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Periodicity of arrhythmias in healthy elderly men at the moderate altitude.

The 24-hour periodicity of supraventricular (SVPB) and ventricular (VEB) extrasystoles in healthy elderly men (age 49-69 years) was studied at two altitudes during 24 h Holter ECG monitoring. At the low altitude (200 m, n = 26), SVPB were more frequent than VEB. The highest occurrence of SVPB was at 17:00 h, the lowest at 01:00 and 02:00 h (P<0.001). The highest occurrence of VEB was at 09:00 h, the lowest one at 04:00 h (P<0.001). At 1350 m (n=9) the incidence of both SVPB and VEB was approximately twofold higher compared to that at the low altitude (P<0.001). The highest occurrence of SVPB was at 13:00 h, the lowest at 06:00 h (P<0.001). VEB were the most frequent at 10:00 h and 13:00 h, while the lowest frequency was observed at 06:00 h (P<0.001). Our results indicate that the incidence of SVPB and VEB in healthy persons at the moderate altitude is twofold and its periodicity is shifted compared to the low altitude. The cause of increased occurrence of extrasystoles is probably due to beta-adrenergic activation of the heart at the higher altitude.

Aged↗

L-Tryptophan does not influence acute ventilatory response at moderate altitude.

Altitude induced insomnia is a very common symptom in mountaineering. Conventional hypnotics such as benzodiazepines potentially can be associated with untoward side effects because they can impair ventilatory adaptation to hypoxia at altitude. The objective of our study was to evaluate the effect of a alternative potentially sedative drug, L-tryptophan on ventilation at moderate altitude. STUDY DESIGN, METHODS AND RELEVANT RESULTS: Randomised, double blind, placebo controlled crossover trial. Blood gas analysis of 8 healthy subjects was performed before and one hour after oral administration of 500 mg L-tryptophan or placebo at altitudes of 171 m and at 3,000 m. PaO2 and PaCO2 before and after L-Tryptophan or placebo medication did not change significantly at neither level of altitude investigated. CONCLUSION: L-tryptophan does not impair ventilatory adaptation to mild hypoxia at moderate altitude.

Adaptation, Physiological↗

Plasma volume by Evans blue: effects of eating and comparison with other methods at altitude.

HYPOTHESIS: Measurements of plasma volume (PV) and its changes (delta%PV) by Evans blue (EB) dye are presumed to be valid only in fasting subjects. In addition, delta%PVEB with acute altitude exposure has not been compared with other methods employing the concentration or dilution of naturally occurring blood (hematocrit (Hct), hemoglobin (Hb)) and plasma (density, proteins) components, but should be similar if capillary permeability and the sampled vein/whole body Hct ratio remain unchanged. METHODS: PVEB was determined in six subjects while fasting or eating on different days, with injection and sampling in the same arm, 4-h extrapolation to time zero and correcting readings with the 620-740 A method. For 93 experiments at altitude, delta%PVEB was obtained similarly from a 3-h extrapolation near the end of a 12-h chamber exposure to 426 mm Hg (-4,880 m =16,000 ft) and at the same time on the preceding control day. RESULTS: Mean PVEB with and without eating was not significantly different (SE of absolute difference = +/- 2.8%). The EB decay curves had significantly more scatter with eating than fasting. The fasting vs. non-fasting values for the single 20-min post-injection point also gave a close comparison (r = +0.97). At altitude the loss in PV measured with EB was significantly greater (delta%PVEB = -6.3%) than losses estimated from Hct-Hb (-2.9%), plasma protein (-3.7%), and plasma density (-3.9%). The expected larger PV loss in subjects tolerant to altitude sickness compared with intolerant ones was most clearly shown by delta%PVEB (8.8%). CONCLUSIONS: Obtaining more samples can offset reproducibility lost by eating. The delta%PVEB were largest and nearest to values previously reported at altitude, perhaps because the single baseline and altitude samples utilized by the other methods are more sensitive to subtle, transient fluctuations in body water and vasomotor tone associated with apprehension, vomiting, fluid intake, and regional vasodilation and constriction.

