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.     

硝苯吡啶对急进高原现场幼猪氧动力学的影响

目的 :了解硝苯吡啶 (Nifedipine ,NF)对急性缺氧幼猪氧动力学的影响。方法 :利用右心漂浮导管法对快速进入高原急性缺氧幼猪应用NF后氧动力学的变化进行观察。结果 :应用NF后 ,急性缺氧幼猪的肺动脉平均压 (mPAP)、肺血管阻力 (PVR)显著降低 (其中mPAP :P <0 .0 1,PVR :P <0 .0 0 1) ;心输出量 (CO)、SaO2 、PaO2 、氧输送 (DO2 )、氧消耗 (VO2 )、氧摄取率 (O2Ext)显著提高 (CO :P <0 .0 1,SaO2 、PaO2 、DO2 、VO2 、O2Ext:P <0 .0 0 1)。结论 :NF能降低急性缺氧幼猪的PVR ,通过改变CO而提高组织的DO2 、VO2 ,改善组织因缺氧引起的氧代谢障碍。     

蒜油抗高原缺氧效应初探

目的:探讨蒜油对急进模拟高原大鼠的抗缺氧效应。方法:低压氧舱复制大鼠急进高原模型,观察蒜油对血气、血液动力学、自由基等指标的影响。结果:蒜油提高了大鼠急进高原模型动脉血氧分压(PaO_2)、血氧饱和度(SaO_2),P<0.05;降低了肺动脉压(PAP),P<0.01;主动脉收缩压(SAP)、左室收缩压(LVSP)、左心室压力最大上升速率(+dp/dt_(max)),P<0.001;增加了血浆超氧化物歧化酶(SOD)含量,P<0.001。结论:蒜油具有抗高原缺氧效应,其作用可能是通过降低肺动脉高压(HPAP)及心肌氧耗,纠正自由基代谢失衡来实现。大蒜是较有潜力的抗高原缺氧药物。     

Air transportation of patients with acute respiratory failure: theory

Adult respiratory distress syndrome (ARDS) that results from severe trauma often occurs in remote places, making it necessary to transport the patients to tertiary medical facilities by air. Since these severely hypoxic patients are exposed to additional risk of reduced inspired oxygen tension due to decreased barometric pressure, the feasibility of transportation of these patients was investigated by computer analysis. Mathematical models of pulmonary gas exchange in patients with ARDS were developed to calculate arterial and mixed venous blood tensions while breathing room air and oxygen at sea level, 8,000 ft, and 40,000 ft. Under each condition the following parameters were varied: alveolar ventilation (VA), cardiac output (Q), metabolic rate (VO2), hematocrit (Hcrit), and membrane diffusing capacity for oxygen (DmO2). Most of the gas exchange problems at altitude could be overcome by breathing oxygen as long as cardiac output and hematocrit were adequate. Hypoxemia in ARDS patients will not be greatly affected by the reduced inspired oxygen tensions at altitude in much the same way that hypoxemia in ARDS is poorly responsive to increased inspired oxygen tensions at sea level.     

Hypoxic ventilatory response of rats born at simulated altitude

Steady-state ventilatory response to isocapnic hypoxia was measured in awake rats: a) resident at sea level (Control); b) born at sea level and acclimatized to a simulated altitude of 3500 m (Newcomers); c) born and raised for two generations at a simulated altitude of 3500 m (HA-II Generation). Arterial PO2, PCO2, and pH were measured at the same time as ventilation. Resting ventilation (mean +/- SE) on room air in Control, Newcomers, and HA-II Generation was 707 +/- 25, 811 +/- 28 and 878 +/- 21 ml.min-1.kg-1, respectively. The ratios of ventilations measured at PaO2 55 and 100 Torr were 1.61 for Control, 1.52 for Newcomers, and 1.60 for HA-II Generation and were not significantly different from one another. The ventilatory response to 5% CO2 in air was also similar in all three groups. After four days at sea level, ventilatory responses of HA-II Generation to normoxia or isocapnic hypoxia were the same as those of sea level control. We conclude that the HA-II Generation groups had ventilatory responses to hypoxia that did not differ from those of Newcomers acclimatized to the same altitude. Unlike man, rats that were born and raised at altitude for two generations did not show any "blunting" of the ventilatory response to hypoxia.     

