Visual fields during acute exposure to a simulated altitude of 7620 m

BACKGROUND: The hypoxia associated with sudden exposure to high altitude is known to impair vision and may thereby affect flight safety. However, no data were available regarding hypoxic effects on visual fields. The aim of this study was to evaluate black-and-white visual field sensitivity with acute hypoxia during acute exposure to a simulated altitude of 7620 m. METHODS: Subjects were 15 male pilots 26-39 yr of age. We measured arterial oxygen saturation (S(aO2)%) using transdermal pulse oximetry while the visual field was measured within a 30 degrees eccentricity in the right eye by computerized perimetry. The subject breathed 100% O2 for 30 min before and during chamber ascent, then removed his mask while measurements were performed. RESULTS: The S(aO2)% and visual field sensitivities (mean +/- SD) at ground level were 99.1 +/- 0.4% and 43.9 +/- 2.1 dB, respectively. During hypoxia, the S(aO2)% dropped to 64.0 +/- 5.4% within 3 min. Mean visual sensitivity was significantly reduced by 7.2 +/- 1.6 dB. Furthermore, peripheral sensitivity was slightly but significantly more diminished than central sensitivity. CONCLUSIONS: Severe acute hypoxia reduces central and moderate peripheral black-and-white vision by a factor of two with the strongest effect in the periphery.     

Effects of sildenafil on exercise capacity in hypoxic normal subjects

The phosphodiesterase-5 inhibitor sildenafil has been reported to improve hypoxic exercise capacity, but the mechanisms accounting for this observation remain incompletely understood. Sixteen healthy subjects were included in a randomized, double-blind, placebo-controlled, cross-over study on the effects of 50-mg sildenafil on echocardiographic indexes of the pulmonary circulation and on cardiopulmonary cycle exercise in normoxia, in acute normobaric hypoxia (fraction of inspired O2, 0.1), and then again after 2 weeks of acclimatization at 5000 m on Mount Chimborazo (Ecuador). In normoxia, sildenafil had no effect on maximum VO2 or O2 saturation. In acute hypoxia, sildenafil increased maximum VO2 from 27 +/- 5 to 32 +/- 6 mL/min/kg and O2 saturation from 62% +/- 6% to 68% +/- 9%. In chronic hypoxia, sildenafil did not affect maximum VO2 or O2 saturation. Resting mean pulmonary artery pressure increased from 16 +/- 3 mmHg in normoxia to 28 +/- 5 mmHg in normobaric hypoxia and 32 +/- 6 mmHg in hypobaric hypoxia. Sildenafil decreased pulmonary vascular resistance by 30% to 50% in these different conditions. We conclude that sildenafil increases exercise capacity in acute normobaric hypoxia and that this is explained by improved arterial oxygenation, rather than by a decrease in right ventricular afterload.     

Hearing thresholds under acute hypoxia and relationship to slowing in the auditory modality

BACKGROUND: Acute hypoxia slows reaction time to visual stimuli and it has been proposed that this slowing can be accounted for by a decrease in perceived brightness. Auditory slowing could be accounted for in an analogous manner if hypoxia decreases perceived loudness, as reflected by an increase in pure-tone thresholds. However, evidence concerning the effects of hypoxia on auditory thresholds is contradictory and we performed an experiment to clarify this issue. Pilot work suggested that thresholds were raised due to noise from our breathing apparatus used to deliver the low O2 mixtures and we eliminated this artifact by measuring thresholds while the subjects held their breath. METHODS: The six subjects breathed either air as a control through an oro-nasal mask or low O2 mixtures to maintain arterial blood oxygen saturation at 74% while thresholds between 500-4000 Hz were measured with an audiometer during breathholding. RESULTS: Hypoxia produced a statistically significant but practically insignificant decrease in thresholds of 1 dB across all frequencies tested. CONCLUSIONS: Our results are consistent with the view that audition is relatively insensitive to hypoxia and that the slowing observed with auditory stimuli cannot be accounted for by an increase in auditory thresholds. Some alternative hypotheses which could account for this slowing are proposed.     

