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Birth weight and altitude: a study in Peruvian communities.

We tested the hypothesis that at high altitude birth weight decreases once a critical barometric pressure (Pb) is reached. Birth weight data covering the 1-year period from November 1997 to October 1998 were collected in Peru from the data files of 15 community and mining centers between sea level and 4575 m altitude. These centers are scattered along the main road that joins Lima (on the Pacific shore) to Cerro de Pasco (4330 m) and surroundings. Above approximately 2000 m (ie, at Pb below approximately 590 mm Hg, inspired O(2) partial pressure of approximately 114 mm Hg) and up to approximately 4500 m altitude birth weight declined at an average of 65 g for every additional 500 m altitude (or 105 g for every additional 50 mm Hg drop in Pb). This pattern did not differ between sexes. Averages and modal distributions of the birth weight from 2 hospitals in Cerro de Pasco (4330 m) serving different social groups were similar. Body length at birth was similar at various altitudes, with the exception of the 2 highest locations above 4500 m, where it was slightly reduced. From these data, together with additional data collected in the North of Peru (Chacas, 3360 m) and with results from other ethnic groups previously published, we conclude that the drop in birth weight at altitude is (1) apparent once the critical Pb of approximately 590 mm Hg is reached, corresponding to an altitude of approximately 2000 m, (2) proportional to the increase in altitude between approximately 2000 m and 4500 m, and (3) independent from socioeconomic factors.

Altitude↗

Altitude and endurance training.

The benefits of living and training at altitude (HiHi) for an improved altitude performance of athletes are clear, but controlled studies for an improved sea-level performance are controversial. The reasons for not having a positive effect of HiHi include: (1) the acclimatization effect may have been insufficient for elite athletes to stimulate an increase in red cell mass/haemoglobin mass because of too low an altitude (< 2000-2200 m) and/or too short an altitude training period (<3-4 weeks); (2) the training effect at altitude may have been compromised due to insufficient training stimuli for enhancing the function of the neuromuscular and cardiovascular systems; and (3) enhanced stress with possible overtraining symptoms and an increased frequency of infections. Moreover, the effects of hypoxia in the brain may influence both training intensity and physiological responses during training at altitude. Thus, interrupting hypoxic exposure by training in normoxia may be a key factor in avoiding or minimizing the noxious effects that are known to occur in chronic hypoxia. When comparing HiHi and HiLo (living high and training low), it is obvious that both can induce a positive acclimatization effect and increase the oxygen transport capacity of blood, at least in 'responders', if certain prerequisites are met. The minimum dose to attain a haematological acclimatization effect is > 12 h a day for at least 3 weeks at an altitude or simulated altitude of 2100-2500 m. Exposure to hypoxia appears to have some positive transfer effects on subsequent training in normoxia during and after HiLo. The increased oxygen transport capacity of blood allows training at higher intensity during and after HiLo in subsequent normoxia, thereby increasing the potential to improve some neuromuscular and cardiovascular determinants of endurance performance. The effects of hypoxic training and intermittent short-term severe hypoxia at rest are not yet clear and they require further study.

Acclimatization↗

Physiological effects of altitude training on elite male cross-country skiers.

Seven elite male cross-country skiers trained for 3 weeks at an altitude of 1900 m. Haemoglobin concentration ([Hb]), haematocrit (Hct) (obtained from venous blood), maximal oxygen uptake (VO2 max) and energy expenditure during a standard submaximal workload were measured before and after training at altitude, and 1 year later while training at sea level (control). Both [Hb] and Hct increased significantly, and the skiers with the lowest initial [Hb] and Hct experienced the largest increases during training at altitude. The increase in blood lactate (BLa) concentration (using haemolysed capillary blood) during a standard submaximal exercise test was significantly lower after training at altitude than before it or 1 year later (control). A significant correlation was found between the magnitude of increase in [Hb] and Hct and the difference in the lactate response to the standard submaximal workload pre- and post-altitude training. Although VO2 max remained unchanged, lower BLa concentration during the submaximal test probably reflects an improved ability to exercise at higher submaximal workloads shortly after training at altitude compared with pre-altitude training. It is suggested that subjects with low initial [Hb] and Hct improve their aerobic performance capacity most during altitude training.

Altitude↗

Effects of altitude on endogenous carboxyhemoglobin levels.