Cardiopulmonary transition in the high altitude infant

The perinatal cardiopulmonary transition at high altitude differs from that at sea level because oxygen plays a fundamental role in the developmental changes from fetus to newborn infant. Under conditions of high altitude hypoxia, arterial oxygen saturations are lower, breathing patterns and maturation of respiratory control reflexes differ, and regression of fetal characteristics of the pulmonary vasculature proceeds more slowly. Several aspects of transition vary not only with postnatal age and altitude, but also with population group, suggesting an effect of genetic adaptation on perinatal physiology. Exposure to chronic high altitude hypoxia during the perinatal transition also results in apparent lifelong alterations in respiratory reflex responses and pulmonary vasoreactivity. Disruption of the normal process of cardiopulmonary transition can result in symptomatic high altitude pulmonary hypertension. The exaggerated hypoxemia associated with acute respiratory infections in young infants still undergoing transition contributes to infant mortality at high altitude.     

Circulatory response to acute hypobaric hypoxia in conscious dogs.

Hemodynamics were studied in seven conscious dogs during acute hypobaric stress at 14,000 ft simulated altitude. Silastic catheters were chronically implanted in the pulmonary artery, left atrium, and aorta. Pulmonary and central aortic pressures, cardiac output, and pulmonary blood volume were determined under conditions of normoxia and acute hypoxia in a hypobaric chamber maintained at 446 mm Hg pressure (14,000 ft). Altitude resulted in significant increases in heart rate, cardiac output, pulmonary blood volume, and pulmonary artery pressure. Left atrial pressure and calculated systemic vascular resistance decreased during hypobaric hypoxia while stroke volume, stroke work index, arterial pressure and pulmonary vascular resistance remained unchanged. Arterial blood PO2 decreased markedly at altitude, and all animals hyperventilated with resultant systemic hypocarbic alkalosis. The combination of elevated pulmonary arterial pressure and increased pulmonary blood volume may by an etiologic factor in the development of high-altitude pulmonary edema.     

不同生理等效高度的富氧环境对大鼠急进高原肺水肿的防护作用

目的研究不同生理等效高度的富氧环境对大鼠急进高原肺水肿的防护作用。方法50只雄性Wistar大鼠按随机数字表法分为地面对照组、缺氧组、富氧1组、富氧2组及富氧3组,每组10只。除地面对照组外,分别将各实验组大鼠置于实验舱内,均以10m／s的速度上升至气压高度6000m,上升同时缺氧组输入空气,富氧1组和富氧2组分别输入氧浓度35％和30％的富氧气体,富氧3组则每4h交替输入空气与35％富氧气体,流量均为7L／min。24h后实验舱下降至地面,处死大鼠,测肺部含水率及病理学效应,测肺组织匀浆中的内皮素-1浓度和-氧化氮合酶活力。结果地面对照组大鼠肺含水率最低（0．80％±0．01％）,与其它各组比差异有统计学意义（P〈0．01）;缺氧组最高（0．83％±0．01％）,与地面对照组和富氧3组比差异有统计学意义（P〈0．01）;3个供氧组居中,其中富氧3组以o．81％土0．01％显著低于富氧1组和富氧2组（P〈0．05）。病理结果表明各实验组出现了不同程度肺水肿表现,由重至轻依次为缺氧组、富氧2组、富氧1组和富氧3组。内皮素-1浓度各组间差异无统计学意义。地面对照组一氧化氮合酶活力最高,为（1．49土0．24）U／mg,与其它各组比差异有统计学意义（P〈0．01）;缺氧组最低,为（0．78±0．28）U／mg,富氧1组和富氧3组一氧化氮合酶活力较强,分别为（1．06±0．17）U／mg、（1．09土0．20）U／mg,与缺氧组比较差异有统计学意义（P〈0．01）。结论在6000m停留24h后大鼠出现了高原肺水肿。氧浓度为35％富氧环境（生理等效高度约2500m）能够有效预防肺水肿,而氧浓度为30％的富氧环境（生理等效高度约3500m）防护效果不显著。4h间断供给含氧35％气体同样可以有效预防大鼠在6000m出现的高原肺水肿。     

Physiological implications of altitude training for endurance performance at sea level: a review.

