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PubMed1981

Variability of oxygen affinity of blood: human subjects native to high altitude.

Whole blood O2 equilibrium curves (OEC) were measured in 46 Peruvians native to high altitude (4,540 m) and in 25 sea-level controls. A method was employed that records the entire OEC from 0 to 150 Torr with constant pH and PCO2. The data were analyzed by fitting the Adair equation describing the successive oxygenation of hemoglobin. At pH 7.4 the PO2 at which hemoglobin is half-saturated with O2 (P50) was significantly higher in the high-altitude population (31.2 +/- 1.9 Torr) than in controls (29.2 +/- 1.8 Torr, P less than 0.001). The acid-base status of the high-altitude subjects, however, was that of compensated respiratory alkalosis (plasma pH 7.439 +/- 0.065), and when the P50's were corrected to the subjects' plasma pH the values (30.1 +/- 2.2 Torr) could no longer be distinguished from the controls. We conclude that, on the average, increased P50 resulting from increased red cell 2,3-diphosphyoglycerate concentration at high altitude is offset by compensated respiratory alkalosis with the net result that the position of the OEC more closely approaches that of sea-level humans than has hitherto been thought. Considerable variation exists in P50, both at sea level and high altitude. This variation might have important consequences for acclimatization and survival under adverse environmental conditions.

2,3-Diphosphoglycerate↗
PubMed1982

Man at extreme altitude.

The history of man's attempts to learn more about the physiology of extreme altitudes is briefly reviewed. The earliest exploits were by balloonists who were often exposed to very severe hypoxia, sometimes with fatal consequences. A turning point was the work by Paul Bert using low-pressure chambers; he was able to prove that the deleterious effects of low barometric pressures were caused by the low PO2, though other explanations for mountain sickness such as a low aterial PCO2 continued to be promoted for some time. Many early physiologists believed that active secretion of oxygen by the lungs was necessary to explain man's tolerance of extreme altitudes. Indeed, Haldane championed this view until his death in 1936, though strong evidence to the contrary had accumulated since the work of Krogh and others in the first decade of the century. High climbs by mountaineers have stimulated much interest in the physiology of severe hypoxia. Norton reached over 8,500 m on Mt. Everest in 1924, but the summit was not attained without supplementary oxygen until 1978--the last 300 m took 54 years! This suggests that the summit, altitude 8,848 m, is very near the limit of human tolerance, and predictions based on maximal work levels measured at lower altitudes are consistent with this. The American Medical Research Expedition to Everest, 1981, was specifically planned to obtain data on human physiology at extreme altitudes, and a number of measurements were made over 8,000 m, including some on the summit itself. It is apparent that the mountain can be climbed without supplementary oxygen only because the barometric pressure at the summit is not as low as has often been predicted, and because of the extreme hyperventilation that man develops under these conditions.

Altitude↗
PubMed1982

Effect of change in P50 on exercise tolerance at high altitude: a theoretical study.

Acclimatization to altitude often results in a rightward shift of the O2 dissociation curve (ODC). However, a left-shifted ODC is reported to increase exercise tolerance in humans at medium altitude and increase survival in rats breathing hypoxic gas mixtures. We examined this paradox using a computer model of pulmonary gas exchange. A Bohr integration procedure allowed for alveolar-capillary diffusion. When diffusion equilibration was complete, mixed venous (PVO2) and arterial PO2 fell as O2 consumption (VO2) was increased, but PVO2 approached a plateau. Under these conditions a right-shifted ODC is advantageous (higher PVO2) at all but very high altitudes. However, diffusion limitation of O2 transfer may occur at any altitude if VO2 is increased sufficiently. If this occurs, a left-shifted ODC results in higher calculated VO2max (compared with the standard ODC). Further, diffusion limitation always occurs at a lower VO2 with a right-shifted ODC than with a left-shifted ODC. We conclude that whether a leftward or rightward shift in the ODC is advantageous to gas exchange at altitude depends on the presence or absence of diffusion limitation.