The effects of carbon monoxide (CO) on blood carboxyhemoglobin (COHb) levels, though well studied at sea level, have not been investigated in populations at altitude. COHb levels were measured in laboratory rats following 6 wk exposure to either clean air or air containing 9 ppm CO at ambient altitude (3300 ft), 10,000 ft, or 15,000 ft simulated high altitude. In animals breathing clean air, COHb levels increased with increasing altitude from 0.68 +/- 0.09% at 3300 ft to 1.16 +/- 0.28% and 1.68 +/- 0.14%, respectively, at 10,000 and 15,000 ft. The relationship between COHb levels and increasing altitude is linear with a correlation coefficient of 0.90 (p less than .001). In animals breathing 9 ppm CO, COHb levels also increased with increasing altitude from 0.99 +/- 0.06% at 3300 ft to 1.77 +/- 0.17% and 2.10 +/- 0.08%, respectively, at 10,000 and 15,000 ft. The relationship between COHb levels and increasing altitude in animals breathing CO is also linear with a correlation coefficient of .92 (p less than .001). These data indicate that, compared with animals at sea level, animals at altitude have an increased body burden of COHb and will attain the COHb level associated with the National Ambient Air Quality Standard for CO more quickly when breathing CO.

Altitude↗

Altitude-dependent and -independent variations in Plasmodium falciparum prevalence in northeastern Tanzania.

BACKGROUND: Effective malaria control requires information about intensity of transmission across large areas and populations. Estimates based on entomological factors lack precision and are not cost-effective to obtain. We tested altitude and rainfall measurements as correlates of transmission intensity in different ecological settings. METHODS: We conducted 2 cross-sectional surveys of approximately 12,000 people (1-45 years old) in 6 altitude transects (150-1800 m) in the Kilimanjaro and Tanga regions of Tanzania. Data were analyzed for associations with altitude and rainfall estimates by use of appropriate regression models. RESULTS: Plasmodium falciparum prevalence showed a negative relationship with altitude (19% and 21% decrease/100-m altitude increase, respectively, in children in Kilimanjaro and Tanga) and rainfall during the 3 months before the survey (46% decrease/100-mm rainfall increase in children in Kilimanjaro). Mean hemoglobin concentrations increased with altitude (0.05 and 0.09 g/dL/100-m altitude increase, respectively, in children in Kilimanjaro and Tanga) and rainfall (0.17 g/dL/100-mm rainfall increase in children and adults in Kilimanjaro). DISCUSSION: Altitude and rainfall were correlated with parasite prevalence and mean hemoglobin concentration; however, the relationship varied according to ecological setting. Climatological variables alone cannot predict malarial outcomes. Local variations in seasonality of malaria transmission--together with vector species composition, topography, host and parasite genetics, and socioeconomic factors--may influence malaria prevalence.

Adolescent↗

Potential genetic contributions to control of the pulmonary circulation and ventilation at high altitude.

This review examines evidence that genetic factors may be important determinants of response of the pulmonary circulation and ventilation at high altitude. Early observations of cattle at high altitude with brisket disease-pulmonary hypertension with right heart failure-found that the disorder ran in families. Subsequent studies confirmed a genetic determination of the pulmonary vasoconstrictor response to hypoxia by selective breeding of cattle for high and low responses. Clear interspecies and interstrain differences in the hypoxic pulmonary pressor response also underscore a major role for genetic influence in animals. In humans, differences in pulmonary hemodynamics are also evident among discrete populations living at altitude in the Andes, Himalayas, and North America suggesting an evolutionary, genetic influence on the response of the lung circulation to the hypoxia of altitude. Ventilation is increased by the hypoxia of high altitude. The strength of the ventilatory response to hypoxia shows considerable variation among individuals at low altitude. Family clusters of high and low responses and greater concordance among identical than fraternal twins suggest a strong genetic modulation of the human hypoxic ventilatory response. Similar effects are seen in interstrain differences among inbred strains of rats and mice. Differences among diverse altitude populations support the possible influence of genetic variation in the hypoxic response on ventilation and adaptation at altitude. Mechanisms linking genetic influences to variation in the hypoxic pulmonary pressor and ventilatory responses are unknown, but could reflect effects on hypoxic sensor, mediator or effector limbs of the response.

Adaptation, Physiological↗

Stroke at high altitude: Indian experience.