Adult↗

[Experimental study on changes of sexual hormones in senior males living on high altitude].

OBJECTIVES: To investigate the characteristics of testosterone (T) and estradiol (E2) in senior males living on high altitude METHODS: According to the years of living on 3,100-meter high altitude. 90 senior males who were more than sixty years old were divided into three groups: group 1 (one year on the high altitude, n = 30), group 2 (two years on the high altitude, n = 30) and group 3 (over 10 years on the high altitude, n = 30). Additionally, there was a control group (living on the sea level). Radioimmunoassay technique was used to measure the level of T and E2 in their serum respectively. At the same time, the ratio of T/E2 was also examined. RESULTS: The levels of T, E2 and T/E2 of the three groups were 42.2 +/- 38.5, 70.0 +/- 31.5, 190.3 +/- 73.5 and 44.0 +/- 42.2, 60.6 +/- 28.3, 144.9 +/- 62.0 and 0.96 +/- 0.19, 1.16 +/- 0.11, 1.33 +/- 0.24, respectively. The levels of T, E2 and T/E2 of group 3 increased obviously than those of the other two groups (P < 0.01). CONCLUSIONS: The sexual hormone levels in senior males living on high altitude increase along with the living years.

Aged↗

Effect of altitude on second-generation blood tests to detect erythropoietin abuse by athletes.

BACKGROUND AND OBJECTIVES: ON- and OFF-model scores derived from blood parameters sensitive to erythropoiesis have been shown to be a useful tool to identify athletes who are currently injecting erythropoietin to enhance performance or those who have recently stopped doing so. We investigated changes in blood parameters and model scores during and after exposure to terrestrial and simulated altitudes. DESIGN AND METHODS: We retrospectively evaluated changes in hematologic data collected from 19 elite cyclists who lived and trained 2690 m above sea level for 26-31 days, from six elite Kenyan runners who lived 2100 m above sea level but descended to compete at sea level competitions, and from 39 well-trained subjects who resided at sea level but slept at a simulated altitude of 2650-3000 m for 20-23 days of either consecutive or intermittent nightly exposure. RESULTS: Upon ascent to a terrestrial altitude, ON- and OFF-model scores increased immediately, mainly because of an increase in hemoglobin concentration. Scores had not returned fully to baseline three weeks after return to sea level, because of the persistence of the raised hemoglobin concentration for the ON and OFF scores and a fall in reticulocyte percentage for OFF scores. Effects were smaller or negligible for simulated altitude. For Kenyan runners, ON- and OFF-model scores decreased within seven days of descent to sea level. INTERPRETATION AND CONCLUSIONS: Our results reinforce the notion that caution should be exercised when interpreting blood results from athletes who have recently been exposed to either terrestrial or simulated altitude, and appropriate allowance should be made for the effect of altitude on blood model scores.

Acclimatization↗

Military operations at moderate altitude: effects on physical performance.

The purpose of this study was to examine changes in select anaerobic and aerobic dependent physical performance tasks in U.S. Marines exposured to field operations at moderate altitude. The subjects (N = 16) completed Wingate anaerobic power, submaximal aerobic cycle ergometry, hand grip strength, and push-up tests on three separate occasions. Testing sessions occurred at sea level, at altitude after a 10-day acclimatization period (immediately before field operations), and at altitude immediately after 4.5 days of field operations. Anaerobic power was significantly (p < 0.05) reduced after the field operations at altitude. In contrast, the aerobic cost of doing submaximal exercise was slightly elevated (p < 0.05) after the altitude field operations. No physiologically significant effect was noted for hand grip or push-up results. The findings of this study indicate that field operations at moderate altitude do result in slight, but significant, anaerobic-aerobic performance decrement in U.S. Marines.

Adult↗

[Pathophysiology, prevention and therapy of altitude pulmonary edema].

