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Alterations in enzymes involved in fat metabolism after acute and chronic altitude exposure.

The purpose of this study was to examine the effect of acute (24 h) and chronic (5 wk) hypobaric hypoxic exposure equivalent to a simulated altitude of 4,300 m (446 mmHg) on the enzymes of fat metabolism. Heart, liver, and skeletal muscle were taken from 32 male Sprague-Dawley rats. Altitude exposure did not affect the activity of citrate synthase in any of the tissues, suggesting that mitochondrial content was unchanged. Carnitine palmitoyltransferase-I (CPT-I) activity was significantly reduced in the heart by both acute and chronic high altitude exposure compared with controls. A similar reduction was found for CPT-I activity in extensor digitorum longus after acute and chronic exposure compared with control animals. CPT-I activity was not affected by altitude exposure in the soleus muscle or the liver. 3-Hydroxyacyl-CoA dehydrogenase (beta-HAD) activity was significantly depressed in the hearts of chronically exposed animals compared with controls. No difference between acute and control animals was found in the heart for beta-HAD activity. Liver beta-HAD activity was also significantly decreased in the acclimatized as well as in the acute animals compared with the control group. Quadriceps beta-HAD activity was reduced for the chronic animals only compared with controls. These data suggest that acclimatization to high altitude selectively decreases key enzymes in fat utilization and oxidation in the heart, liver, and select skeletal muscles.

3-Hydroxyacyl CoA Dehydrogenases↗

Interleukin-6 response to exercise and high-altitude exposure: influence of alpha-adrenergic blockade.

Interleukin-6 (IL-6), an important cytokine involved in a number of biological processes, is consistently elevated during periods of stress. The mechanisms responsible for the induction of IL-6 under these conditions remain uncertain. This study examined the effect of alpha-adrenergic blockade on the IL-6 response to acute and chronic high-altitude exposure in women both at rest and during exercise. Sixteen healthy, eumenorrheic women (aged 23.2 +/- 1.4 yr) participated in the study. Subjects received either alpha-adrenergic blockade (prazosin, 3 mg/day) or a placebo in a double-blinded, randomized fashion. Subjects participated in submaximal exercise tests at sea level and on days 1 and 12 at altitude (4,300 m). Resting plasma and 24-h urine samples were collected throughout the duration of the study. At sea level, no differences were found at rest for plasma IL-6 between groups (1.5 +/- 0.2 and 1.2 +/- 0.3 pg/ml for placebo and blocked groups, respectively). On acute ascent to altitude, IL-6 levels increased significantly in both groups compared with sea-level values (57 and 84% for placebo and blocked groups, respectively). After 12 days of acclimatization, IL-6 levels remained elevated for placebo subjects; however, they returned to sea-level values in the blocked group. alpha-Adrenergic blockade significantly lowered the IL-6 response to exercise both at sea level (46%) and at altitude (42%) compared with placebo. A significant correlation (P = 0.004) between resting IL-6 and urinary norepinephrine excretion rates was found over the course of time while at altitude. In conclusion, the results indicate a role for alpha-adrenergic regulation of the IL-6 response to the stress of both short-term moderate-intensity exercise and hypoxia.

Adrenergic alpha-Agonists↗

Strenuous physical exercise inhibits granulocyte activation induced by high altitude.

To test the hypothesis of whether strenuous physical exercise inhibits neutrophils that can get activated by hypobaric hypoxia, we analyzed the effects of both high altitude and strenuous exercise alone and in combination on potentially cytotoxic functions of granulocytes in healthy volunteers (n = 12 men; average age 27.6 yr; range 24-38 yr). To this end, a field study was prospectively performed with an open-labeled within-subject design comprising three protocols. Protocol I (high altitude) involved a helicopter ascent, overnight stay at 3,196 m, and descent on the following day. Protocol II (physical exercise) involved hiking below an altitude of 2,100 m with repetitive ascents amounting to a total ascent to that of protocol III. Protocol III (combination of physical exercise and high altitude) involved climbing from 1,416 to 3,196 m, stay overnight, and descent on the following day. In protocol I, number of granulocytes did not change, but potentially cytotoxic functions of cells (CD18 expression and superoxide production) were early and significantly upregulated. In protocol II, subjects developed granulocytosis, but functions of cells were inhibited. In protocol III, granulocytosis occurred at higher values than those observed under protocol II. Potentially cytotoxic functions of cells, however, were strongly inhibited again. In conclusion, high altitude alone, even moderate in extent, can activate potentially cytotoxic functions of circulating granulocytes. Strenuous physical exercise strongly inhibits this activation, which may give protection from an otherwise inflammatory injury.