UNLABELLED: Stroke is a common medical emergency. There is limited knowledge about stroke at high altitude. We present the clinical profile of 30 cases of stroke at high altitude seen at our center between November 1998 to July 2000. A detailed neurological and systemic examination was carried out. Cases were investigated with blood counts, lipid profile, cardiac evaluation, and CT scan/MRI. Coagulation parameters were studied in some cases. Strokes formed 13.7/1000 of hospital admissions from high altitude area, compared to 1.05/1000 in nonhigh altitude area. All our cases from high altitude area were males (serving soldiers of armed forces). Their mean high altitude stay was 10.2 months, and they were all located at heights greater than 4270 m. Age ranged from 22 to 48 years (mean 33.4 yr). Except for smoking (in four cases), they had no preexisting risk factors. Twenty-two cases were of ischemic stroke, 2 of intracerebral hemorrhage, 4 of TIA/RIND (transient ischemic attack/reversible ischemic neurological deficit), and 2 had cerebral venous thrombosis. Out of 30 cases, 28 were of "stroke in young" (<45 yr) and were compared with cases in the same age group from nonhigh altitude areas. Polycythemia with Hb ranging from 16.2 to 22 g.dL(-1) was seen in 21 of these 28 cases (75%). Protein C and S deficiency was found in 1 case in each group. CT scan showed massive infarcts involving at least 50% of one cerebral hemisphere in 12 cases. Multiple infarcts were seen in one case. CONCLUSION: Long-term stay at high altitude is associated with higher risk of stroke. Although all types of stroke were seen, ischemic stroke was the commonest. Massive infarcts were common. Polycythemia was an important risk factor.

Adult↗

Prelude to Everest: Alexander M. Kellas and the 1920 high altitude scientific expedition to Kamet.

Following his untimely death due to illness during the early stages of the first Mount Everest Reconnaissance Expedition in 1921, Alexander M. Kellas has received relatively little attention in either mountaineering or scientific literature. He remains an obscure figure despite his noteworthy contributions to high altitude physiology and exploration. He can be considered not only one of the finest exploratory Himalayan mountaineers in history, but also the first person to apply state-of-the-art knowledge of high altitude physiology to field investigations at altitudes over 6000 m. By the time of his death, it is extremely likely that Kellas had spent more time above 6000 m than anyone on Earth, undertaking no fewer than eight Himalayan expeditions between 1907 and 1921. This article revisits and examines in some detail the most ambitious high altitude physiological field study undertaken through the second decade of the 20th century, A. M. Kellas and Henry T. Morshead's 1920 Kamet Expedition. This undertaking by Kellas and Morshead was unique because it specifically emphasized investigation of the practical difficulties inherent in climbing at very high altitudes. During this endeavor, Kellas carried out the first rigorous tests of the value of supplementary oxygen for climbing at high altitude. The results of the field studies conducted during the 1920 Kamet Expedition provided strong support for the use of supplementary oxygen at high altitude. However, after Kellas died on the approach march to Everest the following year, the British mountaineering establishment did not again have a similar proponent or exponent of extreme altitude field research until physiologist Griffith Pugh once again took up the challenge in the early 1950s.

Altitude Sickness↗

High density lipoprotein cholesterol increases with living altitude.

BACKGROUND: The relationship between high density lipoprotein cholesterol (HDL) serum level and the altitude at which people live is controversial. METHODS: A cross-sectional study was carried out in the adult population (30-64 years) of the Island of El Hierro (Canary Islands, Spain). In all, 594 individuals representative of the El Hierro population for gender, age, district and the altitude at which they lived were included. The factors measured included HDL, living altitude, body mass index (BMI), smoking habits, alcohol consumption, diabetes, menopause in women, and physical activity and dietary habits. RESULTS: The HDL showed a correlation with living altitude (r = 0.14, P < 0.01) and with BMI (r = -0.19, P < 0.01). Smokers had lower HDL levels than ex-smokers and non-smokers (P < 0.05). Men who were moderate drinkers had higher HDL levels than heavy or mild drinkers and non-drinkers (P < 0.01). Physical activity was only related to HDL in men with levels >1.52 mmol/l, who walked on the average more than the rest (P < 0.05). Variables not showing the expected relationship with HDL were diabetes and the menopause in women (probably due to a low statistical power of their subsamples). Regression analysis, with HDL as dependent variable showed that the association between HDL and altitude persists when taking altitude as a categorical or a continuous variable. CONCLUSIONS: High density lipoprotein cholesterol levels are linearly and significantly increased when living at a higher altitude. This fact should be taken into account when comparing cardiovascular risk in populations living at different altitudes.

Adult↗

Metabolic and osmoregulatory function at low and high (3800 m) altitude.

