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PubMed2003

Effects of intermittent exposure to high altitude on pulmonary hemodynamics: a prospective study.

Chronic alveolar hypoxia due to disease or low atmospheric pressure at high altitude results in the development of hypoxic pulmonary hypertension. The effects of intermittent hypoxia on pulmonary hemodynamics in healthy men have not been studied. We aimed to investigate, prospectively, pulmonary hemodynamics in workers commuting between an elevation of 3700 and 4200 m (4-week working shift) and lowland, below 500 m (4 weeks of holiday). Pulmonary hemodynamics has been investigated by Doppler echocardiography in 26 healthy Caucasian males, mean age 42 +/- 9 yr. First at lowland (760 m) and next during the fourth week of work at high altitude. Investigations were repeated in 21 subjects 1 year later at the end of the high-altitude exposure. The third series of investigations was performed 2 yr after the initial ones in 10 subjects who earlier had shown the strongest hypoxic vasoconstriction. At lowland, subjects presented with normal pulmonary hemodynamics. At high altitude, mean pulmonary artery pressure (PAPm) rose from 14.7 +/- 2.7 mmHg to 25.8 +/- 8.3 mmHg. One year later the PAPm remained unchanged in hypoxic conditions (25.0 +/- 7.3 mmHg). At the end of a 2-year follow-up of 10 "hyperreactors," PAPm measured at the end of the hypoxic exposure was the same as at the initial investigation, averaging 28 +/- 4.0, 28 +/- 3.5, and 29 +/- 2.5 mmHg at the beginning and at 1 and after 2 yr of intermittent exposure to high altitude. We concluded that intermittent exposure to 4000 m lasting 3 yr does not lead to development of permanent pulmonary hypertension.

Acclimatization↗
PubMed2006

Endothelial nitric oxide synthase polymorphisms do not influence pulmonary artery systolic pressure at altitude.

Previous genetic association studies in high-risk subjects have suggested that polymorphisms in the gene encoding endothelial nitric oxide synthase (eNOS) may be associated with susceptibility to high altitude pulmonary edema (HAPE). We aimed to determine whether eNOS polymorphisms influence systolic pulmonary artery pressure measurements (PASP) in healthy trekkers ascending to high altitude. We examined two polymorphisms of the eNOS gene in Caucasian volunteers: Glu298Asp variant and 27-base pair (bp) variable number of tandem repeats polymorphism (27-bp VNTR). In 33 subjects, the relationships between polymorphisms and absolute pulmonary artery systolic pressure measurements (PASP), determined by echocardiography, were assessed at sea level and 1, 3, and 7 days after acute ascent by vehicle transport to 5200 m. As expected, there was a significant rise in pulmonary artery pressure on ascent to high altitude. By contrast, at sea level and at each time point at high altitude, no difference was found in mean PASP according to eNOS polymorphism. We found no association of Glu298Asp and 27-bp VNTR polymorphisms in the eNOS gene with PASP in a population of healthy trekkers at low or high altitude.

Adolescent↗
PubMed1979

Exercise and altitude.

In studies concerned with the performance at high altitude it is often not possible to separate the effects which are due to hypoxia from those associated with the stress of ascent. Some of the basic observations concerning exercise at high altitude are reviewed and a study is described which was designed to simulate the physical exertion of high altitude mountaineering but performed at altitudes below 1000 m. Some of the changes observed including peripheral oedema might under other circumstances have been ascribed to altitude.

Altitude↗
PubMed1986

Cutaneous vascular responses to heat simulated at a high altitude of 5,600 m.