Alveolar hypoxia and resulting tissue hypoxia initiates the pathophysiological sequence of high altitude pulmonary edema (HAPE). Very rapid ascent to high altitude without prior acclimatization results in HAPE, even in subjects with excellent tolerance to high altitude. Upon acute altitude exposure, HAPE-susceptible individuals react with increased secretion of norepinephrine, epinephrine, renin, angiotensin, aldosterone and atrial natriuretic peptide. In response to exercise at high altitude, subjects developing acute mountain sickness and HAPE secrete more aldosterone and antidiuretic hormone than subjects who remain well. This results in sodium and water retention, reduction of urine output, increase in body weight and development of peripheral edemas. The hypoxic pulmonary vascular response is enhanced in HAPE-susceptible subjects, thus favouring the development of severe pulmonary hypertension on exposure to high altitude. It has been postulated that uneven pulmonary vasoconstriction enhances filtration pressure in non-vasoconstricted lung areas, leading to interstitial and alveolar edema. The high protein content of the edema fluid in HAPE characterizes this edema as a permeability edema. The prophylactic administration of nifedipine prevents the exaggerated pulmonary hypertension of HAPE-susceptible subjects upon rapid ascent to 4559 m and thus prevents HAPE in most cases. This finding illustrates the crucial role of hypoxic pulmonary hypertension in the development of HAPE. The causal treatment of HAPE is descent, evacuation and administration of oxygen. Treatment of HAPE patients with nifedipine results in a reduction of pulmonary artery pressure, clinical improvement, increased oxygenation, decrease of the alveolar arterial oxygen gradient and progressive clearing of pulmonary edema on chest x-ray. Thus nifedipine offers a pharmacological tool for the treatment of HAPE.

Aldosterone↗

[Who gets altitude sickness?].

The author discusses factors promoting the occurrence of acute mountain sickness and high altitude pulmonary edema. The level of altitude as well as the speed of ascent are important determinants and can be influenced by behaviour. A low hypoxic ventilatory drive presents a constitutional factor predisposing to acute mountain sickness and high altitude pulmonary edema. Individuals susceptible to high altitude pulmonary edema also show increased hypoxia vasoconstriction of pulmonary arterioles. The importance of an exaggerated hypoxic pulmonary vascular response for the pathogenesis of high altitude pulmonary edema is demonstrated by the observation that this illness can be treated or prevented by lowering pulmonary artery pressure with nifedipine. In most cases, however, acute mountain sickness and high altitude pulmonary edema can be prevented without the help of drugs, by adjusting the speed of ascent to the degree of susceptibility to these illnesses.

Altitude Sickness↗

Altitude decompression sickness between 6858 and 9144 m following a 1-h prebreathe.

INTRODUCTION: The zero prebreathe altitude threshold for developing 5% decompression sickness (DCS) symptoms in men has been reported to be 6248 m (20,500 ft). However, such an altitude threshold when 1 h of oxygen prebreathe is used has not been well documented and was the primary purpose of this study. METHODS: The 51 male human subjects were exposed to 9144 m (30,000 ft), 8382 m (27,500 ft), 7620 m (25,000 ft), and/or 6858 m (22,500 ft) for 8 h. They were monitored for symptoms of DCS and venous gas emboli (VGE). RESULTS: DCS symptom incidence after 4 h of exposure decreased with exposure altitude from 87% at 9144 m to 26% at 6858 m. VGE were lower during the 4-h 6858-m exposures (32%) than at the higher altitudes (76-85%). The symptom incidences during the first 4 h of exposure were lower at 6858 m and 7620 m following a 1-h prebreathe as compared with analogous zero-prebreathe exposures. There were no differences between incidences of VGE or DCS at any of the four altitudes after 8 vs. 4 h of exposure. CONCLUSION: The altitude threshold for 5% DCS symptoms is below 6858 m after 1 h of prebreathe. However, during 6858-m and 7620-m exposures, a 1-h prebreathe is highly beneficial in reducing DCS incidence and delaying the onset of DCS, keeping the incidence to less than 6% during the first 90 min of exposure. Use of 4-h vs. 8-h exposures does not appear to underestimate DCS risk at or above 7620 m.

Adult↗

Body structure and respiratory efficiency among high altitude Himalayan populations.