Altitude evokes physiological adjustments that include not only respiratory and cardiovascular properties, but also metabolic function, renal and endocrine responses. The purpose of the present study was designed to expand our understanding of the physiological process involved with acclimatisation to high altitude in equids. The study examined temporal effects on metabolic and osmoregulatory function in horses (n = 6) at rest and postexercise at 3800 m. Animals were studied at 225 m (Pb = 743 mmHg) and during a 10 day stay at altitude (Pb = 487 mmHg). Rest samples were taken 90 min postprandial at 0830 h and immediately after the gallop phase of a standard exercise test. Changes in glucose, insulin, cortisol, thyroxine, sodium, potassium, chloride and total protein were assessed at both altitudes. Exercise stimulated increases in cortisol, thyroxine, potassium, and chloride; while the concentrations of glucose, insulin, sodium and total protein (regardless of altitude) decreased. Acute (Day 2) altitude exposure (following transport stress) produced significant increases in glucose, cortisol, thyroxine, chloride and protein at rest and exercise. All variables (except cortisol) appeared to stabilise by Day 4 of altitude exposure. Observations from these data (coupled with haematological and blood gases data) indicate that equids acutely acclimate within 2-3 days to this altitude.

Acclimatization↗

Validity of the 3 min step test in moderate altitude: environmental temperature as a confounder.

The 3 min step test is a widely used method to evaluate physical fitness, but whether this method is valid when performed at altitude is unknown. The purpose of this study was to examine the effect of altitude on the fitness score of the 3 min step test, and the role of ambient temperature in this effect. In study I, 11 healthy volunteers (aged 18.1 +/- 1.1 years) performed a 3 min step test at sea level and at altitude (1950 m). Plasma lactate and stress hormones, as indicators of metabolic stress, were measured before and after the test. To determine the role of ambient temperature, we performed study II at sea level with the same step test simulating the altitude temperature condition (24 degrees C at high altitude versus 32 degrees C at sea level) with 23 subjects (aged 20.4 +/- 0.4 y). In study I, plasma lactate of the subjects was elevated during the step test at sea level and to a greater extent at high altitude. Plasma cortisol and testosterone levels were elevated only at high altitude. However, the heart rate (HR) recovery after the step test was faster at high altitude than at sea level, producing a better physical fitness index. Furthermore, in study II, we demonstrated that the subjects who performed the 3 min step test at 24 degrees C exhibited faster HR recovery than at 32 degrees C. The current study therefore suggests that environmental conditions leading to temperature variation have strong confounding effects on the fitness score of the 3 min step test.

Adolescent↗

Effects of acute exposure to high altitude on ventilatory drive and respiratory pattern.

To assess changes in ventilatory regulation in terms of central drive and timing, on exposure to high altitude, and the effects of induced hyperoxia at high altitude, six healthy normal lowland subjects (mean age 19.5 +/- 1.64 yr) were studied at low altitude (518 m) and on the first 4 days at high altitude (3,940 m). The progressive increase in resting expired minute ventilation (VE; control mean 9.94 +/- 1.78 to 14.25 +/- 2.67 l/min on day 3, P less than 0.005) on exposure to high altitude was primarily due to a significant increase in respiratory frequency (f; control mean 15.6 +/- 3.5 breaths/min to 23.8 +/- 6.2 breaths/min on day 3, P less than 0.01) with no significant change in tidal volume (VT). The increase in f was due to significant decreases in both inspiratory (TI) and expiratory (TE) time per breath; the ratio of TI to TE increased significantly (control mean 0.40 +/- 0.08 to 0.57 +/- 0.14, P less than 0.025). Mouth occlusion pressure did not change significantly, nor did the ratio of VE to mouth occlusion pressure. The acute induction of hyperoxia for 10 min at high altitude did not significantly alter VE or the ventilatory pattern. These results indicate that acute exposure to high altitude in normal lowlanders causes an increase in VE primarily by an alteration in central breath timing, with no change in respiratory drive. The acute relief of high altitude hypoxia for 10 min has no effect on the increased VE or ventilatory pattern.

Adolescent↗

Low acute hypoxic ventilatory response and hypoxic depression in acute altitude sickness.

