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At least 19 recordsLinked to original sources

Improving athletic performance: is altitude residence or altitude training helpful?

Exercise training studies conducted at different altitudes (1250-5700 m) of varying durations (30 min to 19 wk) are critically reviewed to determine the efficacy of using altitude as a training stimulus to enhance sea level and altitude exercise performance. Four strategies are discussed: a) exercise training while residing at the same altitude; b) exercise training at altitude but residing at sea level; c) exercise training at low altitude but residing at a higher altitude; and d) exercise training under sea level and altitude conditions but only after altitude acclimatization has occurred. Residing at altitude causes a multitude of potentially beneficial physiological, ventilatory, hematological and metabolic changes that theoretically should induce a potentiating effect on endurance exercise performance. While it is accepted that endurance performance is greatly enhanced at altitude, there is less support for the view that altitude training while residing at altitude improves subsequent sea level endurance performance. There is some evidence, though also not universally accepted, that training at altitude but residing at sea level may benefit sea level endurance performance. Most recently, the combination of "living high" (e.g., at 2500 m) to obtain beneficial physiological changes associated with altitude acclimatization and "training low" (e.g., at 1250 m) to allow maintenance of high-intensity training is accumulating scientific and popular support as the most advantageous strategy to improve subsequent sea level exercise performance in well-trained, competitive runners.

Altitude↗

Augmented sympathetic activation during short-term hypoxia and high-altitude exposure in subjects susceptible to high-altitude pulmonary edema.

BACKGROUND: Pulmonary hypertension is a hallmark of high-altitude pulmonary edema and may contribute to its pathogenesis. Cardiovascular adjustments to hypoxia are mediated, at least in part, by the sympathetic nervous system, and sympathetic activation promotes pulmonary vasoconstriction and alveolar fluid flooding in experimental animals. METHODS AND RESULTS: We measured sympathetic nerve activity (using intraneural microelectrodes) in 8 mountaineers susceptible to high-altitude pulmonary edema and 7 mountaineers resistant to this condition during short-term hypoxic breathing at low altitude and at rest at a high-altitude laboratory (4559 m). We also measured systolic pulmonary artery pressure to examine the relationship between sympathetic activation and pulmonary vasoconstriction. In subjects prone to pulmonary edema, short-term hypoxic breathing at low altitude evoked comparable hypoxemia but a 2- to 3-times-larger increase in the rate of the sympathetic nerve discharge than in subjects resistant to edema (P<0.001). At high altitude, in subjects prone to edema, the increase in the mean+/-SE sympathetic firing rate was >2 times larger than in those resistant to edema (36+/-7 versus 15+/-4 bursts per minute, P<0.001) and preceded the development of lung edema. We observed a direct relationship between sympathetic nerve activity and pulmonary artery pressure measured at low and high altitude in the 2 groups (r=0.83, P<0.0001). CONCLUSIONS: With the use of direct measurements of postganglionic sympathetic nerve discharge, these data provide the first evidence for an exaggerated sympathetic activation in subjects prone to high-altitude pulmonary edema both during short-term hypoxic breathing at low altitude and during actual high-altitude exposure. Sympathetic overactivation may contribute to high-altitude pulmonary edema.

Adult↗

[A retrospective clinical study of chronic high altitude disease complicated by acute exacerbation in high altitude environment].

OBJECTIVE: To study chronic high altitude disease (CHAD) with concurrent acute high altitude disease (AHAD) in regions of high altitude. METHODS: 18,090 inpatients from Feb. 1956 to Dec. 1995 conforming to a screening standard were observed in a hospital located at altitude 3658 m. 1,028 inpatients suffering from CHAD when hospitalized were collected as a study group. 17,020 inpatients suffering from non-HAD when first hospitalized served as a control group. The morbidity rate of AHAD in these two groups in a follow-up period of 1 - 20 years was analyzed. RESULTS: (1) AHAD morbidity rate was increasing with prolongation of observation time in the control group, but it was not so in the study group. Annual and accumulative morbidity of AHAD in the study group was obviously higher than that in the control group (P < 0.005, OR = 5.03, RR = 4.33). (2) The morbidity rates of three types of AHAD aside from high altitude pulmonary edema (HAPE) of high altitude hypertension (HAH) group and high altitude cerebral edema (HACE) of high altitude heart disease (HAHD) group was obviously higher in the study group than in the control (P < 0.05 - 0.005). AHAD morbidity rate in HAHD group and Monge's disease was 23.5% and 22.0% (OR = 7.33 - 6.71, RR = 5.86 - 5.47). (3) AHAD morbidity rate in HAHD group and Monge's disease group was obviously higher than that in the control, constituting mainly a high morbidity of mild acute high altitude disease. CONCLUSION: The risk of AHAD increases about 5-fold in CHAD patients than in the multitude of high altitude acclimatization, being most evident in HAHD and Monge's disease.