急性缺氧条件下脑认知功能发生障碍的时段

目的 确定急性缺氧条件下脑认知功能障碍的发生阶段。方法 14名被试者在5000m模拟高度（吸低氧混合气体）分别进行2种不同声强值（55dB、80、dB)的听觉Oddball测试,记录脑电图（EEG）、反应时（RT）,EEG经平均叠加处理提取出脑事件相关电位（ERP）中的P3潜时,以P3潜时和RT为主要指标采用加因素法（AFM）评定脑认知功能障碍发和珠具体时段。结果 P3潜时与RT在声强及缺氧。高度间出现交互作用。结论 通过加因素法分析得出急性缺氧影响信息的前加工阶段。     

Effect of normobaric hypoxia on auditory sensitivity

Previous psychophysical studies of hypoxia's effects on auditory sensitivity have provided mixed results but the weight of evidence supports the conclusion that sensitivity is unaffected by hypoxia. This conclusion is discrepant with that drawn from physiological studies in which hypoxia has been found to affect auditory-evoked response (AER) latency. One possible explanation of this discrepancy concerns the relatively low maximum frequency (8 kHz) for which hypoxia's effects were assessed in the psychophysical studies. We have extended the range of frequencies over which hypoxia's effects have been examined to include frequencies up to 16 kHz. Thresholds for 1-, 8-, 10-, 12-, 14- and 16-kHz tones were measured at levels of hypoxia equivalent to altitudes of 0, 1,200, 2,400 and 3,700 m. Our results indicate that sensitivity for frequencies up to 16 kHz is unaffected by hypoxia. We suggest that AER latency does not provide a valid measure of auditory sensitivity.     

Arterial haemoglobin oxygen saturation is affected by F1O2 at submaximal running velocities in elite athletes

This study was conducted to determine whether arterial desaturation would occur at submaximal workloads in highly trained endurance athletes and whether saturation is affected by the fraction of oxygen in inspired air (F(I)O2). Six highly trained endurance athletes (5 women and 1 man, aged 25+/-4 yr, VO2max 71.3+/-5.0 ml x kg(-1) x min(-1)) ran 4x4 min on a treadmill in normoxia (F(I)O2 0.209), hypoxia (F(I)O2 0.155) and hyperoxia (F(I)O2 0.293) in a randomized order. The running velocities corresponded to 50, 60, 70 and 80% of their normoxic maximal oxygen uptake (VO2max). In hypoxia, the arterial haemoglobin oxygen saturation percentage (SpO2%) was significantly lower than in hyperoxia and normoxia throughout the test, and the difference became more evident with increasing running intensity. In hyperoxia, the SpO2% was significantly higher than in normoxia at 70% running intensity as well as during recovery. The lowest values of SpO2% were 94.0+/-3.8% (P<0.05, compared with rest) in hyperoxia, 91.0+/-3.6% (P<0.001) in normoxia and 72.8+/-10.2% (P<0.001) in hypoxia. Although the SpO2% varied with the F(I)O2, the VO2 was very similar between the trials, but the blood lactate concentration was elevated in hypoxia and decreased in hyperoxia at the 70% and 80% workloads. In conclusion, elite endurance athletes may show an F(I)O2-dependent limitation for arterial O2 saturation even at submaximal running intensities. In hyperoxia and normoxia, the desaturation is partly transient, but in hypoxia the desaturation worsens parallel with the increase in exercise intensity.     

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.     