Persons with acute altitude sickness hypoventilate at high altitude compared with persons without symptoms. We hypothesized that their hypoventilation was due to low initial hypoxic ventilatory responsiveness, combined with subsequent blunting of ventilation by hypocapnia and/or prolonged hypoxia. To test this hypothesis, we compared eight subjects with histories of acute altitude sickness with four subjects who had been asymptomatic during prior altitude exposure. At a simulated altitude of 4,800 m, the eight susceptible subjects developed symptoms of altitude sickness and had lower minute ventilations and higher end-tidal PCO2's than the four asymptomatic subjects. In measurements made prior to altitude exposure, ventilatory responsiveness to acute hypoxia was reduced in symptomatic compared to asymptomatic subjects, both when measured under isocapnic and poikolocapnic (no added CO2) conditions. Diminution of the poikilocapnic relative to the isocapnic hypoxic response was similar in the two groups. Ventilation fell, and end-tidal PCO2 rose in both groups during 30 min of steady-state hypoxia relative to values observed acutely. After 4.5 h at 4,800 m, ventilation was lower than values observed acutely at the same arterial O2 saturation. The reduction in ventilation in relation to the hypoxemia present was greater in symptomatic than in asymptomatic persons. Thus the hypoventilation in symptomatic compared to asymptomatic subjects was attributable both to a lower acute hypoxic response and a subsequent greater blunting of ventilation at high altitude.

Adult↗

Effects of acute exposure to simulated altitude on heart rate variability during exercise.

It has been shown that fluctuation of human heartbeat intervals [heart rate variability (HRV)] reflects variations in cardiac autonomic nervous system activity. The present study was designed to investigate whether the acute exposure to moderate levels of simulated altitude and the resultant hypoxia could modify HRV during exercise. Seven healthy men completed one resting measurement in the upright sitting position and two submaximal steady-state cycle ergometer exercises at intensities equivalent to 25 and 50% of their estimated maximal work rate. Experiments were conducted in random order at altitude equivalents of 500, 1,500, 2,500, and 3,500 m within 2 h of exposure to that altitude. Beat-to-beat HRV was measured continuously during the tests. HRV data were analyzed by "coarse-graining spectral analysis" (Y. Yamamoto and R.L. Hughson, Physica 68D: 250-264, 1993) to break down their total power (PT) into harmonic and nonharmonic (fractal) components. The harmonic component was further divided into low (0.0- to 0.15-Hz; PL)- and high (> 0.15-Hz; PH)-frequency components, and the indicators of relative sympathetic (SNS) and parasympathetic (PNS) nervous system activities were calculated by PL/PH and PH/PT, respectively. The fractal component was used to calculate the spectral exponent (beta) to evaluate the overall "irregularity" of HRV. The effects of exercise intensity (increase in heart rate, SNS indicator, and beta and decrease in PNS indicator) were significant (P < 0.05) at all altitude levels. The altitude effects (increase in heart rate and SNS indicator and decrease in PNS indicator) were found only during exercise at 3,500 m (P < 0.05). There was no significant effect of altitude on beta (P > 0.05). These data indicate that acute effects of altitude exposure on HRV were found 1) during exercise at moderate altitude (> 2,500 m) and 2) mainly for the harmonic components of HRV.

Adult↗

Prediction of barometric pressures at high altitude with the use of model atmospheres.

It would be valuable to have model atmospheres that allow barometric pressures (PB) to be predicted at high altitudes. Attempts to do this in the past using the International Civil Aviation Organizations or United States Standard Atmosphere model have brought such models into disrepute because the predicted pressures at high altitudes are usually much too low. However, other model atmospheres have been developed by geophysicists. The critical variable is the change of air temperature with altitude, and, therefore, model atmospheres have been constructed for different latitudes and seasons of the year. These different models give a large range of pressures at a given altitude. For example, the maximum difference of pressure at an altitude of 9 km is from 206 to 248 Torr, i.e., approximately 20%. However, the mean of the model atmospheres for latitude of 15 degrees (in all seasons) and 30 degrees (in the summer) predicts PB at many locations of interest at high altitude very well, with predictions within 1%. The equation is PB (Torr) = exp (6.63268 - 0.1112 h - 0.00149 h2), were h is the altitude in kilometers. The predictions are good because many high mountain sites are within 30 degrees of the equator and also many studies are made during the summer. Other models should be used for latitudes of 45 degrees and above. Model atmospheres have considerable value in predicting PB at high altitude if proper account is take of latitude and season of the year.

Altitude↗

Evidence against an increase in capillary permeability in subjects exposed to high altitude.