Six healthy young men were studied in a high-altitude chamber during a 60-min heat exposure at a simulated altitude of 5,600 m or 0.5 atmosphere absolute (ATA). The heat load was provided by increasing the chamber temperature to 38 degrees C at the rate of 1 degree C/min after a 60-min equilibrium period at thermoneutrality (28 degrees C). Our question was whether or not hypoxia causes differential changes in regional cutaneous circulation during heat exposure. Skin blood flow in the forearm (FBF) and the finger (FiBF), temperatures of the esophagus (Tes) and of the skin, and cardiac output (CO) were measured during the heat exposure at 0.5 ATA and at the sea level (1 ATA). During the equilibrium period, hypoxia increased the mean skin temperature and mean heat transfer coefficient, as well as FBF and forearm vascular conductance. The increased blood flow in the cutaneous circulation during the hypoxic exposure may reflect cutaneous vasodilation and vasoconstriction in other regions of the body, since there was no alteration in CO and total peripheral resistance. During heat exposure, Tes rose faster at high altitude than at sea level. However, at the end of the 60-min heat exposure, all thermal as well as circulatory parameters showed no difference between the two altitudes, except for the FiBF. An attenuated vasodilation in the fingers during heat exposure at high altitude suggests differential vascular controls and possible impairment of thermoregulation when additional stress, such as heat, is imposed. The data suggest that cutaneous blood flow during heat exposure is not uniform throughout the entire skin in a hypoxic environment.

Adult↗
PubMed1990

Operation Everest II: neuromuscular performance under conditions of extreme simulated altitude.

The force output of the ankle dorsiflexors was studied during a 40-day simulated ascent of Mt. Everest in a hypobaric chamber; both electrically activated and maximal voluntary contractions (MVCs) were employed. The purpose of this study was to establish whether, under conditions of progressive chronic hypoxia, there was a decrease in muscle force output and/or increased fatigability. We also attempted to identify the main site of any failure, i.e., central nervous system, neuromuscular junction, or muscle fiber. Muscle twitch torque (Pt), tetanic torque (Po), MVC torque, and evoked muscle compound action potential (M wave) were monitored during 205-s exercise periods in five subjects at three simulated altitudes (760, 335, and 282 Torr). All three types of torque measurement were well preserved at the three altitudes. In some subjects, the responses to stimuli interpolated during repeated MVCs provided evidence of "central" fatigue at altitude. In addition, the rate of fatigue during 20-Hz electrical stimulation was greater (P less than 0.01) at altitude and there was increased fatigability of the twitch (P less than 0.025); however, the M wave amplitude was maintained. We conclude that central motor drive becomes more precarious at altitude and is associated with increased muscle fatigue at low excitation frequencies; the latter is the result, in part, of chronic hypoxia and occurs in the muscle fiber interior because no impairment in neuromuscular transmission could be demonstrated.

Adult↗
PubMed1993

Effects of altitude acclimatization on fluid regulatory hormone response to submaximal exercise.

To determine the effect of altitude acclimatization on plasma levels of atrial natriuretic peptide (ANP) during submaximal exercise and its relationship with renin and aldosterone, seven male volunteers aged 17-23 yr exercised to exhaustion on a cycle ergometer at 80-85% of their maximum O2 uptake at sea level (SL; 50 m), during 1 h in a hypobaric chamber [acute altitude (AA); 4,300 m], and after 14 or 16 days of residence on the summit of Pikes Peak, CO [chronic altitude (CA); 4,300 m]. Plasma samples taken before exercise, 10 min after the start of exercise, and 5 min postexercise were analyzed for ANP, plasma renin activity (PRA), and aldosterone (ALDO). ANP showed a progressive increase from rest to postexercise [7.49 +/- 1.63 to 11.32 +/- 1.80 (SE) pmol/ml and 6.05 +/- 2.55 to 10.38 +/- 7.20 pmol/ml; P = 0.049, exercise] at SL and AA, respectively, but not at CA (P = 0.039, altitude). Similarly, PRA and ALDO rose from rest to postexercise (P < 0.001, exercise), but the rise in ALDO with exercise was less during AA than during SL and CA (P = 0.002, phase). The decreased ANP levels during exercise after altitude acclimatization, with no change in PRA and ALDO, suggest that ANP has little effect on PRA and ALDO under these conditions.

Acclimatization↗
PubMed1980

Ventilatory acclimatization to high altitude is prevented by CO2 breathing.