To understand the morphological and physiological variations among the temporary and permanent residents of high altitude, this study was undertaken at Leh, Ladakh. It is situated at 3500 m (11500 feet) above sea level, the mean barometric pressure was 500 tors and air temperature varied from 2 degrees C to 20 degrees C. The highland Tibetans showed broadest chest and most developed musculature closely followed by Ladakhi Bods. These high altude natives also displayed significantly higher value of vital capacity, forced vital capacity, and inspiratory capacity. The better respiratory efficiency observed among high altitude residents indicates higher degree of adaptation to high altitude hypoxia. Temporary residents were observed to be tallest and fattest with lower trunk fat predominance of all the four groups and showed narrowest chest and lower respiratory efficiency as compared to high altitude natives. The duration of stay at high altitude has clearly brought about a perceptible difference in body dimensions and respiratory functions of various groups of adult males studied at same altitude.

Adaptation, Physiological↗

Oxygen transport during exercise at altitude and the lactate paradox: lessons from Operation Everest II and Pikes Peak.

It seems unlikely that oxygen-limited metabolism explains the increased lactate concentrations in blood or muscle during exercise at high altitude compared with sea level values because: 1. Even marked hypoxia equivalent to that at the summit of Mt. Everest may not be sufficiently severe to impair function or to impair muscle oxidative metabolism markedly during exercise; 2. At this very high altitude, muscle hypoxemia is probably not the limiting factor for exercise performance; other systems, i.e., the cerebral cortex [24, 33], probably fail before hypoxemia impairs muscle metabolism; 3. The traditional view of oxygen-limited aerobic metabolism during exercise at high altitude does not explain a long-standing dilemma in altitude physiology, the lactate paradox (in which blood lactate accumulation during exercise is increased on arrival at high altitude but falls with acclimatization), because the lactate fall is independent of muscle oxygenation; 4. Net lactate release by the leg during exercise is independent of oxygenation; 5. Kinetic studies show that lactate appearance and disappearance are closely linked and both increase with acute altitude exposure and decrease with acclimatization; 6. Lactate appearance rate is strongly correlated with, and may be influenced by, the extent of beta-adrenergic stimulation; 7. The beta-adrenergic stimulation may be, in part, determined by the degree of arterial oxygenation.

Acclimatization↗

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.

Adult↗

[The role of heparin and tissue-type plasminogen activator in the adaptation of the hemostatic system to high altitude].

The role of endogenous heparin and tissue-type plasminogen activator in the middle-period (25 days) adaptation of haemostasis to high altitude (altitude 3200 m) and formation or "high-altitude hypocoagulation" was studied in the experiments on white rats. It was observed that the formation of "high-altitude hypocoagulation" is connected with an increase of heparin and tissue-type plasminogen activator level due to its release from must and endothelial cells to the bloodstream. Histochemical analysis showed that at the course of adaptation to high altitude the increase in blood heparin level was caused by the stimulation of must cells secretory activity. The endothelium of lung vessels is the main source of tissue-type plasminogen activator release into the blood. The existence of interconnection between the changes in haemostasis and stimulation of angiogenesis at high altitude is proposed.

Adaptation, Physiological↗

Altitude decompression sickness: hyperbaric therapy results in 528 cases.

We reviewed 528 cases of decompression sickness (DCS) resulting from altitude exposure (either aircraft or altitude chamber) during the period 1 January 1977 through 31 December 1986, and treated with hyperbaric therapy. Data collected include age, sex, date and place of origin, duty position, type of exposure, altitude, diagnosis, treatment, and result. Analysis of the data described maximum altitudes of exposure, time to onset of symptoms, diagnosis, and the treatment tables used. Significant results include an increased incidence of altitude DCS requiring hyperbaric therapy among females (relative risk for females is 4.3 times that of males), no significant difference in incidence rates between duty positions in the altitude chamber exposures reviewed, and confirmation of the efficacy of hyperbaric oxygen therapy.

Adult↗

Age-dependent influence of a moderate altitude (1,350 m) on the rat cardiopulmonary system.

