Intermittent altitude exposures reduce acute mountain sickness at 4300 m

2004 ◽  
Vol 106 (3) ◽  
pp. 321-328 ◽  
Author(s):  
Beth A. BEIDLEMAN ◽  
Stephen R. MUZA ◽  
Charles S. FULCO ◽  
Allen CYMERMAN ◽  
Dan DITZLER ◽  
...  
Keyword(s):  
Acute Mountain Sickness ◽  
Urine Volume ◽  
Barometric Pressure ◽  
Self Report ◽  
Altitude Exposure ◽  
Cerebral Symptom ◽  
Cycle Training ◽  
Mountain Sickness ◽  
End Tidal ◽  
Rest And Exercise

Acute mountain sickness (AMS) commonly occurs at altitudes exceeding 2000–2500 m and usually resolves after acclimatization induced by a few days of chronic residence at the same altitude. Increased ventilation and diuresis may contribute to the reduction in AMS with altitude acclimatization. The aim of the present study was to examine the effects of intermittent altitude exposures (IAE), in combination with rest and exercise training, on the incidence and severity of AMS, resting ventilation and 24-h urine volume at 4300 m. Six lowlanders (age, 23±2 years; body weight, 77±6 kg; values are means±S.E.M.) completed an Environmental Symptoms Questionnaire (ESQ) and Lake Louise AMS Scoring System (LLS), a resting end-tidal partial pressure of CO2 (PETCO2) test and a 24-h urine volume collection at sea level (SL) and during a 30 h exposure to 4300 m altitude-equivalent (barometric pressure=446 mmHg) once before (PreIAE) and once after (PostIAE) a 3-week period of IAE (4 h·day-1, 5 days·week-1, 4300 m). The previously validated factor score, AMS cerebral score, was calculated from the ESQ and the self-report score was calculated from the LLS at 24 h of altitude exposure to assess the incidence and severity of AMS. During each IAE, three subjects cycled for 45–60 min·day-1 at 60–70% of maximal O2 uptake (VO2 max) and three subjects rested. Cycle training during each IAE did not affect any of the measured variables, so data from all six subjects were combined. The results showed that the incidence of AMS (%), determined from both the ESQ and LLS, increased (P<0.05) from SL (0±0) to PreIAE (50±22) at 24 h of altitude exposure and decreased (P<0.05) from PreIAE to PostIAE (0±0). The severity of AMS (i.e. AMS cerebral symptom and LLS self-report scores) increased (P<0.05) from SL (0.02±0.02 and 0.17±0.17 respectively) to PreIAE (0.49±0.18 and 4.17±0.94 respectively) at 24 h of altitude exposure, and decreased (P<0.05) from PreIAE to PostIAE (0.03±0.02 and 0.83±0.31 respectively). Resting PETCO2 (mmHg) decreased (i.e. increase in ventilation; P<0.05) from SL (38±1) to PreIAE (32±1) at 24 h of altitude exposure and decreased further (P<0.05) from PreIAE to PostIAE (28±1). In addition, 24-h urine volumes were similar at SL, PreIAE and PostIAE. In conclusion, our findings suggest that 3 weeks of IAE provide an effective alternative to chronic altitude residence for increasing resting ventilation and reducing the incidence and severity of AMS.

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 Exercise exacerbates acute mountain sickness at simulated high altitude

2000 ◽  
Vol 88 (2) ◽  
pp. 581-585 ◽  
Author(s):  
R. C. Roach ◽  
D. Maes ◽  
D. Sandoval ◽  
R. A. Robergs ◽  
M. Icenogle ◽  
...  
Keyword(s):  
High Altitude ◽  
Minute Ventilation ◽  
Arterial Oxygen Saturation ◽  
Acute Mountain Sickness ◽  
Urine Volume ◽  
Barometric Pressure ◽  
Arterial Oxygen ◽  
Simulated High Altitude ◽  
Mountain Sickness ◽  
Exercise Induced