The hypoxia of high altitude stimulates ventilation. If the resultant respiratory alkalosis inhibits the initial increase in ventilation, then with prevention of alkalosis, ventilation should rise immediately to a stable plateau. 4 subjects inspired CO2 (3.77%) from ambient air in a hypobaric chamber (PB = 440-455 Torr) during 100 h at high altitude. Ventilation (for given oxygen uptakes at rest and during exercise) increased promptly and remained stable. 4 control subjects exposed to high altitude without CO2 supplementation showed the expected progressive increases in ventilation with time. The hyperoxic CO2 ventilatory response curve shifted progressively to the left with time in the control subjects, but not in those given supplemental CO2. The latter group also failed to increase the ventilatory response to isocapnic hypoxia. Thus, CO2 supplementation at high altitude prevented the so-called "ventilatory acclimatization' from occurring. Prevention of respiratory alkalosis at high altitude probably permitted maintenance of [H+] at some central nervous system locus, thus allowing an uninhibited hypoxic stimulation of ventilation.

Acclimatization↗
PubMed1997

Pulmonary circulation at high altitude.

Hypoxia constricts the pulmonary vessels. An increase in pulmonary vascular resistance is seen in normal subjects during hypoxic breathing at sea level, in acclimatized lowlanders and in high-altitude natives. Hypoxic pulmonary hypertension in all these circumstances is most generally moderate, except in high-altitude natives at exercise. Pulmonary hypertension may become severe during high-altitude pulmonary edema, during infantile or adult forms of subacute mountain sickness, and during chronic mountain sickness. Subacute and chronic mountain sickness may be associated with a right heart failure that would be the human counterpart of brisket disease described in cattle. Subjects susceptible to high-altitude pulmonary edema present with a slight increase in pulmonary vascular resistance at rest and at exercise, and often with an enhanced pulmonary vascular reactivity to hypoxia. However, compared to unselected controls, the overlap is great, so that noninvasive echo-Doppler studies of the pulmonary circulation at sea level are of little predictive value of tolerance to altitudes on an individual basis.

Acclimatization↗
PubMed1998

Effects of high-altitude periodic breathing on sleep and arterial oxyhaemoglobin saturation.

This study aimed to investigate the effect of periodic breathing (PB) at high altitude on sleep structure and arterial oxygen saturation (Sa,O2). Five healthy subjects underwent polysomnographic studies at sea level, and during the first and the fourth week of sojourn at 5,050 m. Their breathing pattern, sleep architecture and Sa,O2 were analysed. PB was detected in the high-altitude studies during nonrapid eye movement (NREM) sleep and tended to increase from the first to the fourth week. Stages 3-4 were absent in four subjects at the first week, but only in one at the fourth week, irrespective of the amount of PB. The arousal index was 11.6+/-3.8 at sea level, 30.1+/-15.5 at the first week at altitude and 33.0+/-18.2 at the fourth week. At altitude, arousal index in NREM sleep was higher during PB than during regular breathing. In NREM sleep, the mean highest Sa,O2 levels in NREM epochs with PB were higher than in those with regular breathing by 2.8+/-1.7% at the first week and 2.9+/-1.5% at the fourth week (p<0.025). From the first to the fourth week, mean Sa,O2 increased significantly during wakefulness (5.6%), NREM (5.2% with regular breathing and 5.3% with PB) and rapid eye movement sleep (7.6%). The data demonstrate a slight role of periodic breathing in altering sleep architecture at high altitude and also show that periodic breathing induces only a minor improvement in arterial oxygen saturation during nonrapid eye movement sleep.

Acclimatization↗
PubMed2005

Sildenafil for the treatment of altitude-induced hypoxaemia.

Exposure to high altitude causes alveolar hypoxia and induces pulmonary hypertension (PH) with consequent limitation of exercise capacity. To assess the impact of sildenafil on haemodynamic and clinical parameters, and on aerobic performance, 12 young healthy unacclimatised subjects were studied (6 received sildenafil 40 mg t.i.d. and 6 received placebo) at sea level and high altitude. Systolic pulmonary artery pressure increased at high altitude, but normalised with sildenafil. The altitude-induced decrease in maximal O2 consumption was significantly smaller with sildenafil than with placebo. Enhancing pulmonary circulation with sildenafil safely protects against the high altitude-induced PH and improves gas exchange.

Altitude↗
PubMed1964

EFFECTS OF MODERATE ALTITUDE ON PATIENTS WITH PULMONARY AND CARDIAC IMPAIRMENT.