The aim of the study was to determine whether a moderate altitude (1,350 m, Strbské Pleso, High Tatras) would act as a hypoxic stimulus on the cardiopulmonary system of young and adult rats. We used three experimental groups of animals differing in the duration of time for which they were kept at the given altitude (60 and 120 days) and the age at which they were acclimatized (from the 5th and the 60th day of life). The controls were kept at an altitude of 200 m (Prague). We found that an altitude of 1,350 m produced a significant increase in blood pressure in the lesser circulation; this response did not depend on the animals' age. Right ventricular enlargement occurred at the same time and was more pronounced in rats which had been acclimatized from infancy. The systemic blood pressure fell mildly, but significantly, only in animals exposed to altitude from adulthood; elevation of the haematocrit was likewise recorded only in this group. The results show that even a moderate altitude influences the cardiopulmonary system of the rat in a manner characteristic of the effect of chronic hypoxic hypoxia.

Acclimatization↗

Altitude hypocapnia at 2,800 m does not affect development of the chicken embryo.

Eggs laid at sea level and incubated at high altitude are subject to hypoxia, hypocapnia, and excessive water loss, resulting in retarded development and poor hatchability. The effect of altitude hypocapnia alone was studied in two series of eggs incubated at a simulated altitude of 2,800 m, PB = 542 torr; the incubator was ventilated at a low flow rate with O2-enriched air; the relative humidity was 70-74%, PH2O 34.4-36.4 torr; ambient PO2 about 130 torr at the plateau stage. In the normocapnic series, CO2 produced by the embryos increased ambient PCO2 to 14 torr at 18-19 days; altitude hypoxia, hypocapnia, and excessive water loss were practically compensated for. In the hypocapnic series, ambient CO2 was almost completely absorbed by soda lime, so that only hypocapnia was not compensated for. In 17-19-day eggs with similar sea level mass specific shell conductances [sp GH2O = 0.26-0.25 mg [g.d.torr]-1], the measured PO2 in the gas space, hematocrit, hemoglobin concentration, lengths of beak and third toe, and masses of body and brain were essentially the same in both series. The masses of heart, liver, and left wing were slightly different on day 19. Altitude hypocapnia alone, without altitude hypoxia and excessive water loss, had almost no significant effect on the embryos' development and hatchability.

Altitude↗

Age, alcohol, and simulated altitude: effects on performance and breathalyzer scores.

Trained men in two age groups, 30-39 (n = 12) and 60-69 (n = 13), each performed at the Multiple Task Performance Battery in four separate full-day sessions with and without alcohol (2.2 ml of 100-proof vodka per kilogram of body weight) at ground level and at a simulated altitude of 12,500 ft (3,810 m). Subjects breathed appropriate gas mixtures through oxygen masks at both ground level and altitude. Mean breathalyzer readings peaked near 88 mg% and did not differ between age groups or altitude conditions. Younger subjects performed better than older subjects; performance of both age groups was significantly impaired by alcohol but these adverse effects were greater for the older subjects. No significant effects on performance were obtained due to altitude or to the interaction of altitude with alcohol. These results and those from several other studies suggest that prevalent views regarding the nature of the combined effects of alcohol and altitude on blood alcohol levels and on performance need to be redefined.

Adult↗

Altitude, low birth weight, and infant mortality in Colorado.

A decrease in birth weight occurs at high altitude, but its relationship to infant mortality is unclear. We examined Colorado vital statistics recorded from 1979 through 1982 to determine whether high altitude increased infant mortality and whether decreased birth weight contributed to the mortality observed. Retardation of intrauterine growth reduced birth weight and doubled the frequency of low-birth-weight infants from the lowest (915 to 1523 m [3000 to 4999 ft]) to the highest (greater than or equal to 2744 m [greater than or equal to 9000 ft]) altitude in the state. Low birth weight increased mortality risk, but the mortality risk of low birth weight was decreased at high compared with low altitudes, resulting in similar infant mortality rates throughout the state. This finding differed from that of 1969 through 1973 when infant mortality doubled at high altitude. A 46% infant mortality reduction had occurred statewide over the ten years due chiefly to decreased mortality risk for preterm low-birth-weight infants. This reduction, particularly pronounced at high altitude, might have been due to better identification and transport of high-risk pregnancies to hospitals with tertiary neonatal treatment centers.

Altitude↗