Saccadic velocity and pupillary reflexes during acclimatization to altitude (4300 m)

INTRODUCTION: Oculometrics have been shown to be responsive to acute hypoxemia. We investigated whether oculometrics could be used as an objective index of a hypoxic effect on the central nervous system (CNS) during altitude acclimatization. We hypothesized that oculomotor reflexes [pupil diameter (PD), constriction amplitude (CA), constriction latency (CL), and saccadic velocity (SV)] changed in concert with a select number of accepted acclimatization variables and that these changes correlated with the severity of acute mountain sickness (AMS). METHODS: After sea-level, baseline (SLB) measurements were obtained, 18 men (19-33 yr) were transported to Pikes Peak, CO (4300 m), where they remained for 14 d. Periodic measurements (days 1-4, 6, 7, 9, 10, and 12) were made of PD, CA, CL, and SV in addition to heart rate (HR), pulse oximetry (SpO2), end-tidal PO2 and PCO2, 24-h urinary catecholamine concentrations, and AMS severity (environmental symptoms questionnaire, ESQ). RESULTS: PD and CL decreased from SLB on days 1-4 and subsequently returned toward SLB; these changes paralleled changes in ventilatory and circulatory variables. CA decreased on days 1 and 2 and remained decreased for 12 d. SV increased over days 1-6 then returned toward SLB with continued exposure, similar to changes in urinary catecholamines. With acclimatization, CL correlated with HR and SpO2; SV correlated with PCO2, HR, and SpO2. AMS severity peaked during days 2-4, returned toward SLB over the next 10 d, and correlated only with CL (p = 0.045). CONCLUSIONS: Oculometrics can be used as an indicator of CNS hypoxia and altitude acclimatization, although there was no strong correlation with AMS severity.     

Speech motor control and acute mountain sickness

BACKGROUND: An objective method that accurately quantifies the severity of Acute Mountain Sickness (AMS) symptoms is needed to enable more reliable evaluation of altitude acclimatization and testing of potentially beneficial interventions. HYPOTHESIS: Changes in human articulation, as quantified by timed variations in acoustic waveforms of specific spoken words (voice onset time; VOT), are correlated with the severity of AMS. METHODS: Fifteen volunteers were exposed to a simulated altitude of 4300 m (446 mm Hg) in a hypobaric chamber for 48 h. Speech motor control was determined from digitally recorded and analyzed timing patterns of 30 different monosyllabic words characterized as voiced and unvoiced, and as labial, alveolar, or velar. The Environmental Symptoms Questionnaire (ESQ) was used to assess AMS. RESULTS: Significant AMS symptoms occurred after 4 h, peaked at 16 h, and returned toward baseline after 48 h. Labial VOTs were shorter after 4 and 39 h of exposure; velar VOTs were altered only after 4 h; and there were no changes in alveolar VOTs. The duration of vowel sounds was increased after 4 h of exposure and returned to normal thereafter. Only 1 of 15 subjects did not increase vowel time after 4 h of exposure. The 39-h labial (p = 0.009) and velar (p = 0.037) voiced-unvoiced timed separations consonants and the symptoms of AMS were significantly correlated. CONCLUSIONS: Two objective measures of speech production were affected by exposure to 4300 m altitude and correlated with AMS severity. Alterations in speech production may represent an objective measure of AMS and central vulnerability to hypoxia.     

Hemodynamic and sympathoadrenal responses to altitude in humans: effect of dexamethasone

Altitude exposure alters hemodynamics and sympathoadrenal function and elicits acute mountain sickness (AMS). Since dexamethasone prevents AMS and influences responsiveness to catecholamines, we studied hemodynamic and sympathoadrenal responses to 4,570 m simulated altitude in 8 subjects treated with dexamethasone or placebo. Mean pulse rates were less at altitude with dexamethasone (96.1 for placebo and 84.1 for dexamethasone; treatment-altitude interaction, p = 0.0045). Altitude led to a postural decline in mean arterial pressure (posture-altitude interaction, p = 0.0026), but this was not affected by dexamethasone. Dexamethasone reduced urinary epinephrine to a greater extent during altitude exposure (from 9.41 ng.mg-1 creatinine with placebo to 4.16 with dexamethasone) when compared with sea level (from 3.24 to 3.08). Urinary excretion of norepinephrine was unchanged at altitude. We conclude that acute altitude exposure is associated with stimulation of the adrenal medulla and not the sympathetic nervous system. Dexamethasone blocks the adrenal medullary response and blunts the pulse rate increase at altitude.     