Twenty ambulatory patients with severe chronic pulmonary disease and 24 with severe heart disease were exposed in an altitude chamber to a simulated altitude of 8000 feet such as might exist in pressurized aircraft. Eight of the patients in the pulmonary group experienced undersirable reactions related to hypoxia, hypoventilation, inability to hyperventilate and expansion of gases. None of the 24 patients with cardiac disease experienced this same difficulty and all tolerated the procedure well. The ability to tolerate the stress of moderate altitude is related more to ventilatory efficiency and the maintenance of adequate oxygen saturation than to cardiovascular factors. It is recommended that a thorough evaluation of the cardio-pulmonary patient by clinical and physiological tests be made before exposure to altitude. When severe impairment is demonstrated, the subject may still be able to tolerate moderate altitudes if appropriate measures are provided to cope with the altered physiologic conditions.

Aerospace Medicine↗
PubMed2003

Hypoxia and pulmonary acclimatisation at 4578 m altitude: the role of acetazolamide and dexamethasone.

OBJECTIVES: To quantify the changes in ventilatory response and arterial blood gases in healthy male volunteers on acute ascent to 4578 meters altitude along with evaluating the role of acetazolamide and dexamethasone prophylaxis in acclimatisation. METHODS: Forty four lowlander male subjects participated as two groups in the study. Twenty four lowlander healthy male adults (age mean +/- SE 27.8 +/- 1.24 years) comprised the non-acclimatised group. They were sub grouped in a double blind fashion into four. Each subgroup (n=6) received placebo (multivitamin) or acetazolamide (250 mg) or dexamethasone (4 mg) or combined regimen of the two drugs twice daily for 5 days commencing 24 hours before ascent. The volunteers reached the altitude of 4578 meters within a span of one day. The second group (acclimatised) comprised of age and height matched twenty volunteers who had arrived 4 and 8 weeks earlier at the same altitude. Arterial PO2, PCO2, SO2 and minute respiratory rate pH were measured. The pulmonary functions (FVC, %FEV1 PEF, FEF(25-75%) and MVV) were recorded by Compact Spirometer (Vitalograph). Pre and post ascent measurements were carried out in non-acclimatised group whereas one measurement of the same parameters were made in acclimatised group. RESULTS: The study revealed a significant increase in respiratory rate min-1 after 24 hours of ascent along with reduction in PaO2 and SaO2. The gradual increase in PaO2 and SaO2 and reduction in PaCO2 was observed after 4 weeks at the same altitude. The reduction in FVC, %FEV1, PEF, FEF(25-75%) and MW were recorded in our subjects after 24 hours of acute ascent. Nevertheless, all pulmonary parameters in volunteers having 8 weeks of stay at 4578 m altitude, were found equivalent to the non-acclimatised group. The greater increase in minute respiratory rate, PaO2, SaO2 and pulmonary functions was found in volunteers taking acetazolamide. CONCLUSION: It is concluded that hyperventilation and increase in lung volumes are the adaptive pulmonary responses which help in improving levels of PaO2 and SaO2. The acetazolamide-dexamethasone prophylaxis appears beneficial in promoting pulmonary acclimatisation during hypobaric hypoxia.

Acclimatization↗
PubMed1992

High-altitude illness.

Acute mountain sickness, high-altitude cerebral edema, and high-altitude pulmonary edema are illnesses associated with acute exposure to altitudes greater than 8000 ft. Although usually self-limiting problems, they can be severe and life threatening. Gradual ascent to allow acclimatization can lessen or prevent symptoms. Acetazolamide is the drug of choice for pharmacologic prophylaxis; descent to lower elevation is the definitive treatment for altitude illness. Individuals who have chronic cardiac, respiratory, or certain other medical conditions may require supplemental oxygen and should be aware of restrictions regarding high-altitude exposure.

Acute Disease↗
PubMed2005

Effect of hypobaric hypoxia on visual evoked potential at high altitude.