Adaptation, Physiological↗

Physiological changes at altitude in nonasthmatic and asthmatic subjects.

Exercised-induced asthma is not due to exercise itself per se, but rather is due to cooling and/or drying of the airway because of the increased ventilation that accompanies exercise. Travel to high altitudes is accompanied by increased ventilation of cool, often dry, air, irrespective of the level of exertion, and by itself, this could represent an 'exercise' challenge for asthmatic subjects. Exercise-induced bronchoconstriction was measured at sea level and at various altitudes during a two-week trek through the Himalayas in a group of nonasthmatic and asthmatic subjects. The results of this study showed that in mild asthmatics, there was a significant reduction in peak expiratory flow at very high altitudes. Contrary to the authors' hypothesis, there was not a significant additional decrease in peak expiratory flow after exercise in the asthmatic subjects at high altitude. However, there was a significant fall in arterial oxygen saturation postexercise in the asthmatic subjects, a change that was not seen in the nonasthmatic subjects. These data suggest that asthmatic subjects develop bronchoconstriction when they go to very high altitudes, possibly via the same mechanism that causes exercise-induced asthma.

Adolescent↗

Pulmonary vascular changes in young and aging rats exposed to 5,486 m altitude.

Young (YNG) and middle-aged (MA) male rats were exposed to 5,486 m for durations ranging from 1 to 42 days to determine the effect of age on the progression of polycythemia, right ventricular hypertrophy (RVH), lung vascular muscularization, and pulmonary vascular responsiveness. Other rats were exposed for 42 days at 5,486 m and were then allowed to recover at 1,520 m for periods up to 42 days. The progression and subsequent regression of polycythemia and RVH with altitude exposure were similar for YNG and MA rats. However, YNG rats exhibited vascular muscularization during the altitude exposure, characterized by hypertrophy of smooth muscle cells, whereas MA rats exhibited little or no change in vascular morphology. Lungs from both altitude-exposed YNG and MA rats exhibited blunting of acute hypoxic pulmonary vasoconstriction upon exposure to 5,486 m, with more severe blunting apparent in MA rats. Pressor responses to angiotensin II (AII) were potentiated in lungs from high altitude rats, particularly in the YNG rats, and this increased responsiveness persisted during the recovery period. A positive correlation was found in YNG rats between the degree of vascular muscularization and the pressor response to AII, suggesting that increased muscle mass was partially responsible for the potentiated AII responses. However, MA rats did not exhibit the same correlation for AII, and neither YNG nor MA rats exhibited increased responsiveness to 5-hydroxytryptamine. The results indicate that age influences the morphologic responses to altitude exposure and vascular responsiveness to AII, but does not affect the polycythemic response or the degree of RVH.

Aging↗

Compliance of the respiratory system in infants born at high altitude.

Populations living at high altitude are known to have a number of distinctive physiologic traits, including an increase in lung volume and compliance. We asked whether the factors that result in the increased compliance of high altitude natives were sufficiently expressed in utero that an increase in respiratory system compliance (Crs) could be detected at birth. Measurements were performed at about 1 day after birth on 34 infants born in La Paz, Bolivia (3,600 m, Pb about 495 mm Hg) and 36 born in Santa Cruz (400 m, Pb about 735 mm Hg). All infants were full-term and healthy, with body weights of at least 2,700 g. We measured Crs from expirations within the tidal volume range by the multiple occlusion method. Breathing pattern was measured from the spirometric record, and an index of chest wall distortion was obtained from the ratio of volume and abdominal displacement during spontaneous breathing and relaxations against closed airways. Rib cage and abdomen dimensions did not differ between the two groups. Crs values in Santa Cruz were similar to those previously obtained in Montreal and in other Caucasian infant populations at low altitudes. Crs was 33% and Crs/kg 37% greater (p less than 0.001) in the high altitude group, which included equal numbers of Amerindians and Mestizos of European ancestry. Dynamic elevation of the end-expiratory level was similar in both groups. Ventilation/kg and the distortion ratio were slightly yet significantly higher in the high altitude infants, suggesting an increased ventilatory drive.(ABSTRACT TRUNCATED AT 250 WORDS)

Adaptation, Physiological↗

The effect of ozone and simulated high altitude on murine lung elastin: quantitation by image analysis.