.—We hypothesized that exercise would cause greater severity and incidence of acute mountain sickness (AMS) in the early hours of exposure to altitude. After passive ascent to simulated high altitude in a decompression chamber [barometric pressure = 429 Torr, ∼4,800 m (J. B. West, J. Appl. Physiol. 81: 1850–1854, 1996)], seven men exercised (Ex) at 50% of their altitude-specific maximal workload four times for 30 min in the first 6 h of a 10-h exposure. On another day they completed the same protocol but were sedentary (Sed). Measurements included an AMS symptom score, resting minute ventilation (V˙e), pulmonary function, arterial oxygen saturation ([Formula: see text]), fluid input, and urine volume. Symptoms of AMS were worse in Ex than Sed, with peak AMS scores of 4.4 ± 1.0 and 1.3 ± 0.4 in Ex and Sed, respectively ( P < 0.01); but restingV˙e and[Formula: see text] were not different between trials. However, [Formula: see text] during the exercise bouts in Ex was at 76.3 ± 1.7%, lower than during either Sed or at rest in Ex (81.4 ± 1.8 and 82.2 ± 2.6%, respectively, P< 0.01). Fluid intake-urine volume shifted to slightly positive values in Ex at 3–6 h ( P = 0.06). The mechanism(s) responsible for the rise in severity and incidence of AMS in Ex may be sought in the observed exercise-induced exaggeration of arterial hypoxemia, in the minor fluid shift, or in a combination of these factors.

Acclimatization to 4,300-m altitude decreases reliance on fat as a substrate

1996 ◽  
Vol 81 (4) ◽  
pp. 1762-1771 ◽  
Author(s):  
A. C. Roberts ◽  
G. E. Butterfield ◽  
A. Cymerman ◽  
J. T. Reeves ◽  
E. E. Wolfel ◽  
...  
Keyword(s):  
Glucose Uptake ◽  
Hypobaric Hypoxia ◽  
Barometric Pressure ◽  
Cycle Ergometry ◽  
Glycerol Release ◽  
Altitude Acclimatization ◽  
Altitude Exposure ◽  
Consumption Rates ◽  
Uptake And Release ◽  
Rest And Exercise

Roberts, A. C., G. E. Butterfield, A. Cymerman, J. T. Reeves, E. E. Wolfel, and G. A. Brooks. Acclimatization to 4,300-m altitude decreases reliance on fat as a substrate. J. Appl. Physiol. 81(4): 1762–1771, 1996.—We tested the hypothesis that exposure to altitude decreases reliance on free fatty acids (FFA) as substrates and increases dependency on blood glucose. Therefore, the effects of exercise, hypobaric hypoxia, and altitude acclimatization on FFA, glycerol and net glucose uptake and release [ = 2(leg blood flow)(arteriovenous concentration)] and on fatty acid (FA) consumption by the legs (= 3 × glycerol release + FFA uptake) were measured. Because sympathetic responses have been implicated, we utilized nonspecific β-blockade and observed responses to exercise, altitude, and altitude acclimatization. We studied six healthy β-blocked men (β) and five matched controls (C) during rest and cycle ergometry exercise (88 W) at 49% of sea-level (SL) peak O2 uptake at the same absolute power output on acute altitude exposure (A1; barometric pressure = 430 Torr) and after 3 wk of chronic altitude exposure to 4,300 m (A2). During exercise at SL, FA consumption rates increased ( P < 0.05). On arrival at 4,300 m, resting leg FFA uptake and FA consumption rates were not significantly different from those at SL. However, after acclimatization to altitude, at rest leg FA consumption decreased to essentially zero in both C and β groups. During exercise at altitude after acclimatization, leg FA consumption increased significantly, but values were less than at SL or A1 ( P < 0.05), whereas glucose uptake increased relative to SL values. Furthermore, β-blockade significantly increased glucose uptake relative to control. We conclude that 1) chronic altitude exposure decreases leg FA consumption during rest and exercise; 2) relative to SL, FFA uptake decreases while glucose uptake increases during exercise at altitude; and 3) β-blockade potentiates these effects.

Atrial Natriuretic Peptide, Altitude and Acute Mountain Sickness

1989 ◽  
Vol 77 (5) ◽  
pp. 509-514 ◽  
Author(s):  
J. S. Milledge ◽  
J. M. Beeley ◽  
S. McArthur ◽  
A. H. Morice
Keyword(s):  
Body Weight ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Packed Cell Volume ◽  
Sodium Excretion ◽  
Acute Mountain Sickness ◽  
Urine Volume ◽  
Symptom Scores ◽  
Mountain Sickness ◽  
Atrial Natriuretic