Acclimatisation to environmental hypoxia initiates a series of metabolic and musculocardio-respiratory adaptations that influence oxygen transport and utilisation, or better still, being born and raised at altitude, is necessary to achieve optimal physical performance at altitude, scientific evidence to support the potentiating effects after return to sea level is at present equivocal. Despite this, elite athletes continue to spend considerable time and resources training at altitude, misled by subjective coaching opinion and the inconclusive findings of a large number of uncontrolled studies. Scientific investigation has focused on the optimisation of the theoretically beneficial aspects of altitude acclimatisation, which include increases in blood haemoglobin concentration, elevated buffering capacity, and improvements in the structural and biochemical properties of skeletal muscle. However, not all aspects of altitude acclimatisation are beneficial; cardiac output and blood flow to skeletal muscles decrease, and preliminary evidence has shown that hypoxia in itself is responsible for a depression of immune function and increased tissue damage mediated by oxidative stress. Future research needs to focus on these less beneficial aspects of altitude training, the implications of which pose a threat to both the fitness and the health of the elite competitor. Paul Bert was the first investigator to show that acclimatisation to a chronically reduced inspiratory partial pressure of oxygen (P1O2) invoked a series of central and peripheral adaptations that served to maintain adequate tissue oxygenation in healthy skeletal muscle, physiological adaptations that have been subsequently implicated in the improvement in exercise performance during altitude acclimatisation. However, it was not until half a century later that scientists suggested that the additive stimulus of environmental hypoxia could potentially compound the normal physiological adaptations to endurance training and accelerate performance improvements after return to sea level. This has stimulated an exponential increase in scientific research, and, since 1984, 22 major reviews have summarised the physiological implications of altitude training for both aerobic and anaerobic performance at altitude and after return to sea level. Of these reviews, only eight have specifically focused on physical performance changes after return to sea level, the most comprehensive of which was recently written by Wolski et al. Few reviews have considered the potentially less favourable physiological responses to moderate altitude exposure, which include decreases in absolute training intensity, decreased plasma volume, depression of haemopoiesis and increased haemolysis, increases in sympathetically mediated glycogen depletion at altitude, and increased respiratory muscle work after return to sea level. In addition, there is a risk of developing more serious medical complications at altitude, which include acute mountain sickness, pulmonary oedema, cardiac arrhythmias, and cerebral hypoxia. The possible implications of changes in immune function at altitude have also been largely ignored, despite accumulating evidence of hypoxia mediated immunosuppression. In general, altitude training has been shown to improve performance at altitude, whereas no unequivocal evidence exists to support the claim that performance at sea level is improved. Table 1 summarises the theoretical advantages and disadvantages of altitude training for sea level performance. This review summarises the physiological rationale for altitude training as a means of enhancing endurance performance after return to sea level. Factors that have been shown to affect the acclimatisation process and the subsequent implications for exercise performance at sea level will also be discussed. Studies were located using five major database searches, which included Medline, Embase, Science Citation Index, Sports Discus, and Sport, in     

PH2O and simulated hypobaric hypoxia

Some manufacturers of reduced oxygen (O2) breathing devices claim a comparable hypobaric hypoxia (HH) training experience by providing F1O2 < 0.209 at or near sea level pressure to match the ambient oxygen partial pressure (iso-PO2) of the target altitude. I conclude after a review of literature from investigators and manufacturers that these devices may not properly account for the 47 mmHg of water vapor partial pressure that reduces the inspired partial pressure of oxygen (P1O2), which is substantial at higher altitude relative to sea level. Consequently, some devices claiming an equivalent HH experience under normobaric conditions would significantly overestimate the HH condition, especially when simulating altitudes above 10,000 ft (3048 m). At best, the claim should be that the devices provide an approximate HH experience since they only duplicate the ambient PO2 at sea level as at altitude. An approach to reduce the overestimation and standardize the operation is to at least provide machines that create the same P1O2 conditions at sea level as at the target altitude, a simple software upgrade.     