Arterial oxygen saturation and hemoglobin mass in postmenopausal untrained and trained altitude residents

Because of lacking ventilatory stimulation by sex hormones in postmenopausal women (PW), one might expect a lowered arterial oxygen saturation (S(O(2))) in hypoxia and therefore a stronger erythropoietic reaction than in young women (YW). Nine untrained (UTRPW) and 11 trained (TRPW) postmenopausal altitude residents (2600 m) were compared to 16 untrained (UTRYW) and 16 trained young women (TRYW) to check this hypothesis and to study the combined response to hypoxia and training. S(O(2)) was decreased in PW (89.2% +/- 2.2 vs. 93.6 +/- 0.7% in YW, p < 0.01). Hb mass, however, was similar in UT (UTRYW: 9.2 +/- 0.9 g/kg(1), UTRPW: 8.7 +/- 1.0 g/kg). But if body fat rise with age was excluded by relation to fat-free mass, Hb mass was increased in UTRPW (+1.2 g/kg, p < 0.05) compared to UTRYW. Training caused a similar rise of Hb mass in PW and YW (0.3 g/kg per mL/kg x min(1) rise in V(O(2peak))). There was no difference in erythropoietin among the groups. Ferritin was higher in PW than YW. The results show that female hormones and fitness level have to be considered in studies on erythropoiesis at altitude. The role of erythropoietin during chronic hypoxia still has to be clarified.     

Physiologic response to moderate altitude exposure among infants and young children

Substantial numbers of children are exposed to moderate altitude while traveling to mountain resorts with their families. Although there has been extensive study of the adult physiologic response to altitude exposure, few studies of infants and young children exist. This investigation examines the acute physiologic responses to moderate altitude exposure among young children and the relationship of these responses to the development of acute mountain sickness (AMS). Children 3 to 36 months old participated in the prospective observational study, which included baseline measurements at 1610 m and measurements after a 24-h exposure to 3109 m. Measurements included pulse and respiratory rate, end-tidal CO(2), arterial oxygen saturation (pulse oximetry), cerebral tissue oxygenation (St(O2)) by near-infrared spectroscopy, middle cerebral artery resistive index by transcranial Doppler, lateral ventricle volumes (ultrasound), and clinical evaluation for the presence of acute mountain sickness (Children's Lake Louise Score). Twenty-four children (13 girls and 11 boys, age 14.5 +/- 10.2 months) participated. After acute exposure to 3109 m, these children showed an increase in respiratory rate from 45 +/- 13 to 51.9 +/- 15 breaths/min (p < 0.008), accompanied by a decrease of end-tidal CO(2) from 31 +/- 3 to 28 +/- 2 mm Hg (p < 0.001) and a reduction of arterial oxygen saturation from 95 +/- 2 to 91 +/- 2% (p < 0.001). St(O2) also decreased from 78 +/- 8 to 67 +/- 13% (p < 0.001), and this reduction appeared to be related to age (r = 0.58, p < 0.05), with lower saturations found in younger children. No evidence of increased intracranial pressure, as assessed by middle cerebral artery resistive index, was seen during ascent. Seven subjects developed symptoms of AMS; however, no relationship was found between the physiologic changes observed and the presence of symptoms. Ascent from 1610 to 3109 m resulted in tachypnea, relative hypoxia, hypocapnia, and a reduction in cerebral tissue oxygenation (St(O2)). The reduction in St(O2) appeared to be related to age, with infants appearing to be the most susceptible to cerebral tissue oxygen desaturation at high altitude. No relationship appears to exist between the presence of AMS and the physiologic measurements.     

Differential fMRI-BOLD signal response to apnea in humans and anesthetized rats.

