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PubMed2001

The evidence for hereditary factors contributing to high altitude adaptation in Andean natives: a review.

Humans have occupied the high plateaus and mountain valleys of the Andes and the Himalayas for thousands of years. Although sea level natives can, and often do, travel in these rarefied reaches, there is little doubt that natives born and raised in the "thin" air are better equipped to deal with the reduced availability of oxygen at altitude. What fraction of the hypoxia defense response of high altitude native populations is due to developmental adaptations acquired during growth and what fraction is due to a genetic component reflecting the effects of selective transmission of beneficial genetic variants through hundreds of generations of antecedents is as yet unresolved. This paper summarizes some of the studies that have been undertaken to address this issue in Andean indigenous populations, primarily with respect to those adaptations thought to be involved in the uptake, distribution and utilization of oxygen in children and adults. Specifically, it focuses on changes in chest morphology, pulmonary function, metabolism and hematology. Space constraints preclude extending this review to the large body of literature concerning prenatal and maternal adaptations although this critical stage in development has likely been subject to significant selective pressures. It is apparent that both nature and nurture influence the acquisition of a high altitude phenotype in humans and while there is some evidence for genetic adaptation in Andean highlanders, it is evident that these characteristics are expressed in concert with substantial environment-dependent developmental adjustments.

Acclimatization↗
PubMedDate not supplied

[Reactions of the human cardiovascular system to orthostasis following high altitude adaptation].

Orthostatic tolerance of 18 healthy test subjects (three groups of 6 persons each) who were exposed to an altitude of 2200 m for 12 days and 3200 m for 12 days was studied. The first group subjects remained in bed with minimized motor activity. The second group test subjects rested in bed and twice a day performed physical exercises with energy expenditures of 300 kcal/day. The third group subjects led a normal mode of life. The studies demonstrated that a prolonged restriction of motor activity and a decrease in the blood hydrostatic pressure of healthy test subjects in highlands resulted in their diminished orthostatic tolerance. Physical exercises proved ineffective in that case. The subjects who led a normal mode of life showed increased cardiovascular reactions to orthostatic tests.

Acclimatization↗
PubMed1992

[Functional morphology of resistant pulmonary vessels and capillaries in individual and species adaptation to high altitude].

Morphological and structural rearrangement of resistant pulmonary vessels and alveolar capillaries was assessed in lowland animals (rabbits) during high-altitude adaptation, in aboriginal high-altitude species (yaks, mountain goats) and on native highlanders. Structural adaptive developments in pulmonary vessels and capillaries of high-altitude animals contribute to maximal facilitation of gas diffusion. Similar adaptive changes in pulmonary resistant vessels and capillaries of laboratory animals and in native highlanders are associated with pathological alterations manifest in the elevation of pulmonary vascular resistance, right ventricular hypertrophy, increases in the thickness of the basal membrane of the air-blood barrier. In all the subjects studied the process of high-altitude adaptation is associated with hypertrophy of pulmonary endothelium. The intensification of pulmonary endothelium. The intensification of pulmonary endothelium metabolic activity may be directed at regulation of vascular tone.

Adaptation, Physiological↗
PubMed2000

[Physical exercise impairs the acute stage of adaptation to moderate altitude].

UNLABELLED: A recent study has reported the impairment of high altitude adaptation capacity by physical exercise in a decompression chamber. The aim of our protocol was to evaluate if physical exercise at moderate altitude in the Alps would show a similar effect. 8 alpinists were examined in a randomised cross-over trial at 171 m and at 3000 m altitude under sedentary and under exercise condition (50% maximal workload on the bicycle ergometer four times 30 minutes during the first 6 hours of an 8 hour observation period at each altitude). At the beginning and at the end of each observation period AMS scores and arterial oxygen saturation SaO2 were measured. The differences of the AMS scores and the differences of SaO2 at both test conditions were compared at both altitudes. RESULTS: In comparison to sedentary condition, the differences between initial and final AMS scores at 3000 m altitude were significantly higher (-0.38 +/- 0.52 vs. -1.25 +/- 0.46, diff 0.88, 95% CI 0.58 to 1.17, p < 0.01), as well as the difference between initial and final SaO2 (-0.25 +/- 0.71% vs. 2.25 +/- 1.04%, diff. -2.5%, 95% CI for the diff. -3.59 to -1.41, p < 0.01). AMS score and SaO2 did not change after exercise at 171 m altitude. CONCLUSION: Physical exercise impairs the acute stage of adaptation to moderate altitude. This is mainly due to the exercise-induced exaggeration of arterial hypoxaemia.

Acute Disease↗
PubMed1992

[Prostacyclin-thromboxane imbalance after adrenergic damage of the heart and aorta and its correction with calcium antagonist finoptin and the adaptation to high-altitude climate].