Postural control and venous gas bubble formation during hypobaric exposure

BACKGROUND: Earlier studies have shown that acute hypoxia at simulated altitudes up to 18,000 ft affects postural control. The main objective of this study was to investigate whether this is caused by hypoxia or by other effects of reduced barometric pressure. Doppler monitoring was included to rule out venous gas emboli (VGE) as a possible cause of disturbed postural control. A secondary objective was to evaluate two conventional altitude chamber training profiles regarding release of VGE. HYPOTHESIS: Chamber flights up to 18,000 ft affect postural control due to acute hypoxia or other effects of reduced barometric pressure such as bubble formation. VGE probably will not be formed at the altitude chamber flight profiles and procedures selected for this study. METHODS: Repeated registrations of postural control and Doppler monitoring for detection of possible VGE were performed on 12 subjects before, during, and after exposure to two different altitude chamber flight profiles. In chamber flight profile 1 the subjects were first preoxygenated for 45 min and then exposed to a normoxic environment at altitudes of 25,000, 18,000, 14,000, and 8000 ft. Chamber flight profile 2 consisted of an 80 min exposure to 14,000 ft without preoxygenation or supplemental oxygen for the first 60 min. RESULTS: In chamber flight profile 1, where normoxic conditions were achieved during all balance testing, no significant changes in postural control were found. No VGE were observed and no subjective dizziness was reported during this exposure. In chamber flight profile 2, a significant influence on postural control was reported for the eyes-open condition, when breathing air at 14,000 ft. These changes normalized when reaching ground level. VGE were observed in one of the 12 subjects after 75 min at 14,000 ft. Another subject complained of severe dizziness during the initial part of the decompression to 14,000 ft, and was excluded from further experiments. CONCLUSIONS: Changes in postural control at altitudes up to 18,000 ft is probably due to acute hypoxia. VGE may form during acute altitude exposure to 14,000 ft.     

模拟4000m高原下犬脂肪栓塞综合征模型制作及其急性肺损伤预警指标观察

目的 :研究高原脂肪栓塞综合征 (FES)模型制作及其急性肺损伤预警指标。方法 :1 4只犬在模拟 40 0 0m高原随机分为FES组与对照组。FES组以 1 3ml/kg同种脂肪液静脉注射。结果 :伤后犬立即呼吸窘迫 ,PaO2 下降 ,双下肺可闻及湿性罗音 ,病理检查见肺内广泛粒细胞浸润、脂肪栓塞、肺泡水种。 (PaO2 /F1 0 2 )× (吸入气体压 /平原空气压 ) <30 0。结论 :以 1 3ml/kg同种脂肪液静脉注射可建立较好的犬高原FES模型。 (PaO2 /F1 0 2 )× (吸入气体压 /平原空气压 ) <30 0 ,对高原FES诊断有一定帮助。伤后早期呼吸窘迫 ,外周血PMN和血小板计数及FN含量下降 ,PaO2 下降 ,GPT、共轭二烯、唾液酸的一过性升高 ,对高原FES的发生有一定预测意义     

急性缺氧幼猪吸入一氧化氮后血流动力学的动态变化

目的 :观察急性缺氧幼猪吸入一氧化氮 (NO)及突然停吸一氧化氮后血流动力学的动态变化。方法 :将 8头平原幼猪空运到高原 ,形成急性缺氧性肺动脉高压模型。幼猪吸入浓度为10 ppm的NO气体 ,经漂浮导管每间隔 5分钟测量一次肺动脉压、心输出量 ,经股动脉插管测股动脉压、抽血做血气分析。突然停吸NO ,重复上述测定。结果 :吸入NO气体后平均肺动脉压 (mPAP)与吸NO前比较有显著降低 (P <0 .0 1) ,股动脉血氧分压 (PaO2 )明显升高 (P <0 .0 5 )。突然停吸NO气体后 5至 10分钟mPAP迅速升高 ,并且超过吸NO前的水平 (P <0 .0 5 ) ,PaO2 迅速降至吸NO前的水平 ,15分钟后mPAP逐渐恢复到吸NO前的水平。吸NO及停NO期间 ,股动脉压、心输出量变化不明显。结论 :急性缺氧幼猪吸入低浓度一氧化氮气体后肺动脉压显著降低 ,动脉血氧分压明显升高 ;但突然停吸NO后肺动脉压迅速升高 ,且超过吸NO前的水平 ,存在反跳现象     