Altitude↗
PubMed1983

Fluid and electrolyte homeostasis during prolonged exercise at altitude.

The combined effect of exercise and altitude on fluid and electrolyte homeostasis was studied over 13 days on six male subjects eating a diet with constant sodium and potassium content. During the first 4 and last 4 days subjects were semisedentary at an altitude of 900 m. In the middle 5 days subjects exercised by hill walking for about 7 h daily at altitudes between 2,678 and 3,629 m. There was a retention of sodium (mean of 202 mM by the end of the exercise-altitude period) and a small retention of water (mean of 0.49 liters). Plasma volume increased by 0.76 liters and packed cell volume fell from a mean of 44.5 to 41.8%. There was no change in plasma sodium concentration. The retention of sodium implies an expansion in the extracellular space of 1.44 liters at the expense of the intracellular space, which decreased by a calculated 1.05 liters. These changes are similar to those resulting from comparable exercise at sea level and opposite to the effect of altitude on resting subjects.

Adult↗
PubMed1983

Effect of prolonged exercise at altitude on the renin-aldosterone system.

The combined effect of exercise and altitude on the renin-aldosterone system was studied in six male subjects on a fixed diet. After 4 control days at rest and at low altitude, subjects ascended to 3,100 m and took about 7 h exercise daily for 5 days. There followed a 4-day recovery period at low altitude. Daily blood samples were taken for estimation of plasma renin activity (PRA), plasma aldosterone concentration (PAC), and angiotensin converting-enzyme (ACE) activity. Results showed a maximal rise in PRA and PAC with exercise at altitude maximal on the first 2 days. ACE activity fell by 23% at altitude. Compared with similar exercise at sea level, the rise in PAC was comparable but the rise in PRA was four times greater, indicating a marked decrease in PAC response to PRA. It is suggested that this loss of sensitivity of PAC to PRA is mediated by the measured reduction in ACE activity.

Adult↗
PubMed1983

Cardiorespiratory response to exercise in men repeatedly exposed to extreme altitude.

The ventilatory and heart rate responses to exercise were studied in four experienced high-altitude climbers at sea level and during a 6-wk period above 4,500 m to discover whether their responses to hypoxia were similar to those of high-altitude natives. Comparison was made with results from four scientists who lacked their frequent exposure to extreme altitude. The climbers had greater Vo2max at sea level and altitude but similar ventilatory responses to increasing exercise. On acute hypoxia at sea level their ventilatory response was less than that of scientists. Their heart rate response did not differ from that of scientists at sea level, but with acclimatization the reduction in response was significantly greater. Alveolar gas concentrations were similar after acclimatization, but climbers achieved these changes more rapidly. The increase in hematocrit was similar in the two groups. It is concluded that these climbers, unlike high-altitude residents, have cardiorespiratory responses to exercise similar to those of other lowlanders except that their ventilatory response was lower and the reduction in their heart rate response was greater.

Adult↗
PubMed1984

Strength and cycle time of high-altitude ventilatory patterns in unacclimatized humans.

Respiration was monitored with magnetometers in 12 healthy supine young adults at sea level and in an altitude chamber at simulated high altitudes of 8,000, 9,000, 11,000, and 14,000 ft. Periodic breathing that was strong enough to include apnea at the time of minimum ventilation was seen in all subjects at high altitude. Cycle time of periodic breathing ranged from 12 to 34 s. On average across the population the incidence of periodic breathing increased with altitude. Cycle time of the periodic pattern increased as strength of the pattern increased. After normalizing to a standard pattern strength, cycle time decreased as altitude increased. The study included two series of experiments, the second occurring 3 wk after the first and involving seven of the same subjects. The standard cycle time at 14,000 ft for each subject in the second series was the same as in the first series to within, on the average, 6%. Each subject studied at 11,000 ft in both series reproduced his cycle time to within, on the average, 9%. The variation of standard cycle time for a given subject is less than the variation across the population, indicating characteristic cycle times for some individuals (one-way analysis of variance, P less than 0.025).