Blood oxygenation level dependent (BOLD) signal intensity (SI) and regional cerebral blood flow (CBF) during a 20-s apnea stimulus in awake humans and pentobarbital-anesthetized rats were measured to assess the usefulness of apnea in estimating cerebral vasodilatory capacity for functional MRI (fMRI) experiments. Rats were ventilated with either room air or 100% O(2.) While breathing room air, apnea for 20 s increased the BOLD SI in humans but decreased it in rats. However, in rats ventilated with 100% O(2), BOLD SI increased upon apnea for 20 s. CBF measurements in rats using laser Doppler flowmetry (LDF) showed a 45% +/- 8% increase during apnea with room air ventilation, and a 10% +/- 3% increase with 100% O(2). Arterial blood oxygen saturation fell from 96% +/- 1% to 29% +/- 5%, and cerebral tissue PO(2) decreased from 15 +/- 3 mmHg to 6 +/- 2 mmHg by the end of 20-s apnea in rats breathing room air. However, with 100% O(2) respiration, apnea produced no change in the arterial blood oxygen saturation, which remained at 99%, but increased tissue PO(2) from 35 +/- 9 mmHg to 39 +/- 10 mmHg. From the results obtained in rats ventilated with room air, it is concluded that apnea induces hypoxia that results in a decrease in fMRI-BOLD signal. The signal decrease occurred despite an increase in P(a)CO(2) and CBF. This BOLD response is the opposite of that observed in humans, who presumably do not develop hypoxia within the applied apnea period. These studies highlight the importance of the choice of ventilating gas mixture on the outcome of BOLD experiments during systemic perturbations.     

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.     

Acute moderate hypoxia affects the oxygen desaturation and the performance but not the oxygen uptake response

The purpose of this study was to examine the influence of hypoxia on the O2 uptake response, on the arterial and muscular desaturation and on the test duration and test duration at VO2max during exhaustive exercise performed in normoxia and hypoxia at the same relative workload. Nine well-trained males cyclists performed an incremental test and an exhaustive constant power test at 90 % of maximal aerobic power on a cycling ergometer, both in normoxia and hypoxia (inspired O2 fraction = 16 %). Hypoxic normobar conditions were obtained using an Alti Trainer200 and muscular desaturation was monitored by near-infrared spectroscopy instrument (Niro-300). The mean response time (66 +/- 4 s vs. 44 +/- 7 s) was significantly lower in hypoxia caused by the shorter time constant of the VO2 slow component. This result was due to the lower absolute work rate in hypoxia which decreased the amplitude of the VO2 slow component. The arterial (94.6 +/- 0.3 % vs. 84.2 +/- 0.7 %) and muscular desaturation (in the vastus lateralis and the lateral gastrocnemius) were reduced by hypoxia. The test duration (440 +/- 31 s vs. 362 +/- 36 s) and the test duration at VO2max (286 +/- 53 s vs. 89 +/- 33 s) were significantly shorter in hypoxia. Only in normoxia, the test duration was correlated with arterial and muscular saturation (r = 0.823 and r = 0.828; p < 0.05). At the same relative workload, hypoxia modified performance, arterial and muscular oxygen desaturation but not the oxygen uptake response. In normoxia, correlation showed that desaturation seems to be a limiting factor of performance.     

Oxyhemoglobin saturation following rapid decompression to 18,288 m preceded by diluted oxygen breathing.

This investigation studied oxyhemoglobin saturation (SaO2) and cardiovascular indices after rapid decompression (RD). Before RD, fractional inspired O2 concentration (FIO2) simulated the range of product gas from molecular sieve O2 generating systems (MSOGS). Four subjects breathed 1.0-0.80 FIO2 at 6,858 m. After decompression to 18,288 m, the subject received 1.0 FIO2 at a positive pressure of 70 mm Hg for 3 min. There were no incidents of severe hypoxia. The mean SaO2 was 98.0% before RD. After RD, SaO2 was maintained at the pre-RD level for 8 s, decreased rapidly over the next 10 s, and over the rest of the 1st min decreased more gradually to reach approximately 82%. Varying FIO2 before RD had no effect on the alteration in SaO2, heart rate, stroke index, and blood pressure after RD. The MSOGS O2 product range offers adequate protection against hypoxia during RD to 18,288 m.     