Intraocular pressure at a simulated altitude of 9000 m with and without 100% oxygen

INTRODUCTION: Exposure to high altitude may affect intraocular pressure (lOP). This study aimed to determine how IOP was altered by two different inspired oxygen tensions at altitude. METHODS: There were 34 healthy male pilots, ages 26-39 yr (mean 31.9 yr), who were studied at the Air Health Examination and Physiological Training Centre in Eskisehir, Turkey. They were studied at ground level, which is 792 m (2414 ft), and during a training session in a hypobaric chamber at a simulated altitude of 9144 m (30,000 ft). IOP was measured with a Tone-pen XL tonometer before subjects entered the chamber, at altitude while breathing 100% oxygen by mask and after removing the mask, and again 30 min after leaving the chamber. RESULTS: Ground level values for IOP (mean +/- SD) were 12.31 +/* 2.98 mmHg. Levels increased significantly at altitude on oxygen (16.75 +/- 4.14 mmHg) and decreased slightly on breathing ambient air (14.37 +/- 3.44 mmHg). In 30 min after leaving the chamber, IOP was 12.81 +/- 1.74 mmHg, indistinguishable from pre-test values. DISCUSSION: Healthy subjects whose baseline IOP is in the normal range experience only a small, temporary elevation of IOP during passive exposure to high altitude with either normoxia or acute hypoxia.     

Cysteinyl leukotriene blockade does not prevent acute mountain sickness

BACKGROUND: Acute Mountain Sickness (AMS) is a multi-system disorder that is characterized by headache, anorexia, nausea, vomiting, insomnia, lassitude, and malaise. The syndrome is common in unacclimatized low altitude residents who rapidly ascend to terrestrial elevations exceeding 2,500 m. AMS may be a manifestation of hypoxia-induced cerebral edema resulting, in part, from increased capillary permeability. HYPOTHESIS: We hypothesized that cysteinyl leukotrienes (CysLTs) may be involved in the pathogenesis of AMS, as these compounds are known to increase endothelial permeability. METHODS: To test this hypothesis, we orally administered a CysLTs type-1 receptor antagonist (montelukast) to 11 subjects prior to and during exposure to high altitude (4,300 m) in a hypobaric chamber in a randomized, placebo-controlled, crossover design. We measured the resulting prevalence and/or severity of AMS, plasma CysLTs levels and urinary CysLTE4, and associated physiological responses. RESULTS: At 12 h exposure, AMS prevalence and symptom severity was lower (p = 0.002) during montelukast administration compared with placebo, but not different at 22 h exposure. Plasma CysLTs and urinary LTE4 levels were not significantly elevated at 22 h exposure, nor did these CysLTs levels correlate with AMS severity. Compared with placebo, montelukast administration was not associated with any significant differences in physiologic measures at sea level or high altitude. CONCLUSIONS: These results do not support a role for the CysLTs mediating the early development of AMS through the CysLT-1 receptor.     

Substrate oxidation is altered in women during exercise upon acute altitude exposure

PURPOSE: The purpose of this study was to determine whether substrate oxidation during submaximal exercise in women is affected by an acute exposure to 4300-m altitude and menstrual cycle phase. METHODS: Eight female lowlanders (mean +/- SD; 33 +/- 3 yr, 58 +/- 6 kg, 163 +/- 8 cm) completed a peak oxygen uptake (VO2peak) and submaximal exercise to exhaustion (EXH) test at 70% of their altitude-specific VO2peak at sea level (SL) and during an acute altitude (AA) exposure to 4300 m in a hypobaric chamber (446 mm Hg) in their early-follicular and midluteal menstrual cycle phase. The respiratory exchange ratio (RER) was calculated from oxygen uptake and carbon dioxide output measurements made during the EXH tests, and used to estimate the percent contribution of fat and carbohydrate to energy metabolism. Blood samples were taken at rest and every 15 min during the EXH tests. Blood samples were evaluated for glucose, lactate, glycerol, free fatty acids, insulin, growth hormone, cortisol, glucagon, epinephrine, norepinephrine, estradiol, and progesterone concentrations. RESULTS: Despite increased (P < 0.05) estradiol and progesterone levels in the midluteal phase, substrate oxidation, energy substrates, and metabolic hormones were not affected by cycle phase at SL or AA. However, free fatty acids and cortisol were increased (P < 0.05) whereas RER was decreased (P < 0.05) during exercise upon AA exposure compared with SL in both cycle phases. CONCLUSIONS: These data suggest that substrate oxidation is altered in women during exercise at AA compared with SL but is not affected by cycle phase. Whether increased fat or protein oxidation accounts for the lower RER values during the AA exposure cannot be determined from this study but warrants further investigation.     