Acclimatization↗
PubMed1985

Headache at high altitude is not related to internal carotid arterial blood velocity.

The cause of headache in persons going to high altitude is unknown. Relatively severe hypoxemia in susceptible subjects could induce large increases in cerebral blood flow that then could initiate the headache. Thus we measured noninvasively, by Doppler ultrasound, changes in internal carotid arterial blood velocity (velocity) in 12 subjects in Denver (1,600 m) and repeatedly up to 7 h at a simulated altitude of 4,800 m (barometric pressure = 430 Torr). Six subjects, selected because of prior history of high-altitude headache, developed comparatively severe headache at 4,800 m, and four subjects, without such history, remained well. Two subjects developed moderate headache. Velocity at 4,800 m did not correlate with symptom development, arterial O2 saturation, or end-tidal PCO2. Also, neither velocity nor blood pressure was consistently elevated above the Denver base-line values. During measurements of hypercapnic ventilatory response in Denver, velocity increased linearly with end-tidal PCO2, confirming that our Doppler method could demonstrate an increase. Also, 30 min of isocapnic or poikilocapnic hypoxia caused small increases in velocity (+8 and +6%) during the base-line measurement at low altitude. Although even a small increase in cerebral perfusion could contribute to headache symptoms at high altitude, cerebral blood flow does not appear to play a primary role.

Adult↗
PubMed1986

Physiological profile of world-class high-altitude climbers.

The functional characteristics of six world-class high-altitude mountaineers were assessed 2-12 mo after the last high-altitude climb. Each climber on one or several occasions had reached altitudes of 8,500 m or above without supplementary O2. Static and dynamic lung volumes and right and left echocardiographic measurements were found to be within normal limits of sedentary controls (SC). Muscle fiber distribution was 70% type I, 22% type IIa, and 7% type IIb. Mean muscle fiber cross-sectional area was significantly smaller than that of SC (-15%) and of long-distance runners (LDR, -51%). The number of capillaries per unit cross-sectional area was significantly greater than that of SC (+ 40%). Total mitochondrial volume was not significantly different from that of SC, but its subsarcolemmal component was equal to that of LDR. Average maximal O2 consumption was 60 +/- 6 ml X kg-1 X min-1, which is between the values of SC and LDR. Average maximal anaerobic power was 28 +/- 2.5 W X kg-1, which is equal to that of SC and 40% lower that that of competitive high jumpers. All subjects were characterized by resting hyperventilation both in normoxia and in moderate (inspired O2 partial pressure = 77 Torr) hypoxia resulting in higher oxyhemoglobin saturation levels in hypoxia. The ventilatory response to four tidal volumes of pure O2 was similar to that of SC. It is concluded that elite high-altitude climbers do not have physiological adaptations to high altitude that justify their unique performance.

Adaptation, Physiological↗
PubMed1986

Pulmonary gas exchange in humans exercising at sea level and simulated altitude.

In a previous study of normal subjects exercising at sea level and simulated altitude, ventilation-perfusion (VA/Q) inequality and alveolar-end-capillary O2 diffusion limitation (DIFF) were found to increase on exercise at altitude, but at sea level the changes did not reach statistical significance. This paper reports additional measurements of VA/Q inequality and DIFF (at sea level and altitude) and also of pulmonary arterial pressure. This was to examine the hypothesis that VA/Q inequality is related to increased pulmonary arterial pressure. In a hypobaric chamber, eight normal subjects were exposed to barometric pressures of 752, 523, and 429 Torr (sea level, 10,000 ft, and 15,000 ft) in random order. At each altitude, inert and respiratory gas exchange and hemodynamic variables were studied at rest and during several levels of steady-state bicycle exercise. Multiple inert gas data from the previous and current studies were combined (after demonstrating no statistical difference between them) and showed increasing VA/Q inequality with sea level exercise (P = 0.02). Breathing 100% O2 did not reverse this increase. When O2 consumption exceeded about 2.7 1/min, evidence for DIFF at sea level was present (P = 0.01). VA/Q inequality and DIFF increased with exercise at altitude as found previously and was reversed by 100% O2 breathing. Indexes of VA/Q dispersion correlated well with mean pulmonary arterial pressure and also with minute ventilation. This study confirms the development of both VA/Q mismatch and DIFF in normal subjects during heavy exercise at sea level. However, the mechanism of increased VA/Q mismatch on exercise remains unclear due to the correlation with both ventilatory and circulatory variables and will require further study.