Acute Disease↗

[Travelling to high altitude areas--acute high altitude sickness].

BACKGROUND: People show increasing interest in travelling to high altitude areas such as the Himalayas, the Andes and mountains like Kilimanjaro in Tanzania. MATERIAL AND METHODS: Based on personal experience and published articles, an overview of acute high altitude sickness (acute mountain sickness) is given. RESULTS AND INTERPRETATION: High altitude sickness may be mild, moderate or severe, i.e. life threatening. There is a gradual shift in symptoms between these three syndromes. Mild to moderate high altitude sickness are recognized by various degree of headache, apathy, reduced appetite, nausea and vomiting, and when moderate, also peripheral oedemas and fluid retention. High altitude pulmonary oedema and high altitude cerebral oedema are life threatening conditions. High altitude sickness can be prevented by slow ascent. It is important to discover symptoms early. Descent is always the best treatment, but oxygen, portable pressure chambers and medication can be used in special situations. Acetazolamid is effective both to prevent and treat acute altitude sickness. Dexamethasone is an alternative, especially indicated for the treatment of high altitude cerebral oedema. Nifedipine is indicated in the treatment of high altitude pulmonary oedema.

Altitude Sickness↗

Altitude convulsion threshold and time to altitude convulsion in gold thioglucose obese mice.

Gold thioglucose-induced hypothalamic obesity caused a higher altitude convulsion threshold and a decrease in the time to altitude convulsion. The average altitude convulsion threshold for the obese mice was 151 torr (38,500 ft). In contrast, the average value for the controls was 131 torr (41,500 ft). It was also observed that at 206 torr (32,000 ft), the average time until altitude convulsion of the obese mice was 69 s; at 179 torr (35,000 ft), 27 s; at 141 torr (40,000 ft), 17 s; at 111 torr (45,000 ft), 10 s; at 87 torr (50,000 ft), 9 s; and at 69 torr (55,000 ft), 8 s. On the other hand, the average control time until altitude convulsion at the above-mentioned altitudes was 97, 37, 26, 11, 9, and 8 s, respectively. Moreover, the average accumulation of fat between pleura and lungs in obese mice was 154 (Table I) or 181 mg (Table II), while the value of the control group was only 72 to 67 mg. Such an increase of fat accumulation in the thoracic cage could decrease the tidal volume. The altitude convulsion threshold and the time until altitude convulsion might thus be changed. The time until altitude convulsion may be regarded as a convenient objective measure of altitude tolerance in mice.

Altitude↗

[Altitude adaptation. Part III. Altitude acclimatization as a problem of human biology (II. Morphology, physiology, biochemistry)].

The physiological mechanisms of adaptation will be reported. In a primary step of adaptation, the body reacts with immediate response, which already leads to a first classification: whether or not altitude will be tolerated by an individual. More steady biological processes follow with the same intention of balancing oxygen deficiency. They may be successful and acclimatization is possible, or they do not achieve the necessary level, i.e. that consequently developing pathological conditions of different severity lead to a next assortation of individuals with insufficient adaptability. The first state of lability can be compensated, or the intolerance will make a further stay in high altitudes impossible. No parameters exist which could allow a prognosis as to what kind of individuals will tolerate altitude or not. A different pattern of biological reaction is seen in permanent inhabitants of high altitudes who have been residing there for generations and haven't experienced conditions other than those of their special altitude in their individual lives. While ascending to higher altitudes, permanent residents also have to undergo new adaptation, as well as when descending to lower altitudes. Returning to their native environment requires reacclimatization. The mechanisms of adaptation on the organ level will be reviewed, as well as on the fluid and cellular level. All those functional and morphological mechanisms of adaptation to oxygen deficiency in high altitudes tend to maintain optimal equilibrium. Maladaptation may result. Expected genetically determined physiological alterations of adaptational value in permanent residents, which could have manifested themselves by way of "soft" selection and change of gene frequency in those high altitude populations, will be discussed. Genetical determination in such physiological parameters does not seem probable, although some pecularities such as the "blunted response" ventilation, the higher Bohr-Effect in Quenchua etc. might be interpreted in this direction.