Respiratory response and muscle function during isometric handgrip exercise at high altitude

The purpose of this investigation was to determine if the hyperventilatory response to fatiguing isometric exercise at sea level could predict resting ventilation and acute mountain sickness (AMS) at 4300 m altitude. Exercise consisted of four successive endurance handgrips held to complete fatigue at 40% of maximum isometric handgrip strength (MHS). There was no relationship between the magnitude or pattern of exercise-induced hyperventilation at sea level and the severity of AMS later at altitude. Sea level hyperventilatory response was not predictive of resting ventilation at altitude. Altitude exposure progressively increased both the incidence and magnitude of the hyperventilatory response to exercise and prolonged it for 60-90 s into the recovery period, providing support for the "central command" theory of ventilatory control during isometric exercise. MHS was significantly increased at altitude--by 11% on day 2 and 16% on day 6. Endurance times to fatigue were reduced, but not always significantly so. A follow-up study involving more practice at sea level demonstrated MHS to be significantly increased throughout an entire 18-d stay at 4300 m and for 3, but not 5, days after descent. Significant changes in endurance could not be demonstrated. Neither AMS nor changes in body weight or circulating norepinephrine levels can account for the temporal pattern of increased grip strength, but the respiratory alkalosis occurring at altitude appears to be a likely mechanism.     

Changes in ventilatory threshold at high altitude: effect of antioxidants

PURPOSE: To investigate the effects of prolonged hypoxia and antioxidant supplementation on ventilatory threshold (VT) during high-altitude (HA) exposure (4300 m). METHODS: Sixteen physically fit males (25 +/- 5 yr; 77.8 +/- 8.5 kg) performed an incremental test to maximal exertion on a cycle ergometer at sea level (SL). Subjects were then matched on VO2peak, ventilatory chemosensitivity, and body mass and assigned to either a placebo (PL) or antioxidant (AO) supplement group in a randomized, double-blind manner. PL or AO (12 mg of beta-carotene, 180 mg of alpha-tocopherol acetate, 500 mg of ascorbic acid, 100 mug of selenium, and 30 mg of zinc daily) were taken 21 d prior to and for 14 d at HA. During HA, subjects participated in an exercise program designed to achieve an energy deficit of approximately 1400 kcal.d(-1). VT was reassessed on the second and ninth days at HA (HA2, HA9). RESULTS: Peak power output (Wpeak) and VO2peak decreased (28%) in both groups upon acute altitude exposure (HA2) and were unchanged with acclimatization and exercise (HA9). Power output at VT (WVT) decreased from SL to HA2 by 41% in PL, but only 32% in AO (P < 0.05). WVT increased in PL only during acclimatization (P < 0.05) and matched AO at HA9. Similar results were found when VT was expressed in terms of % Wpeak and % VO2peak. CONCLUSIONS: VT decreases upon acute HA exposure but improves with acclimatization. Prior AO supplementation improves VT upon acute, but not chronic altitude exposure.     

Prediction of acute mountain sickness by monitoring arterial oxygen saturation during ascent

Acute mountain sickness (AMS) is a common problem while ascending at high altitude. AMS may progress rapidly to fatal results if the acclimatization process fails or symptoms are neglected and the ascent continues. Extensively reduced arterial oxygen saturation at rest (R-Spo?) has been proposed as an indicator of inadequate acclimatization and impending AMS. We hypothesized that climbers less likely to develop AMS on further ascent would have higher Spo? immediately after exercise (Ex-Spo?) at high altitudes than their counterparts and that these postexercise measurements would provide additional value for resting measurements to plan safe ascent. The study was conducted during eight expeditions with 83 ascents. We measured R-Spo? and Ex-Spo? after moderate daily exercise [50?m walking, target heart rate (HR) 150?bpm] at altitudes of 2400 to 5300?m during ascent. The Lake Louise Questionnaire was used in the diagnosis of AMS. Ex-Spo? was lower at all altitudes among those climbers suffering from AMS during the expeditions than among those climbers who did not get AMS at any altitude during the expeditions. Reduced R-Spo? and Ex-Spo? measured at altitudes of 3500 and 4300?m seem to predict impending AMS at altitudes of 4300?m (p?相似文献   