Adult↗
PubMed1986

Nocturnal periodic breathing at altitudes of 6,300 and 8,050 m.

Nocturnal periodic breathing was studied in eight well-acclimatized subjects living at an altitude of 6,300 m [barometric pressure (PB) 350-352 Torr] for 3-5 wk and in four subjects during one night at 8,050 m altitude (PB 281-285 Torr). The measurements at 6,300 m included tidal volume by inductance plethysmography, arterial O2 saturation by ear oximetry (calibrated by arterial blood samples), electrocardiogram (ECG), and electrooculogram. At 8,050 m, periodic breathing was inferred from the cyclical variation in heart rate obtained from a night-long ECG record. All subjects at 6,300 m altitude showed well-marked periodic breathing with apneic periods. Cycle length averaged 20.5 s with 7.9 s apnea. Minimal arterial O2 saturation averaged 63.4% corresponding to a PO2 of approximately 33 Torr, i.e., approximately 6 Torr lower than the normal value at rest during daytime. This was probably the most severe hypoxemia of the 24-h period. At 8,050 m altitude, the cycle length averaged 15.4 s, much longer than predicted by a theoretical model. Cyclical variations in heart rate caused by periodic breathing occurred in all subjects, but abnormal cardiac rhythms such as ventricular premature contractions were uncommon. The severe arterial hypoxemia caused by periodic breathing may be an important determinant of tolerance to these great altitudes.

Adult↗
PubMed1986

Control of ventilation in extreme-altitude climbers.

Ten climbers who participated in the Nepal-Japan Kangchenjunga Expedition (altitude, 8,478-8,586 m) in 1984 were examined for their hypercapnic and isocapnic hypoxic ventilatory responses (HCVR and HVR) at sea level before and after the expedition. Five climbers who reached an altitude higher than 8,000 m, [designated high-performance climbers (HPC)] exhibited significantly higher HVR than five climbers who did not [low-performance climbers (LPC)]. On the other hand, no significant difference in HCVR was seen between HPC and LPC. Our results were in agreement with the findings reported by Schoene et al. (J. Appl. Physiol. 56: 1478-1483, 1984) obtained in the American Medical Research Expedition to Everest in 1981. Significant depression in HVR in five climbers was found even 35-40 days after the expedition, which was accompanied by decreased arterial partial pressure of CO2 and increased pH at rest. Hence, the effect of altitude acclimatization in the climbers exposed to extreme altitude may have still persisted at the time of the postexpedition study. Our results confirmed that HRV evaluated at sea level may be used as an indicator of a climber's capability at great high altitude.

Adult↗
PubMed1987

Operation Everest II: man at extreme altitude.

Rapid ascent to high altitude may cause serious problems for climbers, skiers, and aviators. In contrast, gradual ascent enables humans to function where the unacclimatized cannot. To examine changes in the O2 transport system that produce acclimatization, eight men were taken in a decompression chamber (without other stresses experienced on high mountains) to a simulated altitude of 8,840 m (29,028 ft, ambient PO2 = 43 Torr) in 40 days. Maximal O2 uptake fell to 1.2 l/min, and arterial PO2 and PCO2 were 30 and 11 Torr, respectively, with arterial pH of 7.56. Many sophisticated studies were done: Swan-Ganz catheterization and inert gas diffusion studies at three altitudes showed that normal cardiac function persisted, pulmonary vascular resistance increased and at extreme altitude was not lowered by O2, and pulmonary ventilation-perfusion mismatch increased, though variably. This appears to be an important factor limiting performance at extreme altitude. This paper presents the background, general approach, and a summary of major observations reported in detail in other papers.