Acclimatization↗

Glucose tolerance of lowlanders during prolonged stay at high altitude and among high altitude natives.

The fasting blood sugar level and glucose tolerance were investigated in seven amle lowlanders at sea level, during their stay at an altitude of 4,000 m at intervals of 2 weeks, 10, 15, 20, and 24 months and again on return to sea level during the first week and after 1 month. For comparison, the glucose tolerance of six male Ladakhis (natives of high altitude area) was also determined at altitude. The fasting blood sugar among lowlanders increased to 136.0 plus or minus 4.39 mg per 100 ml during 10 months of stay at altitude followed with a gradual decrease to a value of 76.4 plus or minus 3.8 at the end of 24 months. On return to sea level, the blood glucose showed a tendency to increase. Ladakhis had a lower blood sugar level at altitude (86.4 plus or minus 7.28) as compared with lowlanders at sea level (92.6 plus or minus 2.29). The glucose tolerance curves of lowlanders ran paralell to each other at altitude and at sea level. However, the peak of the glucose tolerance curve shifted towards the left during the 20th and 24th months of stay at altitude and at sea level. However, the peak of the glucose tolerance curve shifted towards the left during the 20th and 24th months of stay at altitude and on return to sea level. The tolerance curve of Ladakhis was similar to that of lowlanders at altitude, but showed a sharper blood sugar decline rate.

Acclimatization↗

[Comparison study on uterine and umbilical artery blood flow during pregnancy at high altitude and at low altitude].

OBJECTIVE: To evaluate the effect of high altitude on uterine and umbilical artery blood flow dynamics during normal pregnancy. METHOD: Uterine artery blood flow parameters of the pregnant (34) and nonpregnant (37) subjects and umbilical artery blood flow parameters of 119 subjects living at high altitude or at low altitude were measured with color Doppler flow imaging system. RESULTS: Uterine artery diameter, blood flow volume increased during pregnancy at both altitude, and uterine artery blood flow volume and diameter were smaller at high altitude than at low altitude [(0.35 +/- 0.04) cm vs (0.45 +/- 0.04) cm, (280 +/- 48) ml/min vs (425 +/- 55) ml/min, P < 0.01]. Umbilical artery blood flow velocity systolic to diastolic (S/D) value, resistant index of different pregnant period were greater at high altitude than at low altitude (P < 0.01). CONCLUSION: High altitude has effect on placental and infant blood flow that causes the decrease of placental blood infusion and the increase of uterine and umbilical artery flow velocity S/D and reactive index.

Adult↗

High-altitude retinopathy and altitude illness.

OBJECTIVE: To determine the relationship between high-altitude retinopathy (HAR) and other altitude-related illnesses and establish a classification system for HAR. DESIGN: Observational case series. PARTICIPANTS: All 40 climbers among 3 Himalayan expeditions who ascended to altitudes between 16,000 and 29,028 feet above sea level (summit of Mt. Everest) were examined for signs of HAR and altitude illness (AI). METHODS: All subjects had dilated fundus examinations before the ascent, intermittent fundus, and medical examinations during the climb and a dilated fundus and medical examination within 2 days after attaining their highest altitude. MAIN OUTCOME MEASURES: Careful fundus drawings or fundus photography or both were obtained for all participants. All subjects gave a subjective assessment of their symptoms of acute mountain sickness (AMS) and were assessed clinically for signs of high-altitude cerebral edema (HACE). RESULTS: Nineteen of 21 climbers who ascended above 25,000 feet developed HAR. Fourteen of 19 climbers who attained altitudes between 16,000 and 25,000 feet were found to have retinopathy. A grading system for HAR describing the severity of the retinopathy was developed. Correlation of the retinopathy with other AI showed that AMS was endemic and that a statistically significant correlation exists between HAR and HACE (P = 0.0240). CONCLUSION: Recognizing advancing grades of HAR may allow physicians to recommend initiating empiric treatment with oxygen, steroids, diuretics and immediate descent to prevent HAR progression, macular involvement, or potentially fatal HACE. High-altitude retinopathy is both a significant component of and a predictor of progressive AI.