Moderate exercise in hypoxia induces a greater arterial desaturation in trained than untrained men

During moderate exercise breathing a low inspired O(2) fraction (F(I)O(2)), arterial O(2) desaturation may depend on the fitness level. Seven trained (TM) and seven untrained men (UTM) cycled in normoxia and in hypoxia (F(I)O(2)=0.187, 0.173, 0.154, 0.13 and 0.117). We compared TM and UTM at submaximal intensities below the ventilatory threshold. Ventilatory variables were monitored and arterial oxygen saturation was measured by pulse oximetry. O(2) saturation was not different between groups at sea level. In hypoxia, O(2) saturation was lower in TM than in UTM at F(I)O(2)=0.154 (87.3 +/- 2.9% vs 90.4 +/- 1.5% at 90 W) and below. Both the ventilatory-equivalent and the end-tidal O(2) pressure were lower in TM at sea level and at every F(I)O(2), with the differences between TM and UTM becoming apparent at lower exercise intensity and increasing in magnitude as the severity of hypoxia increased. O(2) saturation was correlated with the ventilatory parameters at every F(I)O(2) and the correlations were stronger in severe hypoxia. These results demonstrate that a moderate exercise carried out in hypoxia, contrary to normoxic conditions, can lead to a greater arterial desaturation in TM compared with UTM. This phenomenon could be partly attributed to a relative hypoventilation in trained subjects.     

Serial changes in spirometry during an ascent to 5,300 m in the Nepalese Himalayas

The aims of the present study were to determine the changes in forced vital capacity (FVC), forced expiratory volume in 1 sec (FEV1) and peak expiratory flow (PEF), during an ascent to 5,300 m in the Nepalese Himalayas, and to correlate the changes with arterial oxygen saturation measured by pulse oximetry (SpO2) and symptoms of acute mountain sickness (AMS). Forty-six subjects were studied twice daily during an ascent from 2,800 m (mean barometric pressure 550.6 mmHg) to 5,300 m (mean barometric pressure 404.3 mmHg) during a period of between 10 and 16 days. Measurements of FVC, FEV1, PEF, SpO2, and AMS were recorded. AMS was assessed using a standardized scoring system. FVC fell with altitude, by a mean of 4% from sea level values [95% confidence intervals (CI) 0.9% to 7.4%] at 2,800 m, and 8.6% (95% CI 5.8 to 11.4%) at 5,300 m. FEV1 did not change with increasing altitude. PEF increased with altitude by a mean of 8.9% (95% CI 2.7 to 15.1%) at 2,800 m, and 16% (95% CI 9 to 23%) at 5,300 m. These changes were not significantly related to SpO2 or AMS scores. These results confirm a progressive fall in FVC and increase in PEF with increasing hypobaric hypoxia while FEV1 remains unchanged. The increase in PEF is less than would be predicted from the change in gas density. The fall in FVC may be due to reduced inspiratory force producing a reduction in total lung capacity; subclinical pulmonary edema; an increase in pulmonary blood volume, or changes in airway closure. The absence of a correlation between the spirometric changes and SpO2 or AMS may simply reflect that these measurements of pulmonary function are not sufficiently sensitive indicators of altitude-related disease. Further studies are required to clarify the effects of hypobaric hypoxia on lung volumes and flows in an attempt to obtain a unifying explanation for these changes.     

Unchanged anaerobic and aerobic performance after short-term intermittent hypoxia

INTRODUCTION: Repeated short-term exposures to a severe degree of hypoxia, alternated with similar intervals of normoxia, are recommended for performance enhancement in sports. However, scientific evidence for the efficiency of this method is controversial with regard to anaerobic performance. Therefore, we conducted a randomized, double-blind, placebo-controlled study to investigate the effects of this new method on both anaerobic and aerobic performance. METHODS: During 15 consecutive days, 20 endurance-trained men (V O2max (mean +/- SD) 60.2 +/- 6.8 mL x kg(-1) x min(-1)) were exposed each day to breathing (through mouthpieces) either a gas mixture (11% O2 on days 1-7 and 10% O2 on days 8-15; hypoxia group, N = 10) or compressed air (control group, N = 10), six times for 6 min, followed by 4 min of breathing room air for a total of six consecutive cycles. Before and after the treatment, an incremental cycle ergometer test to exhaustion and the Wingate anaerobic test were performed to assess aerobic and anaerobic performance. RESULTS: Hypoxic treatment did not improve peak power or mean power during the Wingate anaerobic test, nor did it affect maximal oxygen uptake (V O2max), maximal power output (Pmax), lactate threshold or levels of heart rate (HR), minute ventilation (V E), oxygen uptake (V O2), or blood lactate concentration at the submaximal workloads during the ergometer test. Maximal lactate concentration (Lamax) after the tests and HRmax and maximal respiratory exchange ratio (RERmax) during the ergometer test were not significantly different between groups at any time. CONCLUSION: The results of this study demonstrated that 1 h of intermittent hypoxic exposure for 15 consecutive days has no effect on aerobic or anaerobic performance.     