Acclimatization↗
PubMed1992

Heart and lung alterations in neonatal rats exposed to CO or high altitude.

We wished to determine whether cardiac changes produced by CO are related to the development of pulmonary hypertension and whether they are specific for CO or also occur with high-altitude exposure. Newborn male Sprague-Dawley rats were exposed to 500 ppm CO for 32 days (CO) at Detroit, MI or to 11,500-ft simulated altitude at Fort Collins, CO (barometric pressure 495 Torr; 11K); ambient air controls were maintained at Detroit (657 ft, 200 m; AIR) and at Fort Collins (5,000 ft, 1,524 m; 5K). Rats were maintained at Fort Collins after 34 days of age. Hematocrit was elevated to a greater extent in the CO than in the 11K group 2 days postexposure; however, no differences existed 40, 76, or 112 days postexposure. Right ventricle (RV) and left ventricle plus septum (LV + S) mass in CO rats were increased 38.0 and 37.4%, respectively, relative to the AIR group 2 days after CO exposure; RV and LV + S in the 11K group were increased 55.7 and 9.3%, respectively, relative to the 5K group. Cardiac hypertrophy declined in the CO and 11K groups postexposure but remained significant for the RV, reaching 20.7% above the AIR group (CO) and 29.7% above the 5K group (11K) at 145 days of age. By use of an in vitro preparation, pulmonary vascular resistance (PVR) and pulmonary arterial pressure were significantly increased immediately after altitude but not after CO exposure and remained elevated in adulthood after altitude exposure. PVR was correlated with hematocrit in altitude- but not in CO-exposed rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗
PubMed1993

Cognitive performance and event-related brain potentials under simulated high altitudes.

The effects of hypobaric hypoxia on cognitive processing in humans were studied by recording event-related potentials (ERPs) from the scalp in a go/no-go reaction time (RT) paradigm under various simulated high altitudes. Most subjects indicated abrupt impairment of RT at high altitudes. RTs lengthened in association with changes in latency and amplitude of the N2-P3 components, reflecting sensory discrimination and evaluation processes. Some subjects did not suffer any changes in RT up to an extremely high altitude of 6,000 m. In the latter case, although the N2-P3 components did not undergo any changes, the P3 component was followed by a sequence of negative on-going (frontal maximum) and positive on-going (parietal maximum) slow waves. The amplitudes of these slow waves increased as altitude increased. Although these same waves appeared in the ERPs of subjects who demonstrated the increase in RTs at high altitudes, when the subjects failed in the RT task, both of the slow waves either disappeared or diminished. Such slow waves may be associated with attempts to maintain RTs against the deteriorative effects of hypobaric hypoxia.

Adult↗
PubMed1995

Effect of altitude on uterine artery blood flow during normal pregnancy.

To determine whether uterine blood flow was reduced and indexes of pelvic blood flow distribution altered in normotensive pregnancy at high (3,100 m) compared with low altitude (1,600 m), we measured uterine, common iliac, and external iliac artery blood flow velocities and diameters in women during pregnancy and again postpartum. Pregnancy increased uterine artery diameter, blood flow velocity, and volumetric flow at both altitudes. Uterine artery blood flow velocity was greater (69.0 +/- 2.2 vs. 59.4 +/- 3.0 cm/s; P < 0.005) but diameter was smaller at 3,100 m than at 1,600 m (2.5 +/- 0.3 mm vs. 3.4 +/- 0.2 mm; P < 0.005), resulting in volumetric flow that was one-third lower at week 36 of pregnancy (203 +/- 48 vs. 312 +/- 22 ml/min, respectively; P < 0.01). Pregnancy increased common iliac blood flow velocity and decreased external iliac artery blood flow velocity at both altitudes. The uterine artery received a smaller percent of common iliac flow at 3,100 than at 1,600 m (46 +/- 7 vs. 74 +/- 6%; P < 0.005). Gestational age was similar but birth weight was lower at 3,100 m than at 1,600 m. Among subjects at 1,600 m, variation in uterine blood flow velocity correlated positively with infant birth weight. We concluded that reduced uterine blood flow and altered pelvic blood flow distribution during pregnancy at high altitude likely contributed to the altitude-associated reduction in infant birth weight.