Acute Disease↗

Austrian Moderate Altitude Study (AMAS 2000) - fluid shifts, erythropoiesis, and angiogenesis in patients with metabolic syndrome at moderate altitude (congruent with 1700 m).

It was hypothesized that subjects with metabolic syndrome (hypertension, obesity, hyperlipidemia, diabetes mellitus): (1) develop measurable peripheral edema at moderate altitude and (2) might show differences on erythropoiesis, iron status and vascular endothelial growth factor (VEGF) in comparison to healthy subjects during and after a long-term stay (3-week exposure) at moderate altitude (congruent with 1700 m). Twenty-two male subjects with metabolic syndrome were selected. Baseline investigations (t1) were performed in Innsbruck (500 m). All participants were transferred by bus to 1700 m (Alps) and remained there for 3 weeks with examinations on day 1 (after the first night at altitude, t2), day 4 (t3), day 9 (t4) and day 19 (t5). After returning to Innsbruck, post-altitude examinations were conducted after 7-10 days (t6) and 6-7 weeks (t7), respectively. Body mass was decreased from t1 to t7 (P<0.01). Total body water was decreased at t2 (P<0.01), returned to control level (t3, t4), and was found elevated at t7 (P<0.01). Lean body mass did not change, but body fat decreased during the study (P<0.01). Tissue thickness at the forehead decreased during and after altitude exposure (P<0.01), whereas tissue thickness at the tibia did not alter. Erythropoietin (EPO) was elevated as early as t2 and remained increased until t5. Reticulocyte count was increased at t3 and remained above pre-altitude values. VEGF levels were unchanged. After a 3-week exposure to moderate altitude, patients with metabolic syndrome had reduced their body mass, mainly because of a reduction in body fat. The moderate altitude was found to stimulate erythropoiesis in these patients but this was not sufficient to increase serum VEGF concentration.

Adaptation, Physiological↗

"Living high-training low": effect of moderate-altitude acclimatization with low-altitude training on performance.

The principal objective of this study was to test the hypothesis that acclimatization to moderate altitude (2,500 m) plus training at low altitude (1,250 m), "living high-training low," improves sea-level performance in well-trained runners more than an equivalent sea-level or altitude control. Thirty-nine competitive runners (27 men, 12 women) completed 1) a 2-wk lead-in phase, followed by 2) 4 wk of supervised training at sea level; and 3) 4 wk of field training camp randomized to three groups: "high-low" (n = 13), living at moderate altitude (2,500 m) and training at low altitude (1,250 m); "high-high" (n = 13), living and training at moderate altitude (2,500 m); or "low-low" (n = 13), living and training in a mountain environment at sea level (150 m). A 5,000-m time trial was the primary measure of performance; laboratory outcomes included maximal O2 uptake (VO2 max), anaerobic capacity (accumulated O2 deficit), maximal steady state (MSS; ventilatory threshold), running economy, velocity at VO2 max, and blood compartment volumes. Both altitude groups significantly increased VO2 max (5%) in direct proportion to an increase in red cell mass volume (9%; r = 0.37, P < 0.05), neither of which changed in the control. Five-kilometer time was improved by the field training camp only in the high-low group (13.4 +/- 10 s), in direct proportion to the increase in VO2 max (r = 0.65, P < 0.01). Velocity at VO2 max and MSS also improved only in the high-low group. Four weeks of living high-training low improves sea-level running performance in trained runners due to altitude acclimatization (increase in red cell mass volume and VO2 max) and maintenance of sea-level training velocities, most likely accounting for the increase in velocity at VO2 max and MSS.

Acclimatization↗

[Prerequisites and guidelines for acclimatization to great and extreme altitude in prevention of altitude sickness].

Acute mountain sickness is a possible danger of life but it appears in fact absolutely not as fateful or unavoidable because it's evidence occurs as the consequence of missed observation of the specific conditions as much as of individual misbehaviour to altitude. Before someone plans to travel or climb at high altitudes by sharing a trekking-tour or an expedition-team medical advices for prevention of severe incidences caused by the reduced oxygen at altitudes are of utmost importance. Thereby it is not the question of the individual suitability to altitude which appears in the foreground but the need to find out typical health restrictions and, first of all, to develop an individual concept of optimal acclimatization to altitude. In this synopsis therefore all relevant aspects of preparation, precautions and detailed methods of acclimatization to altitude are laid down corresponding to the actual knowledge of altitude medicine and will be presented as crucial guiding principles for trekking and climbing to high altitudes.