Adrenergic cardiac and aortic lesion was reproduced by using intramuscularly a stress-necrogenic epinephrine dose of 2 mg/kg. Following 24 hours, the levels of malonic dialdehyde (MDA) as a TxA2 marker, were measured in the platelets. The antiaggregability of the aortic wall where PGI2 is synthesized was also examined. The adrenergic lesion was found to impair the platelet function-vascular wall balance, creating the condition for enhancing spontaneous platelet aggregation. This led to 50% death of experimental "lowland" rats. The short-term high-altitude adaptation failed to substantially modify the death rates in adrenergic lesion, though the platelets showed a 30% decrease in MDA generation. The combination of high-altitude adaptation and the calcium antagonist finoptin completely prevented the stress-induced increase in the platelet generation of MDA, a TxA2 marker, which was followed by a drastic reduction (16.6% versus 50%) in sudden death cases among the rats during adrenergic cardiac and aortic lesion.

Adaptation, Physiological↗
PubMed1990

Coronary and myocardial adaptations to high altitude in dogs.

The objective of this study was to determine whether exposure to high altitude (hypoxic hypoxemia) induces coronary and/or collateral growth. Fourteen mongrel dogs were maintained at a simulated altitude of 18,000 ft for 1 mo and 7 dogs maintained for 3 mo. Within 2 days after their sojourn, the following data were obtained at ambient pressure: pulmonary, right heart chamber, and wedge pressures as well as cardiac output. On an isolated heart preparation, coronary and collateral flows were determined; each vessel was injected with a different color tracer; and the heart was sliced, separated by perfusion territories, and examined for myocardial hypertrophy. We found that pulmonary artery pressures in altitude-adapted animals were higher compared with controls, and coronary flow per gram was increased after 1 mo of exposure but not different from control after 3 mo. Collateral flows were not significantly different from that of control animals, and biventricular hypertrophy occurred with right ventricular dominance. Comparing these results with those that we obtained previously from anemic animals, we favor the hypothesis that oxygen availability rather than blood flow velocity is most likely linked to vascular growth.

Adaptation, Physiological↗
PubMed1982

[Adrenoreactivity of the vessels of the small intestine during adaptation to high altitude in the cat].

Responses of the resistance and capacitance vessels of small intestine to adrenergic stimulation and blockade were studied in acute experiments on cats after 3-30 days of high altitude adaptation (the Pamirs, 3370 m). In comparison to control (Dushanbe, 830 m) constrictor responses of the resistance vessels to noradrenaline and adrenaline were significantly increases at high altitude, whereas the dilator responses to beta-stimulator propranolol were obviously reduced. Changes of venous blood outflow from small intestine in response to catecholamines at high altitude exceeded the control values. Pharmacological analysis suggests that the reactivity of alpha-adrenoreceptors of the small intestine resistance and capacitance vessels at high altitude was increased, whereas the beta-reactivity of the resistance vessels was reduced. Crucial shifts of the adrenoreactivity occurred after 3-5 and 14-16 days of the adaptation.

Adaptation, Physiological↗
PubMed1977

[Influence of adaptation to altitude hypoxia and subsequent de-adaptation on the retention of a temporary connection].

Adaptation to simulated altitude hypoxia was followed by a significant increase of the degree of retention of active avoidance of the conditioned reflex. Twenty four hours after the reflex elaboration the adapted rats required only half of conditioned and unconditioned stimulus combinations in the reflex retention test than control ones. This effect was reproduced 1 and 5 days after the cessation of hypoxic training. The obtained increase in the degree of the conditioned reflex retention disappeared during deadaptation 10 and 27 days after the cessation of hypoxic training.

Adaptation, Physiological↗
PubMed1982

[Prevention of postischemic reoxygenation disturbances of heart function by using adaptation to altitude hypoxia].

The influence of adaptation to altitude hypoxia (2100 m) on rat myocardial contractility was examined during transitory ischemia induced by ligation of the descending branch of the left coronary artery and subsequent reperfusion. In control animals and those after adaptation, ischemia caused the same depression of heart function, while during reperfusion, the animals after adaptation, unlike the control ones, showed partial recovery of contractile function. Evaluation of heart function after ischemia and reperfusion demonstrated that the hearts of the animals after adaptation preserve the ability to bear the maximal isometric load on the level attained during adaptation to hypoxia, while the control animals experience substantial disorders of heart function because of ischemia and reperfusion. Thus, adaptation to altitude hypoxia increases the heart resistance to the damages that occur during reoxygenation.

Adaptation, Physiological↗
PubMed2000

[Respiratory adaptation to altitude and risk factors due to respiratory illnesses].