Circulatory responses to orthostasis during alpha1-adrenergic receptor blockade at high altitude.

BACKGROUND: Increased blood level of norepinephrine, a primary alpha-adrenergic agonist, is associated with high-altitude exposure, and may help regulate key physiological functions (e.g., blood pressure). We hypothesized that blocking alpha1-adrenergic receptors would impair circulatory compensation for an orthostatic challenge to a greater extent at altitude than at sea level. METHODS: Sixteen healthy women (23 +/- 2 yr) were randomly assigned to receive either 2 mg prazosin (n = 8) or placebo (n = 8) t.i.d. (double-blind design) for 12 d at sea level and during the first 12 d of altitude residence (4300 m). Passive 60 degrees upright tilt was performed at sea level (10 d of treatment), and after 3 and 10 d at altitude. Mean arterial BP (MABP, via auscultation) and heart rate (HR, via ECG) were measured every min during 10 min each of supine rest and tilt. RESULTS: For the prazosin group compared with the placebo group: 1.) Supine and tilt MABP were consistently lower (p < 0.05) at sea level; 2.) MABP did not differ (p > 0.05) for either day at altitude; 3.) HR was similar for both positions at sea level and altitude; and 4.) MABP was consistently less only at sea level and HR was consistently greater only at altitude (both p < 0.05) in response to tilt. CONCLUSIONS: alpha1-adrenergic blockade altered MABP and HR responses to tilt at sea level and altitude, but circulatory responses to orthostasis were well maintained in both environments. At altitude, BP during tilt was sufficiently maintained by a compensatory increase in heart rate, likely mediated by parasympathetic withdrawal.     

Sea level and acute responses to hypoxia: do they predict physiological responses and acute mountain sickness at altitude?

OBJECTIVES: To compare a range of physiological responses to acute sea level hypoxia at simulated altitudes with the same physiological responses and acute mountain sickness (AMS) scores measured at altitude (similar to the simulated altitudes) during a 17 day trek in the Himalayas. METHODS: Twenty men and women aged 18-54 years took part in the study. End tidal CO(2) tension (PETCO(2)) and saturated oxygen (SaO(2)) were measured using a capnograph. Observations made at sea level and some simulated altitudes were compared with those in the Himalayas. Pairwise correlations were used to examine the correlation between variables and regression, with 95% prediction intervals providing information on how well one variable could be predicted from another for a given subject. RESULTS: There was only a significant correlation for a few comparisons. The 95% prediction intervals for individual SaO(2) values at a range of simulated altitudes were fairly wide going from +/- 4% to +/- 5%. All of the correlations between laboratory and Himalayan PETCO(2) values were not statistically significant. There was a significant correlation for the relation between SaO(2)and PETCO(2) at sea level for the laboratory data (r=-0.51; p=0.05). For the Himalayan data, there were significant correlations at Namche Bazaar (3450 m; day 3) (r=-0.56; p=0.01) and Dingboche (4300 m; day 6) (r=-0.48; p=0.03). The correlation between SaO(2) and PETCO(2) and AMS was generally poor. CONCLUSIONS: The results indicate that limited information can be gained on a subject's response to altitude by assessing physiological variables at sea level and a range of simulated altitudes before the subject carries out a trek at altitude.     

