The objective of this study was to determine the efficacy of low-dose acetazolamide (125 mg twice daily) for the prevention of acute mountain sickness (AMS). The design was a prospective, double-blind, randomized, placebo-controlled trial in the Mt. Everest region of Nepal between Pheriche (4243 m), the study enrollment site, and Lobuje (4937 m), the study endpoint. The participants were 197 healthy male and female trekkers of diverse background, and they were evaluated with the Lake Louise Acute Mountain Sickness Scoring System and pulse oximetry. The main outcome measures were incidence and severity of AMS as judged by the Lake Louise Questionnaire score at Lobuje. Of the 197 participants enrolled, 155 returned their data sheets at Lobuje. In the treatment group there was a statistically significant reduction in incidence of AMS (placebo group, 24.7%, 20 out of 81 subjects; acetazolamide group, 12.2%, 9 out of 74 subjects). Prophylaxis with acetazolamide conferred a 50.6% relative risk reduction, and the number needed to treat in order to prevent one instance of AMS was 8. Of those with AMS, 30% in the placebo group (6 of 20) versus 0% in the acetazolamide group (0 of 9) experienced a more severe degree of AMS as defined by a Lake Louise Questionnaire score of 5 or greater (p = 0.14). Secondary outcome measures associated with statistically significant findings favoring the treatment group included decrease in headache and a greater increase in final oxygen saturation at Lobuje. We concluded that acetazolamide 125 mg twice daily was effective in decreasing the incidence of AMS in this Himalayan trekking population.
The purpose of the present study was to elucidate the influence of intermittent hypobaric hypoxia at rest on endurance performance and cardiorespiratory and hematological adaptations in trained endurance athletes. Twelve trained male endurance runners were assigned to either a hypoxic group (n = 6) or a control group (n = 6). The subjects in the hypoxic group were exposed to a simulated altitude of 4500 m for 90 min, three times a week for 3 weeks. The measurements of 3000 m running time, running time to exhaustion, and cardiorespiratory parameters during maximal exercise test and resting hematological status were performed before (Pre) and after 3 weeks of intermittent hypoxic exposure (Post). These measurements were repeated after the cessation of intermittent hypoxia for 3 weeks (Re). In the control group, the same parameters were determined at Pre, Post, and Re for the subjects not exposed to intermittent hypoxia. The athletes in both groups continued their normal training together at sea level throughout the experiment. In the hypoxic group, the 3000 m running time and running time to exhaustion during maximal exercise test improved. Neither cardiorespiratory parameters to maximal exercise nor resting hematological parameters were changed in either group at Post, whereas oxygen uptake ((V) over dot O-2) during submaximal exercise decreased significantly in the hypoxic group. After cessation of intermittent hypoxia for 3 weeks, the improved 3000 m running time and running time to exhaustion tended to decline, and the decreased (V) over dot O-2 during submaximal exercise returned to Pre level. These results suggest that intermittent hypoxia at rest could improve endurance performance and submaximal exercise efficiency at sea level in trained endurance athletes, but these improvements are not maintained after the cessation of intermittent hypoxia for 3 weeks.
A few studies have reported increased body temperature (T-o) associated with acute mountain sickness (AMS), but these usually include exercise, varying environmental conditions over days, and pulmonary edema. We wished to determine whether T-o would increase with AMS during early exposure to simulated altitude at rest. Ninety-four exposures of 51 men and women to reduced P-B (423 mmHg = 16,000 ft = 4850 m) were carried out for 8 to 12 h. AMS was evaluated by LL and AMS-C scores near end of exposure, and T-o was measured by oral digital thermometer before altitude and after 1 (A1), 6 (A6), and last (A12) h at simulated altitude. Other measurements included ventilation,O-2 consumption and autonomic indicators of plasma catecholamines, HR, and HR variability. Average To increased by 0.5degreesF from A1 to A12 in all subjects (p < 0.001). Comparison between 16 subjects with lowest AMS scores (mean LL = 1.0, range = 0 to 2.5) and 16 other subjects with highest AMS scores (mean LL = 7.4, range = 5 to 11) demonstrated a transient decline in T-o from A1 to A6 in AMS, in contrast to a rise in non-AMS (p = 0.001). Catecholamines, HR, and HR variability (increased low F/high F ratio) indicated significant elevation of sympathetic activity in AMS, where T-o fell, but no change in metabolic rate. The apparently greater heat loss during early AMS suggests increased hypoxic vasodilation in spite of enhanced sympathetic drive. Greater hypoxic vasodilation and elevated HR in AMS in the absence of other changes suggest that augmentation of beta-adrenergic tone may be involved in early AMS pathophysiology.
The male reproductive functions of the members of the Masherbrum (7821 m) Expedition in 1999 were examined via semen analyses and endocrine tests. Specimens were collected from three subjects who had stayed above 5100 m for 21 to 24 days and above 6700 m for 4 to 5 days before departure and 1 month, 3 months, and 2 yr after returning from the expedition. Semen analyses showed no change in the semen volume. Sperm counts decreased after 1 month and had not recovered after 3 months, but they had recovered after 2 yr in all subjects. An increase in abnormally shaped sperm was also observed after 1 month, but had nearly recovered to the preexpedition state after 3 months. Endocrine tests revealed slightly decreased testosterone in the blood after 1 month, which had decreased still further after 3 months. The tests were completely normal after 2 yr. We suggest that a high altitude sojourn may induce reversible spermatogenic and Leydig cell dysfunction.