Four subgroups of a colony of 50 mice were housed in environmental chambers supplied by particle- and pollutant-filtered air. The animals were exposed to 0.35 ppm ozone and/or simulated high altitude (380 mm Hg) for four weeks, with exposure 4 1/2 hours/day and 5 days/week. Lung elastin area and alveolar wall area were quantitated by computer assisted image analysis of paraffin embedded sections stained with aldehyde fuchsin and metanil yellow. Compared to the controls, the combination of ozone and simulated high altitude resulted in a 54.5% increase in lung elastin area (p less than 0.005), and simulated high altitude by itself increased elastin area by 19.6% (p less than 0.05). Simulated high altitude with and without ozone exposure also increased alveolar wall area (24.8%, p less than 0.01; and 9.7%, NS, respectively). Ozone exposure alone had a reverse effect: a 16.1% decrease in elastin area (p less than 0.1), and a 6.5% decrease in alveolar wall area (NS). Since an intact lung scaffolding is required for full restoration of injured alveolar epithelium and since intact lung elastin is critical for proper lung compliance, the results suggest that ozone exposure at high altitude is most likely to have an adverse effect on lung structure and function.

Altitude↗

Nasal mucociliary transport is impaired at altitude.

There have been a number of anecdotal reports of rhinitis and nasal obstruction occurring at altitude. To quantify these reports, we investigated nasal obstruction and mucociliary transport in a group of healthy volunteers trekking to Mount Everest Base Camp, Nepal, altitude 5,300 m. Nasal obstruction was estimated by subjective scoring and mucociliary transport was determined by the saccharin method. Subjective assessment showed that nasal obstruction was increased on arrival at 5,300 m in 23 out of 54 subjects, unchanged in 24, and decreased in seven (McNemar's test: chi 2 = 7.5; p < 0.01). The median saccharin time at sea level was 11 min (95% confidence interval (95% CI) 8-17 min) and increased to 60 min (95% CI 27-60 min) on arrival at 5,300 m. Compared to sea level, the saccharin time was prolonged in 25 out of 33 subjects (McNemar's test: chi 2 = 14.7; p < 0.01), and remained prolonged after 2 weeks at altitude (median 60 min; 95% CI 38-60 min). These results confirm the subjective feelings of nasal obstruction and show that nasal mucociliary transport times are increased at altitude. The mechanisms of these findings are not clear, but nasal obstruction may impede breathing and adversely affect performance at altitude.

Adolescent↗

Cough frequency and cough receptor sensitivity to citric acid challenge during a simulated ascent to extreme altitude.

The aim of this study was to determine the frequency of cough and the citric acid cough threshold during hypobaric hypoxia under controlled environmental conditions. Subjects were studied during Operation Everest 3. Eight subjects ascended to a simulated altitude of 8,848 m over 31 days in a hypobaric chamber. Frequency of nocturnal cough was measured using voice-activated tape recorders, and cough threshold by inhalation of increasing concentrations of citric acid aerosol. Spirometry was performed before and after each test. Subjects recorded symptoms of acute mountain sickness and arterial oxygen saturation daily. Air temperature and humidity were controlled during the operation. Cough frequency increased with increasing altitude, from a median of 0 coughs (range 0-4) at sea level to 15 coughs (range 3-32) at a simulated altitude of 8,000 m. Cough threshold was unchanged on arrival at 5,000 m compared to sea level (geometric mean difference (GMD) 1.0, 95% confidence intervals (CI) 0.5-2.1, p=0.5), but fell on arrival at 8,000 m compared to sea level (GMD 3.3, 95% CI 1.1-10.3, p=0.043). There was no relationship between cough threshold and symptoms of acute mountain sickness, oxygen saturation or forced expiratory volume in one second. Temperature and humidity in the chamber were controlled between 18-24 degrees C and 30-60%, respectively. These results confirm an increase in cough frequency and cough receptor sensitivity associated with hypobaric hypoxia, and refute the hypothesis that high altitude cough is due to the inhalation of cold, dry air. The small sample size makes further conclusions difficult, and the cause of altitude-related cough remains unclear.

Adult↗

Can circulatory fetal DNA be used to study placentation at high altitude?