Effects of propranolol on acute mountain sickness (AMS) and well-being at 4,300 meters of altitude

A number of physiological responses and adjustments occur at high altitude to compensate for hypoxia. We hypothesized that interference with one component of the normal compensatory process, the sympathetic nervous system, would hinder altitude acclimatization and thereby exacerbate acute mountain sickness (AMS) and compromise well-being. Twelve young males (21.2 +/- 0.4 years) received either 80 mg propranolol (PRO; n = 6) or placebo (PLA; n = 6), t.i.d. at sea level (SL) and during the first 15 d of a 19-d residence at 4,300 m (HA). Individuals were randomly assigned to each group. The Environmental Symptoms Questionnaire (ESQ) was administered at SL and twice daily (AM and PM) during the entire altitude exposure in order to assess AMS symptoms and subjective feelings of well-being. Supine heart rate (HR) was determined at rest twice at SL and four times at HA. HR in the PLA group increased 40% over SL values (57 +/- 3 to 80 +/- 4 beats/min) by day 7 at HA (p less than 0.01). HR in the PRO group did not increase above SL values during medication at HA. By 4 d after the medication administration was terminated, HR in the PRO group had increased and did not differ from the PLA group. Throughout the entire altitude exposure, ESQ scores for the PRO group were lower than or similar to the PLA group. Furthermore, cessation of PRO treatment did not result in a change in well-being. These findings suggested that interference with the normal acclimatization process by beta-adrenergic blockade did not exacerbate AMS or reduce feelings of well-being.     

中日联合阿尼玛卿山医学科学考察——人在极高高原的生理研究

为了探讨人在极高高原的低氧生理适应,考察队在急速进抵阿尼玛卿山(海拔6282m)进行了一项综合性的生理学研究。在4个不同海拔(2261m,3719m,4 904m及5 200m)动态地检测了静息及运动负荷下的心肺功能、心电图改变、运动动脉血氧饱和度、球结膜微循环、神经反应时、睡眠特征、凝血因子、能量消耗与体重丧失,急性高山病的发生率及生理学评价指标,同时进行了低氧动物实验研究。本研究获取了大量有意义的高原生理资料,特别在若干生理反应和急性高山病的发生率上在汉族队员与藏族世居者间存在明显差别,提示他们生理适应方式的差别和高原藏族的适应优势。     

Phenytoin: ineffective against acute mountain sickness

Phenytoin sodium was evaluated for its effect on the development and intensity of acute mountain sickness (AMS) because of its ability to reduce intracellular Na+ concentrations in brain and thereby minimize any tendency to increase cellular volume, a hypothetical cause of AMS. Six men aged 19-35 were exposed to approximately 4600 m altitude in a hypobaric chamber for 52 h on two occasions separated by 10 d at sea level. Subjects received wither phenytoin or placebo for 18 h before (700 mg, divided dose) and throughout (100 mg t.i.d.) each altitude exposure in a double-blind, repeated-measures (crossover) design. Phenytoin serum concentrations ranged from 4.4-13.9 micrograms/ml during altitude exposure. Twice daily questionnaires and clinical evaluations showed no marked benefit from phenytoin on the occurrence, severity, or duration of AMS symptoms: headache, nausea, insomnia, and general malaise. Overall, 1 subject felt better, 2 felt worse, 1 felt the same; 2 were not suitably comparable. There was no observed relationship between serum levels and symptoms of AMS. Moderate degrees of weakness and dizziness were each reported by 3 subjects with phenytoin but not with placebo, however. Resting pulmonary ventilation, end-tidal PO2 and PCO2, map reading abilities and respiratory mask donning times were not affected by phenytoin. Under the conditions of this trial, phenytoin did not appear to be useful in managing AMS.     

Improvement in hypoxemia at 4600 meters of simulated altitude with carbohydrate ingestion.

BACKGROUND: Carbohydrate ingestion increases the relative production of carbon dioxide which results in an increase in ventilation in normal individuals. An increase in ventilation at altitude can result in improvement of altitude-induced hypoxemia. HYPOTHESIS: Carbohydrate ingestion will increase the arterial blood oxygen tension and oxyhemoglobin saturation during acute high altitude simulation. METHODS: There were 15 healthy volunteers, aged 18-33 yr, who were given a 4 kcal x kg(-1) oral carbohydrate beverage administered 2.5 h into an exposure to 15,000 ft (4600 m) of simulated altitude (5.5 h after the last meal). Altitude was simulated by having subjects breath a 12% oxygen/balance nitrogen mixture while remaining at sea level. Arterial blood gas samples were drawn at baseline and at regular intervals up to 210 min after carbohydrate ingestion. Subjects were evaluated for AMS by use of the Environmental Symptoms Questionnaire (ESQ) and a weighted average of cerebral symptom score (AMS-C). RESULTS: Baseline PaO2 increased significantly (p < 0.01) from 43.0 +/- 3.0 mmHg at 4600 m before carbohydrate ingestion to 46.8 +/- 6.2 mmHg at 60 min after carbohydrate ingestion. Arterial oxygen saturation rose significantly (p < 0.01) from a baseline of 79.5% +/- 5.1 to 83.8% +/- 6.42 at 60 min. CONCLUSIONS: Carbohydrate consumption significantly increased oxygen tension and oxyhemoglobin saturation in arterial blood of normal subjects during simulated altitude. Effects reached statistical significance across all subjects at 60 min. There was no significant difference in arterial oxygen levels or arterial oxygen saturation in subjects who developed AMS vs. those who did not develop AMS.     