Predicted arterial oxygenation at commercial aircraft cabin altitudes

INTRODUCTION: The degree of hypoxia manifested by airline passengers during flight is not well characterized. Statistical models to predict age-specific levels of Pao2 manifest at altitudes between sea level and 8000 ft (Pao2alt) are described. METHODS: The relationship between age and Pao2 at sea level (Pao2sl) and the relationship between Pao2alt, and Pao2sl, Pco2 at sea level (Pco2sl), and pulmonary health status were investigated using linear regression techniques to analyze previously published data. RESULTS: In persons with normal pulmonary health, the relationship between Pao2sl (mmHg) and age (yr) was Pao2sl = 105.9 - 0.44 * age (R2 = 0.582, MSE = 25.314); Pco2sl (38.1 +/- 2.8 mmHg) was not related to age over the range 18-75 yr. In persons with chronic obstructive lung disease (COPD), neither Pao2sl (78.2 +/- 11.3 mmHg) nor Pco2sl (40.5 +/- 5.7 mmHg) were related to age (77.0 +/- 9.0 yrs).The relationship between PaO2alt and Pao2sl, Pco2sl and altitude (ft) was: Pao2alt = 1.59 + 0.98 * Pao2sl + 0.0031 * Alt - 0.000061 * Pao2sl * Alt - 0.000065 * Pao2sl * Alt + 0.000000092 * Alt2 (R2 = 0.932, MSE = 22.774). DISCUSSION: Pao2sl declines with age in persons with normal pulmonary health; Pco2sl remains constant. Neither vary with age in persons with COPD. Pao2alt can be estimated with acceptable precision from knowledge of Pao2sl, Pco2sl, and altitude. These models predict a substantial proportion of older passengers will manifest a Pao2alt at 8000 ft below the threshold at which supplemental oxygen is recommended.     

高压氧预处理对急性低氧大鼠心肌超微结构和心功能保护机制的研究

目的 探讨高压氧(HBO)预处理对急性低氧大鼠心肌超微结构和心脏功能的影响.方法 取13只Wistar大白鼠随机分为2组:低氧组(n=7),将大鼠置于模拟海拔5400 m低压氧舱内3 d;HBO预处理组(HBO组,n=6),进入低压舱前2 d给予HBO预处理2 d,每天1次,然后置于模拟海拔5400 m低压氧舱内3 d.第4天上午在模拟海拔5400 m的低压氧舱内,2组动物用10%氨基甲酸乙酯腹腔麻醉,经右颈外静脉插入心导管至右心室、肺动脉,用多道生理记录仪连续描记肺动脉压力曲线5min,测定心率(HR)、肺动脉压力(PAP)、右室收缩压(RVSP)和舒张压(RVEDP)、右室等容收缩期心室内压力上升最大速率和右室等容舒张期心室内压力下降最大速率(±dp/dtmax>)等血流动力学指标,并观察心肌超微结构的变化.结果HBO组较低氧组HR、RVSP降低,±do/dtmax>增高,差异有统计学意义(P<0.01);肺动脉舒张压降低,差异有统计学意义(P<0.05),肺动脉收缩压、肺动脉平均压、RVEDP差异无统计学意义(P>0.05).低氧组心肌细胞线粒体肿胀、溶解,肌浆网扩张,局部区域形成许多泡状;HBO组心肌无明显病变,仅滑面内质网轻度扩张.结论 高压氧具有改善急性低氧大鼠血流动力学、降低肺动脉压、保护心功能的作用.     

The role of the right ventricle during hypobaric hypoxic exercise: insights from patients after the Fontan operation

OBJECTIVES: The principal objective of this study was to examine the importance of the right ventricle for maximal systemic oxygen transport during exercise at high altitude by studying patients after the Fontan operation. BACKGROUND: High-altitude-induced hypoxia causes a reduction in maximal oxygen uptake. Normal right ventricular pump function may be critical to sustain cardiac output in the face of hypoxic pulmonary vasoconstriction. We hypothesized that patients after the Fontan operation, who lack a functional subpulmonary ventricle, would have a limited exercise capacity at altitude, with an inability to increase cardiac output. METHODS: We measured oxygen uptake (VO2, Douglas bag), cardiac output (Qc, C2H2 rebreathing), heart rate (HR) (ECG), blood pressure (BP) (cuff), and O2 Sat (pulse oximetry) in 11 patients aged 14.5+/-5.2 yr (mean +/- SD) at 4.7+/-1.6 yr after surgery. Data were obtained at rest, at three submaximal steady state workrates, and at peak exercise on a cycle ergometer. All tests were performed at sea level (SL) and at simulated altitude (ALT) of 3048 m (10,000 ft, 522 torr) in a hypobaric chamber. RESULTS: At SL, resting O2 sat was 92.6+/-4%. At ALT, O2 sat decreased to 88.2+/-4.6% (P < 0.05) at rest and decreased further to 80+/-6.3% (P < 0.05) with peak exercise. At SL, VO2 increased from 5.1+/-0.9 mL x kg(-1) x min(-1) at rest to 23.5+/-5.3 mL x kg(-1) x min(-1) at peak exercise and CI (Qc x m(-2)) increased from 3.3+/-0.7 L x m(-2) to 6.2+/-1.2 L x m(-2). VO2 peak, 17.8+/-4 mL x kg(-1) x min(-1) (P < 0.05), and CI peak, 5.0+/-1.5 L x m(-2) (P < 0.05), were both decreased at ALT. Remarkably, the relationship between Qc and VO2 was normal during submaximal exercise at both SL and ALT. However at ALT, stroke volume index (SVI, SV x m(-2)) decreased from 37.7+/-8.6 mL x min(-1) x m2 at rest, to 31.3+/-8.6 mL x min(-1) x m2 at peak exercise (P < 0.05), whereas it did not fall during sea level exercise. CONCLUSIONS: During submaximal exercise at altitude, right ventricular contractile function is not necessary to increase cardiac output appropriately for oxygen uptake. However, normal right ventricular pump function may be necessary to achieve maximal cardiac output during exercise with acute high altitude exposure.     