Pregnancy at high altitude (>2700 m) is associated with higher rates of fetal growth restriction and preeclampsia as well as alterations in placentation, including increased villous vascularization and reduced remodeling of maternal spiral arteries. Because circulatory fetal DNA concentrations were shown to be enhanced in pregnancies affected by preeclampsia, we investigated whether similar elevations are also apparent in pregnancies at high altitude by examining ethnic Tibetans and recent migrant Han Chinese residents in Lhasa (altitude 3650 m) as well as Han Chinese residents in Guangzhou (altitude 7 m). Our data from this preliminary study (n = 10/study group) indicate that circulatory fetal DNA levels were significantly higher in the unremarkable pregnancies of Han women who moved to Tibet when compared to Han women at sea level. No significant difference could be discerned between migrant Han Chinese and ethnic Tibetans living in Lhasa. Our data, therefore, suggest that pregnancy at high altitude is associated with an increased liberation of cell-free fetal DNA and that no major ethnic differences are apparent.

Altitude↗

Clinical features of headache at altitude: a prospective study.

BACKGROUND: Headache is the most common nervous system complication at altitude; however, there have been few attempts to characterize clinical features of high-altitude headaches (HAH). OBJECTIVE: To measure prospectively the incidence of HAH and to determine its risk factors and characteristics. METHODS: Members of an expedition to Kanchenjunga base camp in Nepal (5,100 m) were prospectively studied. Subjects were interviewed prior to the trip and while trekking recorded headaches experienced at >3,000 m using a structured questionnaire incorporating International Headache Society (IHS) and acute mountain sickness (AMS) criteria. In addition, clinical features of headaches in 19 trekkers in other groups above 3,000 m were recorded using the same questionnaire. RESULTS: Eighty-three percent (50/60) reported at least 1 HAH (median 2, range 0 to 10). Those who developed HAH were younger (p = 0.04); women and persons with headaches in daily life were more likely to report severe headaches (p = 0.03 and p = 0.07). One hundred thirty-eight HAH, experienced by 69 persons, are described. The mean altitude at which headaches occurred was 4,723 m. Twenty-six percent of headaches woke subjects at night or occurred upon awakening. HAH reported by migraineurs were accompanied by more phonophobia (p = 0.008). There were no IHS accompanying symptoms in 44% of headaches or symptoms of AMS in 52% of headaches. CONCLUSIONS: Headaches are a frequent complication of ascent to altitude. Older age appears to offer some protection, whereas headaches were more severe in women and persons with headaches in daily life. There is a wide clinical spectrum, with some suggesting intracranial hypertension. There is a need for evidence-based diagnostic criteria for headaches at altitude.

Adaptation, Physiological↗

Effects of altitude and temperature on organ phenotypic plasticity along an altitudinal gradient.

Small mammals living in high-altitude environments must endure decreased ambient temperatures and hypoxic conditions relative to sea-level environments. Previously, it was noted that heart, lung and digestive tract masses and blood hematocrit increase along an altitudinal gradient in small mammals. Increases in digestive organ mass were attributed to lower ambient temperatures and greater food intake, and increases in lung mass and hematocrit were attributed to hypoxia, but these assumptions were not explicitly tested. In addition, it was not clear whether changes in heart and lung mass were a function of an increase in organ blood content or of an increase in organ tissue mass. We used captive deer mice (Peromyscus maniculatus sonoriensis) to determine the relative effects of ambient temperature and oxygen concentration (PO2) on organ mass and blood hematocrit along an altitudinal gradient. We also exsanguinated hearts and lungs to determine whether changes in mass were associated with the blood content or with increases in tissue mass. We found that small intestine mass was, as expected, correlated positively with energy intake and negatively with ambient temperature. Heart mass was also negatively correlated with temperature. Lung mass and hematocrit were, as expected, positively correlated with altitude (and PO2). Interestingly, the masses of both small intestine and kidney were negatively correlated with altitude. For kidney mass, this correlation was apparent in cold-exposed mice but not in warm-exposed mice. We also found that changes in both heart and lung mass were mainly a function of changes in tissue mass rather than blood content. These data show that different abiotic variables have different effects on organ masses at high altitude, but also that phenotypic plasticity in response to cold temperatures and low oxygen pressures at altitude is widespread across several different organ systems, suggesting a general elevated whole-body response.

Altitude↗

Metabolic and cardiovascular parameters in type 1 diabetes at extreme altitude.