Role of airway receptors in altitude-induced dyspnea

PURPOSE: The purpose of this study was to examine the role of airway receptors in respiratory-related sensations after ascent to altitude. METHODS: Ratings of respiratory-related sensations, perceived exertion and acute mountain sickness, heart rate, and peripheral oxygen saturation were recorded at rest and exercise in male and female subjects who had inhaled either aerosolized saline or saline with tetracaine after acute ascent to an altitude of 3500 m and after prolonged acclimatization of 18 d at altitudes between 4000 and 5000 m. RESULTS: Tetracaine had no effect on respiratory-related sensations at altitude either at rest or during exercise, and male and female subjects experienced similar respiratory-related sensations. Sensations of rapid breathing were experienced at rest after acute exposure to 3500 m as compared with sea level, but not after acclimatization to 5000 m. Sensations of rapid breathing, air hunger, and heavy breathing were experienced during exercise after acute and prolonged altitude exposure as compared with sea level, with a sensation of chest tightness experienced at 3500 m and a sensation of gasping experienced at 5000 m. CONCLUSION: These results suggest that airway afferents play no role in the respiratory-related sensations experienced by male and female subjects either during acute ascent to altitude or after prolonged acclimatization at altitude.     

Intraocular pressure measured at ground level and 10,000 feet

BACKGROUND: Intraocular pressure (IOP) may be subject to change during altitude exposure. This may be an important consideration for long-haul flights. In this study, intraocular pressure change was investigated following exposure to an altitude of 10,000 ft during flight in an unpressurized aircraft. METHODS: We measured the IOP of the right eye of 20 healthy volunteers (18 men, 2 women; mean age 34.6 +/- 9.5 yr) at a ground level of 1,760 ft (536 m) above the sea level (ASL) using a Tono-Pen XL tonometer. We then repeated the measurements during a flight in the unpressurized cabin of a CASA (CN235-100 M) aircraft after gaining an altitude of 10,000 ft (3,048 m) ASL. Changes in the IOP were evaluated. RESULTS: Mean IOP was 16.2 +/- 2.46 mmHg at ground level and 15.0 +/- 2.61 mmHg at 10,000 ft (3,048 m) ASL. IOP was reduced in 13 eyes, increased in 6 eyes, and remained unchanged in 1 eye. The mean change in IOP was 1.2 +/- 2.69 mmHg. However, this was not statistically significant (p = 0.06). CONCLUSION: Acute change in altitude resulted in a statistically non-significant reduction in IOP in healthy subjects.     

Increased oxidative stress following acute and chronic high altitude exposure

The generation of reactive oxygen species is typically associated with hyperoxia and ischemia reperfusion. Recent evidence has suggested that increased oxidative stress may occur with hypoxia. We hypothesized that oxidative stress would be increased in subjects exposed to high altitude hypoxia. We studied 28 control subjects living in Lima, Peru (sea level), at baseline and following 48 h exposure to high altitude (4300 m). To assess the effects of chronic altitude exposure, we studied 25 adult males resident in Cerro de Pasco, Peru (altitude 4300 m). We also studied 27 subjects living in Cerro de Pasco who develop excessive erythrocytosis (hematocrit > 65%) and chronic mountain sickness. Acute high altitude exposure led to increased urinary F(2)-isoprostane, 8-iso PGF(2 alpha) (1.31 +/- 0.8 microg/g creatinine versus 2.15 +/- 1.1, p = 0.001) and plasma total glutathione (1.29 +/- 0.10 micromol versus 1.37 +/- 0.09, p = 0.002), with a trend to increased plasma thiobarbituric acid reactive substance (TBARS) (59.7 +/- 36 pmol/mg protein versus 63.8 +/- 27, p = NS). High altitude residents had significantly elevated levels of urinary 8-iso PGF(2 alpha) (1.3 +/- 0.8 microg/g creatinine versus 4.1 +/- 3.4, p = 0.007), plasma TBARS (59.7 +/- 36 pmol/mg protein versus 85 +/- 28, p = 0.008), and plasma total glutathione (1.29 +/- 0.10 micromol versus 1.55 +/- 0.19, p < 0.0001) compared to sea level. High altitude residents with excessive erythrocytosis had higher levels of oxidative stress compared to high altitude residents with normal hematological adaptation. In conclusion, oxidative stress is increased following both acute exposure to high altitude without exercise and with chronic residence at high altitude.     