间歇性低氧训练对高性能战斗机飞行员脑电复杂度及血氧饱和度的影响

目的 通过动态观察间歇性低氧训练前后高性能战斗机飞行员EEG复杂度和血氧饱和度(arterial oxygen saturation,Sa()2)的变化特征,为低氧适应性训练效果评价提供量化指标.方法 对32名高性能战斗机飞行员进行15 d的间歇性低氧训练(模拟高度3500 m),1次/d,每次25 min.于训练前后,分别检测受试者在模拟7500 m高空环境下的EEG、SaO2、红细胞数及血红蛋白含量,并对受试者低氧训练前后的检测数据进行t检验.结果 间歇性低氧训练后,受试者在模拟7500 m高空环境下的EEG复杂度较训练前显著降低,差异有统计学意义(P＜0.01),Sa()2升高,差异有统计学意义(P＜0.01),红细胞和血红蛋白含量则无明显变化(P＞0.05).结论 模拟3500 m间歇性低氧训练可提高机体高空缺氧耐力水平,EEG复杂度和SaO2可作为评价高性能战斗机飞行员间歇性低氧训练的定量生理指标. Abstract： Objective To explore the quantitative index for evaluating the intermittent hypoxia training effects by analyzing the characteristic changes of electroencephalogram (EEG) complexity and saturation of blood oxygen (SaO2) of high performance fighter pilots. Methods Thirty-two pilots were selected as subjects and undertook a 25 min-training (simulated hypoxia at 3500 m-oxygen concentration 13.1%) with Type DY-84 hypoxia training device once a day for 15 d. Before and after training the subjects were put in simulated 7500 m hypoxia condition (oxygen concentration 7.1%,ventilation volume 15L/min) and their EEG, SaO2, number of red blood cell and hemoglobin level were recorded and analyzed by t-test. Results Training effects showed that the subjects' 7500m EE(G complexity was significantly decreased (P＜0.01), but SaO2 was significantly increased (P＜0.01).Number of red blood cell and hemoglobin level had no obvious change (P＞0.05).Conclusions The simulated 3500 m intermittent hypoxia training could improve pilot's hypoxia tolerance. EEG complexity and SaO2, which are measured under simulated 7500 m hypoxia condition,would be the quantitative indices for evaluating the effects of intermittent hypoxia training for pilot.The results application would be hopefully expanded to the population who work at high altitude or in anoxic environment.     

Pulmonary artery pressure increases during commercial air travel in healthy passengers

BACKGROUND: It is not known whether the mild hypoxia experienced by passengers during commercial air travel triggers hypoxic pulmonary vasoconstriction and increases pulmonary artery pressure in flight. Insidious pulmonary hypertensive responses could endanger susceptible passengers who have cardiopulmonary disease or increased hypoxic pulmonary vascular sensitivity. Understanding these effects may improve pre-flight assessment of fitness-to-fly and reduce in-flight morbidity and mortality. Methods: Eight healthy volunteers were studied during a scheduled commercial airline flight from London, UK, to Denver, CO. The aircraft was a Boeing 777 and the duration of the flight was 9 h. Systolic pulmonary artery pressure (sPAP) was assessed by portable Doppler echocardiography during the flight and over the following week in Denver, where the altitude (5280 ft/1610 m) simulates a commercial airliner environment. Results: Cruising cabin altitude ranged between 5840 and 7170 ft (1780 to 2185 m), and mean arterial oxygen saturation was 95 +/- 0.6% during the flight. Mean sPAP increased significantly in flight by 6 +/- 1 mmHg to 33 +/- 1 mmHg, an increase of approximately 20%. After landing in Denver, sPAP was still 3 +/- 1 mmHg higher than baseline and remained elevated at 30 +/- 1 mmHg for a further 12 h. Conclusions: Pulmonary artery pressure increases during commercial air travel in healthy passengers, raising the possibility that hypoxic pulmonary hypertension could develop in susceptible individuals. A hypoxia altitude simulation test with simultaneous echocardiography ('HAST-echo') may be beneficial in assessing fitness to fly in vulnerable patients.     