PURPOSE: The American Diabetes Association states that physical activity can be performed by individuals with Type 1 diabetes. Nevertheless, extreme altitude mountaineering represents a demanding challenge. We present the metabolic and cardiovascular parameters found in individuals with Type 1 diabetes during the ascent to Cho Oyu located at a height of 8201 m. METHODS: Six individuals with Type 1 diabetes and 10 matched controls participated in the expedition. Both groups were evaluated before and after 4 h of trekking for vital indices, blood gases, acute mountain sickness, and metabolic control at 0, 3700, and 5800 m. RESULTS: No difference between the groups was observed in acute mountain sickness scores. There was a progressive elevation in basal heart rates in both groups at increasing altitude while no changes were observed in mean blood pressures. After the 3 h of trekking, a significant increase in heart rate was observed in the controls at 0 m whereas a significant decrease in blood pressure was observed at higher altitude only in controls. HbA1c levels were worse after the expedition in both groups. A progressive increase in insulin requirement was observed in subjects with Type 1 diabetes (38 +/- 6 U x d(-1) at 0 m to 51 +/- 6 at 4200 m, P < 0.001). At an altitude of 5800 m, there was a significant increase in blood lactate concentration, independently of the activity level in the two groups. CONCLUSIONS: At extreme altitude, highly motivated trekkers with Type 1 diabetes but free from long-term complications present metabolic and cardiovascular parameters comparable with those of control subjects despite a worsening in metabolic control. This type of physical activity must be accompanied by careful glucose monitoring.

Adult↗

ACE gene polymorphism and erythropoietin in endurance athletes at moderate altitude.

PURPOSE: To determine the role of the ACE (I/D) gene polymorphism on erythropoietic response in endurance athletes after natural exposure to moderate altitude. METHODS: Erythropoietic activity was measured in 63 male endurance athletes following natural exposure to moderate altitude (2200 m) during 48 h. Erythropoietin (EPO) levels and hemoglobin (Hb) concentrations were measured at baseline and 12, 24, and 48 h after reaching the set altitude. Reticulocyte counts were determined at baseline and 48 h thereafter. Subjects were grouped into two groups (responders and nonresponders) based on significant increase in EPO levels (median: > 16.5 ng x m(-1)) after 24 h at altitude. ACE gene polymorphism was ascertained by polymerase chain reaction (DD, 31 (49%); ID, 24 (38%); II, 8 (13%)). RESULTS: Overall, EPO levels significantly increased at 12 (70%; P = 0.0001) and 24 h (72%; P = 0.0001) above baseline concentration following exposure to 2200 m. Thereafter, EPO concentration decreased at 48 h, but a significant increase in Hb levels (4.6 +/- 4%; P = 0.0001) and reticulocyte count (50.5 +/- 79%; P = 0.0001) was observed at the end of the experiment, suggesting negative feedback. There were no significant differences in EPO and Hb concentration profiles between subjects with DD genotype and those with other genotypes (ID/II). Moreover, responders (N = 42; DD, 50%; ID/II, 50%) and nonresponders (N = 21; DD, 48%; ID/II, 52%) showed a similar erythropoietic profile during the experiment and the ACE gene polymorphism did not influence the time course of the erythropoietic response. CONCLUSIONS: The ACE gene polymorphism does not influence erythropoietic activity in endurance athletes after short-term exposure to moderate altitude.

Adult↗

Do changes in lung function predict high-altitude pulmonary edema at an early stage?

PURPOSE: Ascent to high altitude is associated with alterations in lung function. The mechanisms of these changes and whether they reflect early stages of high-altitude pulmonary edema (HAPE) has been debated. Therefore, we investigated the time course of pulmonary function in relation to hemodynamics and clinical symptoms in mountaineers ascending rapidly to high altitude. METHODS: In 26 unacclimatized subjects we assessed spirometry, single-breath nitrogen washout, diffusing capacity (DLCO), and Doppler echocardiography in Zurich, 490 m, after climbing within 24 h to Monte Rosa, 4559 m, and after one night at 4559 m. RESULTS: Mean (+/- SD) FVC fell from 103 +/- 9% predicted in Zurich to 96 +/- 10% predicted at 4559 m, FEV1/FVC increased from 0.82 +/- 0.06 to 0.84 +/- 0.08, and closing volume increased from 0.35 +/- 0.14 to 0.44 +/- 0.11 L above residual volume (P < 0.05, all changes). On the following day at 4559 m, closing volume remained elevated in 9 of 21 subjects who had a lower DLCO but similar pulmonary artery systolic pressures compared with the remaining 12 subjects (40 +/- 8 vs 43 +/- 7 mm Hg, P = NS). None of the subjects had overt HAPE. CONCLUSION: We conclude that changes in pulmonary function after rapid ascent to high altitude were consistent with interstitial fluid accumulation, but they were not related to changes in pulmonary artery pressure. Individual lung function responses to high-altitude exposure varied largely and did not predict subsequent HAPE.