Conjunctival oxygen tension at high altitude

Transconjunctival oxygen tension (PcjO2) was studied using a hypobaric chamber and during mountaineering excursions. Measurements obtained during acute chamber exposures (15-20 min) at sea level, 1829 m (6,000 ft), 3048 m (10,000 ft), 4267 m (14,000 ft) and return to sea level were (means +/- SEM): 60.1 +/- 2.7, 49.1 +/- 1.8, 38.3 +/- 2.4, 27.4 +/- 1.5, and 61.1 +/- 2.8 mm Hg, respectively (n = 13). The ratio of PcjO2 to arterial blood oxygen tension (PaO2) did not change in a consistent manner between sea level and 4267 m; PcjO2 was 74 +/- 6.9% of PaO2. The 16 subjects participating in the mountaineering phase of the study revealed similar means at sea level and 1829 m (57.4 +/- 2.4 and 46.3 +/- 1.9 mm Hg respectively), but a smaller decrement was observed at 3048 m (43.0 +/- 1.6 mm Hg). The difference between mountain and chamber values may be accounted for by a partial acclimatization to altitude brought about by longer exposure on the mountain excursions. A comparison between PcjO2 and transcutaneous oxygen tension during the chamber study suggests that a greater precision and sensitivity is obtained with measurement of oxygen tension at the conjunctival site. PcjO2 measurement is a non-invasive reflection of PaO2 which is suitable for continuous monitoring during hypoxia studies.     

Residence at moderate altitude improves ventilatory response to high altitude

BACKGROUND: This study compared the distribution of arterial oxygen saturation (SaO2) and susceptibility to Acute Mountain Sickness (AMS) in moderate altitude residents (MAR) and low altitude residents (LAR) following rapid ascent to 4056 m. METHODS: Resting PETCO2 and SaO2 were measured in 38 subjects residing for > 3 mo near Colorado Springs, CO (MAR group), at 1940 m (USAF Academy), and after approximately 1 h at 4056 m on the summit of Pikes Peak, CO, following ascent by car. SaO2 was also measured at 610-m elevation intervals during the ascent. Of the LAR (50 m) group, 39 subjects were exposed to a similar ascent profile in a hypobaric chamber. RESULTS: At 1940 m the MAR SaO2 and PETCO2 were 94 +/- 1% (X +/- SD) and 33.6 +/- 2.8 mmHg, respectively. At 3048 m and higher, MAR SaO2 decreased, reaching 86 +/- 2% (p < 0.001) at 4056 m, and PETCO2 (32.1 +/- 4.5 mmHg) decreased (p < 0.05). At 50 m the LAR SaO2 and PETCO2 were 98 +/- 1% and 38.7 +/- 2.7 mmHg, respectively. At 1940 m and higher, LAR SaO2 decreased (p < 0.001), reaching 82 +/- 5% at 4056 m, and PETCO2 (36.4 +/- 3.5 mmHg) decreased (p < 0.05). Above 2438 m, the MAR SaO2 was higher (p < 0.001) than the LAR. Only one MAR subject, but nine LAR subjects reported AMS symptoms. CONCLUSIONS: Ventilatory acclimatization developed during moderate altitude residence substantially enhances arterial oxygenation during rapid ascents to higher altitudes. Compared with prior studies, the level of ventilatory acclimatization achieved at moderate altitude is similar to residing at 4056 m for approximately 5-9 d.