Hemoglobin mass and peak oxygen uptake in untrained and trained female altitude residents

Total hemoglobin mass has not been systematically investigated in females at altitude. We measured this quantity (CO-rebreathing method) as well as peak oxygen uptake in 54 young women (age 22.5 +/- 0.6 SE years) with differing physical fitness living in Bogota (2600 m) and compared the results with those of 19 subjects from 964 m in Colombia and 75 subjects from 35 m in Germany. In spite of an increased hemoglobin concentration the hemoglobin mass was not changed in highlanders (means 9.0 to 9.5 g . kg (-1) in untrained subjects at all altitude levels). Endurance trained athletes, however, showed a rise in hemoglobin mass by 2 - 3 g . kg (-1) at all sites. Erythropoietin was little increased in Bogota; iron stores were within the normal range. Aerobic performance capacity was lower at high altitude than at sea level and remained so also after correction for the hypoxic deterioration in untrained and moderately trained subjects but not in athletes; possibly the cause was reduced daily physical activity in non-athletic Bogotanians compared to lowlanders. After exclusion of the factor V.O(2peak) by analysis of covariance a mean rise of 6.6 % in hemoglobin mass at 2600 m was calculated being smaller than in males (> 12 %). The attenuated increase of hemoglobin mass in female highlanders possibly results from stimulation of ventilation improving arterial oxygen saturation or from an increased hypoxia tolerance of cellular metabolism both caused by female sexual hormones.     

The effect of hypoxia on thallium kinetics in cultured chick myocardial cells

To assess the effect of hypoxia on cellular thallium-201 (201Tl) uptake and washout independent of coronary flow, we studied thallium kinetics during normoxia and hypoxia in cultured chick ventricular cells. Monolayers of contracting ventricular cells grown on coverslips were placed in a chamber and perfused to asymptote with media containing 201Tl. Perfusates were equilibrated with 5% CO2-95% air or 5% CO2-95% nitrogen for normoxia and hypoxia, respectively. Washout thallium kinetics were then observed during perfusion with unlabeled media. Twenty paired experiments were performed, randomly alternating the sequence of normoxia and hypoxia. Pharmacokinetics for thallium were determined by computer using standard formulae. Thallium uptake and washout were best described by assuming that intracellular thallium was contained within a single compartment. Cellular thallium uptake, as well as transfer rate constants for thallium uptake and for thallium washout during normoxia and hypoxia, were compared using paired t-tests. During normoxia and hypoxia, respectively, thallium uptake was 22 +/- 7% and 19 +/- 7% of asymptote (p less than 0.01); the compartmental rate constant for uptake by the cell was 0.16 +/- 0.07 min-1 and 0.15 +/- 0.06 min-1 (N.S.); and the transfer rate constant for washout from the cell was 0.26 +/- 0.06 min-1 and 0.23 +/- 0.05 min-1 (p less than 0.01). We conclude that there was a small (14%) decrease in thallium uptake during hypoxia. The rate of thallium uptake and washout was slightly less during hypoxia, although only the rate of washout was significantly less. These data show that cellular accumulation of thallium and the rate of washout of thallium were minimally decreased by hypoxia independent of blood flow.