1. To investigate the mechanisms of acute mountain sickness, 22 subjects travelled to 3100 m by road and the following day walked to 4300 m on Mount Kenya. Control measurements were made over 2 days at 1300 m before ascent and for 2 days after arrival at 4300 m. These included body weight, 24 h urine volume, 24 h sodium and potassium excretion, blood haemoglobin, packed cell volume, and symptom score for acute mountain sickness. In 15 subjects blood samples were taken for assay of plasma aldosterone and atrial natriuretic peptide. 2. Altitude and the exercise in ascent resulted in a marked decrease in 24 h urine volume and sodium excretion. Aldosterone levels were elevated on the first day and atrial natriuretic peptide levels were higher on both altitude days compared with control. 3. Acute mountain sickness symptom scores showed a significant negative correlation with 24 h urinary sodium excretion on the first altitude day. Aldosterone levels tended to be lowest in subjects with low symptom scores and higher sodium excretion. No correlation was found between changes in haemoglobin concentration, packed cell volume, 24 h urine volume or body weight and acute mountain sickness symptom score. 4. Atrial natriuretic peptide levels at low altitude showed a significant inverse correlation with acute mountain sickness symptom scores on ascent.

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.

Early fluid retention and severe acute mountain sickness

2005 ◽  
Vol 98 (2) ◽  
pp. 591-597 ◽  
Author(s):  
Jack A. Loeppky ◽  
Milton V. Icenogle ◽  
Damon Maes ◽  
Katrina Riboni ◽  
Helmut Hinghofer-Szalkay ◽  
...  
Keyword(s):  
Acute Mountain Sickness ◽  
Plasma Concentrations ◽  
Free Water ◽  
Plasma Renin ◽  
Barometric Pressure ◽  
Respiratory Alkalosis ◽  
Fluid Retention ◽  
Free Water Clearance ◽  
Water Excretion ◽  
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.

scholarly journals Oxidative stress and erythropoietin response in altitude exposure

2008 ◽  
Vol 31 (6) ◽  
pp. 380 ◽  
Author(s):  
Hsien-Hao Huang ◽  
Chih-Ly Han ◽  
Horng-Chin Yan ◽  
Woei-Yau Kao ◽  
Chu-Dang Tsai ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
High Altitude ◽  
Sea Level ◽  
Ferritin Level ◽  
Acute Mountain Sickness ◽  
Thiobarbituric Acid ◽  
Altitude Exposure ◽  
Delayed Recovery ◽  
Mountain Sickness ◽  
Stress Burden

Purpose: Oxidative stress and erythropoietin (EPO) levels are increased following high altitude exposure. We hypothesized that the altitude-oxidative stress and EPO response would be associated with the presence or absence of acute mountain sickness (AMS) in subjects exposed at high altitude. Methods: The study enrolled 29 healthy volunteers exposed at altitudes without strenuous physical exercise. Oxidative stress was determined by the spectrophotometric measurement of the colour occurring during the reaction of malondialdehyde (MDA) with thiobarbituric acid (TBA) on blood samples. Ferritin and EPO were also measured simultaneously. Results: During a rise in altitude at 2000 and 3000 m, there were no changes in plasma ferritin level in either of the 2 groups with or without AMS. In contrast, EPO increased at an altitude of 3000 m and after returning to sea level (28.2±2.7, 26.9±3.3 vs 12.2±1.4 and 17.1±1.6, P < 0.05, in group without AMS; 29.3±4.5, 22.8±2.7 vs 10.6±1.0 and 16.1±1.5, # P < 0.05, in group with AMS; compared with the baseline level and at the height of 2000 meters). At a height of 3000 m, plasma MDA level was elevated compared with that at the altitude of baseline and 2000 m in both groups of subjects with and without AMS (3.77±0.29 vs 1.14±0.17, and 1.64±0.22, P < 0.001, in subjects with AMS; 3.65±0.39 vs 1.71±0.21, and 1.73±0.21, P < 0.001, in subjects without AMS) . After returning to sea level, subjects without AMS had lower MDA oxidative stress compared with those with AMS (2.58±0.26 vs 3.51±0.24, P = 0.0223). Along with a rise in altitude, the oxidative stress in these both groups was not correlated with the changes in EPO (r2 = 0.0728, P = 0.1096). Conclusion: High altitude-induced oxidative stress, detected by MDA assay, is not different between the two groups of subjects with and without AMS. Upon return to sea level, subjects without AMS had lower MDA oxidative stress burden and higher EPO level than those with AMS. Whether the subjects with altitude illness had delayed recovery from oxidative stress merits further investigation.

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