Adaptation to altitude is a complex ability of the organism which involves primarily the cardiovascular and respiratory system in order to increase the oxygen supply for body tissues. Cardiovascular adaptations to rapid altitude challenge are regulated sympathetically and manifest themselves first of all as variations of cardiac output, systolic blood pressure and heart rate at rest. However, respiration plays an important role in compensating hypobaric hypoxia at altitude. The hypoxic ventilatory response (HVR) to alveolar hypoxia expressed as alveolar hyperventilation happens within a very short period of exposure to hypoxic conditions. This immediate adaptation response is followed by the acclimatization period, which encompasses longer lasting compensation processes such as the increase of blood hemoglobin concentration improving the arterial oxygen content. This final stage of adaptation is reached within days or weeks of persisting exposure and will vary somewhat depending on the degree of altitude. For healthy, acclimatized individuals the oxygen supply to the organism does not limit the exercise performance at moderate altitudes and higher. However, above 5000 meters (15,000 ft) long term adaptation cannot occur because oxygen-diffusion becomes a limiting factor to physical exercise capacity. Altitude-related disorders are contributing significantly to the morbidity and mortality of non-acclimatized individuals. Subjects already suffering from symptomatic underlying respiratory disease and hypoxemia at rest have a higher risk and incidence of altitude adaptation disorders even at lower altitudes. Therefore, several diseases with impaired respiratory function are contraindicated for any stay at altitude.

Acclimatization↗
PubMed1995

Salt excretory capacity in natives adapted to moderate high altitude living after acute mobilization to sea level.

The sodium excretory capacity of six normal subjects born and raised at moderately high altitude (2600 m) was evaluated at high altitude (HA), and after acute mobilization to sea level (SL). The ability of these individuals to respond to an acute salt load was evaluated by infusing a volume of 100 ml.m-2 body surface area (BSA) of 5% sodium chloride solution over a 30-min time period in both experimental conditions. HA natives were able to excrete a significantly greater salt load at HA than at SL (41.8% vs. 31.6%, respectively, p < 0.05) in 3 h. No changes in plasma atrial natriuretic factor (ANF) concentration were found in either experimental condition. Despite an increase in serum osmolality, no vasopressin (AVP) response was noted either at HA or SL. No correlation between serum AVP levels and urine c-AMP concentrations was found. The enhanced excretory response to a salt load at HA was not explained by the measured hormonal changes. The lack of AVP response to increased serum osmolality, both at HA and SL, in high altitude adapted subjects is presently unexplainable.

Adaptation, Physiological↗
PubMed2001

Genetic approaches to understanding human adaptation to altitude in the Andes.

Despite the initial discomfort often experienced by visitors to high altitude, humans have occupied the Andean altiplano for more than 10000 years, and millions of people, indigenous and otherwise, currently live on these plains, high in the mountains of South America, at altitudes exceeding 3000 m. While, to some extent, acclimatization can accommodate the one-third decrease in oxygen availability, having been born and raised at altitude appears to confer a substantial advantage in high-altitude performance compared with having been born and raised at sea level. A number of characteristics have been postulated to contribute to a high-altitude Andean phenotype; however, the relative contributions of developmental adaptation (within the individual) and genetic adaptation (within the population of which the individual is part) to the acquisition of this phenotype have yet to be resolved. A complex trait is influenced by multiple genetic and environmental factors and, in humans, it is inherently very difficult to determine what proportion of the trait is dictated by an individual's genetic heritage and what proportion develops in response to the environment in which the person is born and raised. Looking for changes in putative adaptations in vertically migrant populations, determining the heritability of putative adaptive traits and genetic association analyses have all been used to evaluate the relative contributions of nurture and nature to the Andean phenotype. As the evidence for a genetic contribution to high-altitude adaptation in humans has been the subject of several recent reviews, this article instead focuses on the methodology that has been employed to isolate the effects of 'nature' from those of 'nurture' on the acquisition of the high-altitude phenotype in Andean natives (Quechua and Aymara). The principles and assumptions underlying the various approaches, as well as some of the inherent strengths and weaknesses of each, are briefly discussed.

Adaptation, Physiological↗
PubMed1982

[Intensity of RNA synthesis and the DNA content in the myocardium of newborn rats during adaptation to altitude hypoxia].

Newborn rats were exposed to staged adaptation to altitude hypoxia in a pressure chamber at an atmospheric pressure corresponding to an altitude from 2000 to 9000 m. The time course of changes in the synthesis of RNA and DNA by the nuclei of muscle and connective tissue cells of the heart were studied by light autoradiography with the use of 3H-5-uridine and 3H-thymidine. In the course of early postnatal ontogenesis adaptation to altitude hypoxia was demonstrated to be accompanied by the intensified synthesis of nucleic acids by muscle and non-muscle cells of the heart, which is regarded as a compensatory-adaptation reaction of the myocardium to hyperfunction under the test experimental conditions.

Adaptation, Physiological↗