Author(s):  
Martin J. MacInnis ◽  
Eric A. Carter ◽  
Michael G. Freeman ◽  
Bidur Prasad Pandit ◽  
Ashmita Siwakoti ◽  
...  
Keyword(s):  
High Altitude ◽  
Epidemiological Study ◽  
Acute Mountain Sickness ◽  
Prospective Epidemiological Study ◽  
Mountain Sickness

Abstract 14359: Single Nucleotide Polymorphisms in Genes Involved in L-arginine / Dimethylarginine Metabolism Predispose for Pulmonary Hypertension and Acute Mountain Sickness at High Altitude

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Juliane Hannemann ◽  
Julia Zummack ◽  
PATRICIA SIQUES ◽  
JULIO BRITO ◽  
Rainer Boeger
Keyword(s):  
Pulmonary Hypertension ◽  
Relative Risk ◽  
Genetic Variability ◽  
High Altitude ◽  
Acute Mountain Sickness ◽  
Minor Allele ◽  
Nucleotide Polymorphisms ◽  
Single Nucleotide ◽  
Mountain Sickness ◽  
Study Participants

Introduction: Chronic (CH) and chronic-intermittent (CIH) exposure to hypoxia at high altitude causes acute or chronic mountain sickness and elevation of mean pulmonary arterial pressure (mPAP). This is paralleled by increased plasma levels of ADMA, an endogenous inhibitor of NO synthesis. ADMA is cleaved by dimethylarginine dimethylaminohydrolase (DDAH1 and DDAH2), whilst symmetric dimethylarginine (SDMA) is cleaved by AGXT2. Arginase (ARG1 and ARG2) competes with endothelial NO synthase (NOS3) for L-arginine as substrate. We have shown previously that baseline ADMA (at sea level) determines mPAP after six months of CIH; cut-off values of 25 mm Hg and 30 mm Hg are being used to diagnose high altitude pulmonary hypertension. Hypothesis: We hypothesized that genetic variability in genes coding for core enzymes of ADMA, SDMA, and L-arginine metabolism may predispose individuals for high altitude disease and pulmonary hypertension. Methods: We genotyped 16 common single nucleotide polymorphisms in the NOS3, DDAH1, DDAH2, AGXT2, ARG1 and ARG2 genes of 69 healthy male Chilean subjects. Study participants adhered to a CIH regimen (5d at 3,550m, 2d at sea level) for six months. Metabolites were measured by LC-MS/MS; mPAP was estimated by echocardiography at six months, and altitude acclimatization was assessed by Lake Louise Score and arterial oxygen saturation. Results: Carriers of the minor allele of DDAH1 rs233112 had a higher mean baseline ADMA level (0.76±0.03 vs. 0.67±0.02 μmol/l; p<0.05), whilst the major allele of DDAH2 rs805304 was linked to an exacerbated increase of ADMA in hypoxia (0.10±0.03 vs. 0.04±0.04 μmol/l; p<0.02). Study participants carrying the minor allele of ARG1 rs2781667 had a relative risk of elevated mPAP (>25 mm Hg) of 1.70 (1.56-1.85; p<0.0001), and carriers of the minor allele of NOS3 rs2070744 had a relative risk of elevated mPAP (>30 mm Hg) of 1.58 (1.47-1.69; p<0.0001). The NOS3 and DDAH2 genes were associated with the incidence of acute mountain sickness. Conclusions: We conclude that genetic variability in the L-arginine / ADMA / NO pathway is an important determinant of high altitude pulmonary hypertension and acute mountain sickness. DDAH1 is linked to baseline ADMA, whilst DDAH2 determines the response of ADMA to hypoxia.

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