A potential pathogenetic cofactor for the development of acute mountain sickness and high-altitude pulmonary edema is an increase in capillary permeability, which could occur as a result of an inflammatory reaction and/or free radical-mediated injury to the lung. We measured the systemic albumin escape by intravenously injecting 5 muCi of 125I-labeled albumin and the plasma concentrations of cytokines, F2-isoprostanes (products of lipid peroxidation), and acute-phase proteins in 24 subjects exposed to 4,559 m. Ten subjects developed acute mountain sickness, and four subjects developed high-altitude pulmonary edema. The transcapillary escape rate of albumin was 6.9 +/- 2.0%/h (SD) at low (550 m) and 6.3 +/- 1.9%/h at high (4,559 m) altitude (P = 0.23; n = 24). The subjects with high-altitude pulmonary edema had a modest but insignificant increase in the transcapillary escape rate of albumin (4.6 +/- 1.9%/h at low vs. 5.7 +/- 1.9%/h at high altitude; P = 0.42; n = 4). Plasma concentrations of fibrinogen, alpha 1-acid glycoprotein, C-reactive protein, and interleukin-6 were unchanged in the early phases and significantly increased by the end of the observation period in the subjects with high-altitude pulmonary edema, whereas tumor necrosis factor-alpha and F2-isoprostanes did not change at all. This suggests that the inflammatory reaction was rather a consequence than a causative factor of high-altitude pulmonary edema. In summary, these data argue against a dominant role for increased systemic capillary permeability in the development of acute mountain sickness and high-altitude pulmonary edema.

Acclimatization↗

Altered ion transporter expression in bronchial epithelium in mountaineers with high-altitude pulmonary edema.

Hypoxia inhibits activity and expression of transport proteins of cultured lung alveolar epithelial cells. Here we tested whether hypoxia at high altitude affected the expression of ion transport proteins in tissues obtained from controls and mountaineers with high-altitude pulmonary edema (HAPE) at the Capanna Margherita (4,559 m). Expression was determined by RT-PCR and Western blots from brush biopsies of bronchial epithelium and from leukocytes obtained before and during the stay at high altitude. At low altitude, amounts of mRNAs were not different between control and HAPE-susceptible subjects. At high altitude, the amount of mRNA of Na-K-ATPase, CFTR, and beta-actin of brush biopsies did not change in controls but decreased significantly (-60%) in HAPE-susceptible subjects. There was no change in Na channel mRNAs at high altitude in controls and HAPE. No statistically significant correlation was found between the expression of Na transporters and PO2 and O2 saturation. In leukocytes, 28S-rRNA and Na-K-ATPase decreased at altitude in control and HAPE-susceptible subjects, but no significant change in Na-K-ATPase protein was found. Hypoxia-inducible factor-1alpha mRNA and GAPDH mRNA tended to increase in leukocytes obtained from HAPE-susceptible subjects at high altitude but did not change in controls. These results show that hypoxia induces differences in mRNA expression of ion transport-related proteins between HAPE-susceptible and control subjects but that these changes may not necessarily predict differences in protein concentration or activity. It is therefore unclear whether these differences are related to the pathophysiology of HAPE.

Adult↗

Respiratory function at different altitudes.

For the evaluation of a respiratory test at high altitude, several factors must be taken into account: the decreased barometric pressure, the decreased density of air and the degree of acclimatization which is related to the altitude and to the length of exposure. Several studies have shown a reduction in forced vital capacity (FVC) at high altitude and using simulated conditions, mainly related to an increase in pulmonary blood volume and development of interstitial edema. To assess the daily spirometric patterns during ascending to high altitudes we studied 17 healthy subjects at both Capanna Regina Margherita on the Italian Alps (4,559 m) and the Pyramid Laboratory in Nepal (5,050 m). Respiratory function tests were performed every day. Peak expiratory flow values significantly increased. The mean percent increase was 15% at 3,200 and 3,600 m and 26% at 4,559 m. FVC and MEF25 values showed a significant decrease (p < 0.005) during the first days above 3,500 m and improved only after several days spent above this altitude. For each subject the maximal reductions in FVC and maximal expiratory flow (MEF) at 25% of FVC however were found on different days. In our opinion, these data support the hypothesis that at high altitude the respiratory function can be affected by the presence of an increased pulmonary blood volume and/or the development of interstitial edema. The observed changes in forced expiration curves at high altitude seem to reflect the degree of acclimatization that is related to the individual susceptibility, to the altitude reached and to the duration of the exposure. These changes are transient and resolve after returning to sea level.

Adult↗