The effect of hypobaric hypoxia on visual evoked potential (VEP) was studied in 27 male volunteers at sea level (SL), during the 1st and 3rd weeks of their stay at high altitude (HA) of 3,500 m and in the 1st week of their return to the sea level (RSL). Exposure to high altitude (HA) led to significant changes in VEP. The N1 wave latency of both right and left eye was significantly increased (P<0.05) during 3rd week of stay at the altitude which persisted even after the return to the sea level. The latency of P1 wave of both right and left eye was higher in 3rd week at high altitude but not significant statistically. But the delay in P1 latency persisted in 1st week of their return to sea level which was significant (p<0.05) statistically as compared to sea level. The latency of N2 wave was significantly decreased (P<0.05) during the 1st week of stay at HA and returned back to basal value in the 3rd week of stay at HA in both right and left eye. However, the changes observed in NPN complex in terms of wave latencies were within the physiological limits. The amplitude of wave N1-P1 of both the right and left eye did not show any change. The changes observed reflect the process of acclimatisation to 3500m high altitude.

Adult↗
PubMed1989

Blood pressure, intraocular pressure, and retinal vessels after high altitude mountain exposure.

Identical test protocols were used before and after 2 to 7 weeks of high altitude exposure in 23 climbers participating in 3 separate mountain expeditions in the Himalayas. The three groups reached altitudes of 4,000 m, 5,200, and 5,850 m, respectively. High altitude retinal hemorrhages (HARH) were found in three subjects (13%). Two weeks after the mountain exposure, reduced mean values of systolic (p less than 0.005) and diastolic (p less than 0.05) blood pressure and intraocular pressure (p less than 0.005) were found. Retinal veins were dilated 2.6% (p less than 0.001), and in both arteries (p less than 0.001) and veins (p less than 0.005) we observed a tendency for small vessels to dilate and large vessels to constrict. The intensity of reflection of light ("the central light reflex") from arteries was reduced (p = 0.003), indicating hemorrheology changes in the vessels. This study shows that significant changes in blood pressure, intraocular pressure and retinal vascularity follow hypoxic and physical strain of high altitude. The vascular conditioning of altitude acclimatization can be demonstrated in the retinal circulation 2 weeks after the exposure.

Adult↗
PubMed1988

Effects of exercise at high altitudes on young adults.

Outward Bound programs are carried out throughout the world, and many of these courses occur at altitudes above 3000 m (10,000 ft). As more knowledge is accumulated about health problems at high altitudes, exercise has been implicated as a factor contributing to acute mountain sickness in susceptible individuals. Thus, exercise conditioning programs occurring at high altitudes have come under scrutiny. Twenty-eight young men and women were enrolled in an Outward Bound course at an altitude over 3000 m for a 21-day period. Twelve of the 28 individuals developed shortness of breath, cough, or both by the third day of the course. Of these 12, seven had pulmonary function abnormalities: three having evidence of large airway involvement and four having findings of small airway involvement. The symptoms were not significant enough to interfere with acclimatization and the muscular conditioning aspects of the program. Although at altitudes between 3000 m and 4300 m, pulmonary function abnormalities of acute mountain sickness develop in a significant number of participants, the abnormalities were not significant enough to prevent persons from completing the course or achieving marked improvements in fitness measurements.

Adult↗
PubMed1987

High-altitude medical problems.

A spectrum of medical problems, including self-limited acute mountain sickness, high-altitude retinopathy, and the potentially fatal high-altitude pulmonary and cerebral edemas, may afflict residents and sojourners at higher elevations. However, appropriate prevention and prompt recognition will minimize the impact of these disorders. Prevention is predicated upon slow ascent to altitude and minimizing initial exertion at altitude; in selected cases, preventive drug therapy with Diamox (Lederle, Pearl River, New York) is helpful. Early recognition and descent to lower altitude remain the cornerstones of therapy.

Acute Disease↗
PubMed1986

Cerebral thrombosis at altitude: its pathogenesis and the problems of prevention and treatment.

In analyzing cerebral thrombosis at altitude--own case and in the literature--we anatomically confirmed that cerebral thrombi in mountain sickness were all of venous origin. All climbers went higher than 5,000 m and most stayed in that altitude longer than 3 weeks. Hemoconcentration was confirmed in two cases, including our own patient. It was suspected that hemoconcentration resulting from secondary polycythemia and dehydration at altitude, as well as cerebral circulatory disturbance produced by high-altitude cerebral edema, played a major role in the development of cerebral thrombosis. The problems of prevention and treatment of cerebral thrombosis at altitude are discussed.

Adult↗