Effect of different ascent profiles on performance at 4,200 m elevation

Two groups of sea level residents were studied at the summit of Mauna Kea (4,200 m elevation) following ascent by vehicle. "Commuters" spent 6 h at the summit, while "shiftworkers" lived on the mountain for 5 d. Although PaO2 levels were lower in commuters, they experienced fewer altitude sickness symptoms than shiftworkers on the first day at 4,200 m. After 5 d, shiftworkers reported fewer symptoms and performed better at tests of numerate memory and psychomotor ability than commuters. At high altitude, pulse rates were increased in both groups, but only shiftworkers exhibited an elevation in systemic blood pressure. Arterial-alveolar oxygen tension gradients were not increased at 4,200 m. Despite frequent and rapid ascents and descents, with minimal provision for acclimatization, high altitude pulmonary and cerebral oedema were uncommon.     

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.     

Effect of hypoxia on heart glycogen utilization during exercise

An investigation was made into the effects of physical exercise upon heart glycogen change in rats exposed to decreased barometric pressure in hypobaric chamber simulating the effects of 3,000 m and 5,000 m altitude. Blood and cardiac tissue samples were examined after 1 h and 5 h of treadmill running at sea level and at 3,000 m, and after 1 h at 5,000 m. At sea level, cardiac glycogen level showed a classic biphasic evolution which was not affected by running. At 3,000 m, 1 h of running promoted an initial increase of 16% from control values, while a secondary decrease of 15% was measured after 5 h of running. Running for 1 h at 5,000 m induced a total depletion in cardiac glycogen level, the latter being depressed by 90% from control values. Free fatty acid (FFA) plasma level was increased by physical exercise at all barometric pressures, but the response was gradually enhanced by hypoxia. These data indicate that heart glycogen utilization during prolonged physical exercise is stimulated by acute altitude exposure, which suppresses the sparing effect observed at sea level upon dependence of enhanced FFA availability. The great differences in cardiac glycogen utilization support the views that enhanced glycogenolysis during hypoxia is promoted by different parameters, thus affecting various pathways. The slight decrease at 3,000 m suggests a moderate increase in anaerobic metabolism while the exhaustion observed after 1 h of running at 5,000 m indicates a decrease in cellular respiration response and enhanced heart anaerobic metabolism.     

Effect of hypobaric hypoxia on auditory sensitivity

INTRODUCTION: Previous studies on the effect of hypobaric hypoxia on auditory sensitivity are not readily interpretable, in most cases because the potential effect of ambient pressure on stimulus level was not considered. In this study, auditory sensitivity to 1, 8, 12, and 16 kHz tones was compared between conditions of hypoxia and normoxia at the same simulated altitude (3700 m). METHOD: In the hypoxic condition, the partial pressure of oxygen in the inspired air was allowed to decrease with increasing altitude. In the normoxic condition, the partial pressure of oxygen was maintained at a level equivalent to that experienced at mean sea level (MSL). This comparison also controlled for any effect resulting from physiological consequences of hypobaria other than hypoxia (such as a change in middle-ear impedance). RESULTS: A small (2.57 dB) reduction in sensitivity across the frequency range tested was observed. CONCLUSION: A reduction in sensitivity of this magnitude would not be expected to have a large impact on the effectiveness of information transfer via the auditory modality.