Adult↗
PubMed1996

Augmented hypoxic cerebral vasodilation in men during 5 days at 3,810 m altitude.

The fractional increase in cerebral blood flow (CBF) velocity (VCBF) from the control value with 5-min steps of isocapnic hypoxia and hyperoxic hypercapnia was measured by transcranial Doppler in six sea-level native men before and during a 5-day sojourn at 3,810 m altitude to determine whether cerebral vasoreactivity to low arterial O2 saturation (SaO2) gradually increased [as does the hypoxic ventilatory response (HVR)] or diminished (adapted, in concert with known slow fall of CBF) at altitude. A control resting PCO2 value was chosen each day during preliminary hyperoxia to set ventilation at 140 ml.kg-1.min-1 for this and the parallel HVR study, attempting to establish control cerebrospinal fluid (CSF) and brain extracellular fluid pH values unaltered by acclimatization. The relationship of CBF to SaO2 was nonlinear, steepening at a lower SaO2. A hyperbolic equation was used to describe hypoxic cerebrovascular reactivity: fractional VCBF = x[60/ (SaO2-40)-1], where X is the fractional increase of VCBF at 70%.X rose from 0.346 +/- 0.104 (SD) at sea level to 0.463 +/- 0.084 on altitude day 5 (P < 0.05 by paired t-test, justified by the a priori experimental plan). For comparison with CO2 sensitivity, from these X values, we estimate the rise in CBF in response to a 1% fall in SaO2 at 80% to be 1.30% at sea level and 1.74% after 5 days at altitude. CBF sensitivity to increased end-tidal PCO2 rose from 4.01 +/- 0.62%/Torr at sea level to 5.12 +/- 0.79%/Torr on day 5 (P < 0.05), as expected, at the lower PCO2 due to the logarithmic relationship of PCO2 to CSF pH. This change was not significant after correction to log PCO2. We conclude that the cerebral vascular response to acute isocapnic hypoxia may increase during acclimatization at high altitude. The mechanism is unknown but is presumably unrelated to the parallel carotid chemosensitization that, in these subjects, increased the HVR by 60% in the same 5-day period from 0.91 +/- 0.38 to 1.46 +/- 0.59 l.min-1.% fall in SaO2-1).

Adult↗
PubMed1996

Water balance and acute mountain sickness before and after arrival at high altitude of 4,350 m.

The present study is a first attempt to measure water balance and its components at altitude by using labeled water and bromide dilution and relating the results with acute mountain sickness (AMS). Water intake, total water output, and water output in urine and feces were measured over a 4-day interval before and a subsequent 4-day interval after transport to 4,350 m. Total body water and extracellular water were measured at the start and at the end of the two intervals. There was a close relationship between energy intake and water intake, and the relationship was unchanged by the altitude intervention. Subjects developing AMS reduced energy intake and water intake cor respondingly. The increase in total body water (TBW) in subjects developing AMS was accompanied by a reduction in total water loss. They did not show the increased urine output, compensating for the reduced evaporative water loss at altitude. Subjects showed a significant increase in TBW after 4 days at altitude. Subjects with AMS showed the biggest shifts in extracellular water relative to TBW. In conclusion, fluid retention in relation to AMS is independent of a change in water requirements due to altitude exposure. Subjects developing AMS were those showing a fluid shift of at least 1 liter from the intracellular to the extracellular compartment or from the extracellular to the intracellular compartment.

Adult↗