Adolescent↗

Pulmonary function and hypoxic ventilatory response in subjects susceptible to high-altitude pulmonary edema.

To determine if spirometric changes reflect early high-altitude pulmonary edema (HAPE) formation, we measured the FVC, FEV1, and FEF25-75 serially during the short-term period following simulated altitude exposure (4,400 m) in eight male subjects, four with a history of HAPE and four control subjects who had never experienced HAPE. Three of the four HAPE-susceptible subjects developed acute mountain sickness (AMS), based on their positive Environmental Symptom Questionnaire (AMS-C) scores. Clinical signs and symptoms of mild pulmonary edema developed in two of the three subjects with AMS after 4 h of exposure, which prompted their removal from the chamber. Their spirometry showed small decreases in FVC and greater decreases in FEV1 and FEF25-75 after arrival at high altitude in the presence of rales or wheezing on clinical examination and normal chest radiographs. One of the two subjects had desaturation (59 percent) and tachycardia during mild exercise, and excessive fatigue and inability to complete the exercise protocol developed in the other at 4 h. The six other subjects had minimal changes in spirometry and did not develop signs of lung edema. Further, we measured each subject's ventilatory response to hypoxia (HVR) prior to decompression to determine whether the HVR would predict the development of altitude illness in susceptible subjects. In contrast to anticipated results, high ventilatory responses to acute hypoxia, supported by increased ventilation during exposure to high altitude, occurred in the two subjects in whom symptoms of HAPE developed. The results confirm that HAPE can occur in susceptible individuals despite the presence of a normal or high ventilatory response to hypoxia.

Adult↗

High altitude pulmonary edema and exercise at 4,400 meters on Mount McKinley. Effect of expiratory positive airway pressure.

Breathing against positive expiratory pressure has been used to improve gas exchange in many forms of pulmonary edema, and forced expiration against resistance during exercise has been advocated for climbing at high altitude as a method to optimize performance. To evaluate the effect of expiratory positive airway pressure (EPAP) on climbers with high altitude pulmonary edema (HAPE) and on exercise at high altitude, we studied four climbers with HAPE at rest and 13 healthy climbers during exercise on a bicycle ergometer at 4400 m. We measured minute ventilation (VI, L/min), arterial oxygen saturation (SaO2 percent), end-tidal carbon dioxide (PACO2, mm Hg), respiratory rate (RR), and heart rate (HR) during the last minute of a five minute interval at rest in the climbers with HAPE, and at rest, 300, and 600 kpm/minute workloads on a bicycle ergometer in the healthy subjects. The HAPE subjects demonstrated an increased SaO2 percent, no change in HR or VI, and a decrease in RR on EPAP as compared to control. In normal subjects, SaO2 percent, VI, and heart rate were significantly higher on EPAP 10 cm H2O than 0 cm H2O control (p less than 0.01, 0.01, and 0.05, respectively). The RR and PaCO2 were not significantly different. In summary, EPAP improves gas exchange in HAPE subjects at rest. The EPAP in normal subjects at high altitude resulted in a higher SaO2 percent at the expense of a higher VI and higher HR. These results suggest that the work of breathing is higher and the stroke volume lower on EPAP. The positive pressure mask may be an effective temporizing measure for victims of HAPE who cannot immediately go to a lower altitude.

Adult↗

[Pituitary hormone responses to exercise at high altitudes].

The secretory responses of the anterior pituitary hormone to physiological stress were studied in healthy male volunteers. Measurements of blood LH, FSH, Prolactin, GH, ACTH, lactate, pyruvate and hematocrit were made from blood samples taken at rest, after 15 minutes at sea level, and at an altitude of 4000 m and 5500 m modulated in a climate-controlled room. The results are summarized as follows: Blood levels of Prolactin and ACTH were increased after exercise at a high altitude. Blood levels of LH and FSH after exercise at each altitude were not significantly different from those at rest. Blood GH level was increased after exercise at any altitude. Blood levels of lactate and pyruvate were increased after exercise at any altitude. These results suggest that the secretory response of the anterior pituitary hormone to physiological stress is prominent in Prolactin, GH and ACTH but not in FSH and LH.

Adrenocorticotropic Hormone↗