Acclimatization↗

Operation Everest II: Altitude decompression sickness during repeated altitude exposure.

The incidence of altitude decompression sickness (ADS) was studied in 23 altitude scientists during repeated altitude exposure to 15,000-29,000 ft (4572-8839 m) in a decompression chamber. Prior to each altitude exposure, a 30-60-mm pre-breathing period with 100% oxygen took place. Ascent was made to an altitude at a rate of 2000 ft X min-1. The altitudes studied ranged from 15,000-29,000 ft (4572-8839 m). Symptoms reported appear consistent with previous reports. Incidence of ADS at 26,000-29,000 ft (7925-8839 m) was 29.7%, during 274 chamber flights and 1264.6 h of altitude time. Incidence appeared related to frequency of exposure, severity of altitude, and physical activity. Incidence was not related to age, duration of exposure, or body index (weight/height 2). This high incidence of ADS reported in this study is similar to that reported by NASA.

Adult↗

Austrian Moderate Altitude Study 2000 (AMAS 2000). The effects of moderate altitude (1,700 m) on cardiovascular and metabolic variables in patients with metabolic syndrome.

We investigated the changes in the cardiovascular system [resting blood pressure (BP) and heart rate (HR), measured by means of a 24-h ambulatory BP and a holter-electrocardiogram (ECG)], glycemic parameters, and lipid metabolism of subjects suffering from metabolic syndrome during a 3-week sojourn at 1,700 m in the Austrian Alps. A total of 22 male subjects with metabolic syndrome were selected. Baseline investigations were performed at Innsbruck (500 m above sea level). During the 3-week altitude stay the participants simulated a holiday with moderate sports activities. Examinations were performed on days 1, 4, 9, and 19. After returning to Innsbruck, post-altitude examinations were conducted after 7-10 days and 6-7 weeks, respectively. The 24-h ambulatory BP and holter ECG revealed a decrease in average HR, BP, and rate pressure product (RPP: systolic blood pressure x HR) after 3 weeks of altitude exposure. In some patients, an increase in premature ventricular beats was observed at the end compared to the beginning of the exposure to moderate altitude. The ECG revealed no ischemic ST-segment changes. Maximal physical capacity as measured by symptom-limited maximal cycle ergometry tests remained unchanged during the study. Six weeks after the altitude exposure the blood pressure increased again and returned to pretest levels. The Homeostasis Model Assessment index, which is a measure of insulin resistance, decreased significantly and glucose concentrations obtained after an oral glucose tolerance test were significantly lower after the stay at altitude compared to the basal values. We conclude that after a 3-week exposure to moderate altitude, patients with metabolic syndrome (1) tolerated their sojourn without any physical problems, (2) exhibited short-term favorable effects on the cardiovascular system, and (3) had significant improvements in glycemic parameters that were paralleled by a significant increase in high-density-lipoprotein-cholesterol.

Adaptation, Physiological↗

Reticulocytosis, increased mean red cell volume, and greater blood viscosity in altitude susceptible compared to altitude resistant rats.

We have identified two strains (H and M) of Sprague-Dawley rat with markedly different susceptibilities and cardiopulmonary responses to chronic hypobaria. To further characterize factors responsible for these differing cardiopulmonary responses to chronic hypobaria, the present study examined differences in hematologic responses between the strains and assessed the contribution of differences in blood viscosity to differences in pulmonary vascular resistance. Following a 4-5 week exposure to simulated high altitude (0.5 atm), hemoglobin, hematocrit, mean red cell volume, and reticulocyte count were all increased in the susceptible H compared to the resistant M rats, whereas red blood cell counts were similar. Sea level controls manifested no differences. Blood viscosity, measured in a capillary viscometer, was 53% greater in chronically hypoxic H than in M rats, and plasma viscosities were similar. Blood from high altitude H rats increased pulmonary vascular resistance more than blood from high altitude M rats when perfused into lungs isolated from high altitude rats of either strain. In conclusion, high altitude H rats have an increased population of immature red cells, leading to a greater mean red cell volume and hematocrit than in high altitude M rats. These hematologic differences contribute to the the increased blood viscosity and greater pulmonary vascular resistance of H compared to M rats after 4 weeks' high altitude exposure.

Altitude↗