One essential factor in the development of high altitude pulmonary edema (HAPE) is elevated pulmonary artery pressure, possibly due to a lack of nitric oxide (NO) in pulmonary vessels. NOS3 gene polymorphisms (G894T, T-786C, and CA-repeats greater than or equal to38) might be linked to decreased NO synthesis and increased susceptibility to HAPE, while the C242T polymorphism of the CYBA gene [encoding for the NAD(P)H oxidase subunit p22phox] may increase NO availability and thus convey resistance to HAPE. To test this hypothesis, we genotyped 51 mountaineers susceptible and 52 mountaineers not susceptible to HAPE. Genotyping revealed similar genotype frequencies of the G894T and the T-786C NOS3 polymorphism in both groups (G894T: susceptibles, 39.2% GG, 47.1% GT, 13.7% TT; nonsusceptibles, 48.0% GG, 44.0% GT, 8.0% TT; p = 0.54. T-786C: susceptibles, 45.1% TT, 39.2% TC, 15.7% CC; nonsusceptibles, 53.8% TT, 40.4% TC, 5.8% CC; p = 0.28). Genotype frequencies of the C242T CYBA polymorphism were 43.1% CC, 47.1% CT, and 9.8% TT in HAPE susceptibles and 38.0% CC, 52.0% CT, and 10.0% TT (p = 0.92) in nonsusceptibles. There was also no difference between the two groups in the number of CA repeats (p = 0.57), and individuals with greater than or equal to38 CA repeats were not more likely to develop HAPE (p = 1.0). Haplotype analysis for the NOS3 polymorphisms also revealed no association with HAPE. The results of this study suggest that none of these genetic variants plays a substantial role in the pathogenesis of HAPE in Caucasians, but does not exclude epistatic effects that might still involve the genetic systems studied here.
Wood, Steve; Tsering Norboo; Miles Lilly; Ken Yoneda; Marlowe Eldridge. Cardiopulmonary function in high altitude residents of Ladakh. High Alt. Med. Biol. 4:445-454, 2003. We studied residents of high altitude in Ladakh, India, to determine the effects of altitude, age, gender, and ethnicity on gas exchange and pulmonary function. Physical examinations, including pulse oximetry, hemoglobin concentration, end-tidal P-CO2, and pulmonary function, were conducted on resting Ladakhi and Tibetan subjects at altitudes of 3300, 4200, and 4500 In. A total of 574 men and women, ranging in age from 17 to 82, were studied. At 3300 In, Ladakhis had higher heart rates than Tibetans in both genders and higher P-ETCO2 in women. Above 4000 m, 21 of the 141 men studied (15%) had Hb concentrations higher than 20 g/dL, with one confirmed case of Monge's disease. There was no gender difference in Sa(O2) at any altitude except for pregnant women. At 4600 m, Tibetans had significantly higher peak flows and lower P-ETCO2 than Ladakhis. Ladakhi men had higher diastolic BP than women (91 vs. 81), with no difference in systolic BP. There was no gender difference in BP for Tibetans. An important spirometry finding for both groups was high air flows, with mid-maximal expiratory flow (MMEF) at 130% to 150% of predicted values, compared with 85% for sojourner controls, and FEV1/FVC at 115%, compared with sojourner controls at 98%. Improved lung mechanics may be an important adaptation to the lifelong sustained increase in resting ventilation as well as to indoor biomass smoke and outdoor dust exposure of these populations at high altitude.
Pronk, Marieke; Ivo Tiemessen, Maarten D.W. Hupperets, Brian P. Kennedy, Frank L. Powell, Susan R. Hopkins, Peter Wagner. Persistence of the lactate paradox over 8 weeks at 3800 m. High Alt. Med. Biol. 4:431-443, 2003.-The arterial blood lactate [La] response to exercise increases in acute hypoxia, but returns to near the normoxic (sea level, SL) response after 2 to 5 weeks of altitude acclimatization. Recently, it has been suggested that this gradual return to the SL response in [La], known as the lactate paradox (LP), unexpectedly disappears after 8 to 9 weeks at altitude. We tested this idea by recording the [La] response to exercise every 2 weeks over 8 weeks at altitude. Five normal, fit SL-residents were studied at SL and 3800 m (Pbar = 485 torr) in both normoxia (P-IO2 = 150 torr) and hypoxia (P-IO2 = 91 torr congruent to air at 3800 m). Arterial [La] and blood gas values were determined at rest and during cycle exercise at the same absolute workloads (0, 25, 50, 75, 90, and 100% of initial SL-(V) over dot(O2MAX)) and exercise duration (4, 4, 4, 2, 1.5, and 0.75 min, respectively) at each time point. [La] curves were elevated in acute hypoxia at SL (p < 0.01) and at 3800 m fell progressively toward the SL-normoxic curve (p < 0.01). On the same days, [La] responses in acute normoxia showed essentially no changes over time and were similar to initial SL normoxic responses. We also measured arterial catecholamine levels at each load and found a close relationship to [La] over time, supporting a role for adrenergic influence on [La]. In summary, extending the time at this altitude to 8 weeks produced no evidence for reversal of the LP, consistent with prior data obtained over shorter periods of altitude residence.
Sarybaev Akpay; Grzegorz Palasiewicz; Dinara Usupbaeva; Robert Plywaczewski; Abdirashit Maripov; Akylbek Sydykov; Mirsaid Mirrakhimov; Hans Le Roux; Talant Kadyrov; Jan Zielinski. Effects of intermittent exposure to high altitude on pulmonary hemodynamics: a prospective study. High Alt. Med. Biol. 4:455-463, 2003. Chronic alveolar hypoxia due to disease or low atmospheric pressure at high altitude results in the development of hypoxic pulmonary hypertension. The effects of intermittent hypoxia on pulmonary hemodynamics in healthy men have not been studied. We aimed to investigate, prospectively, pulmonary hemodynamics in workers commuting between an elevation of 3700 and 4200 In (4-week working shift) and lowland, below 500 m (4 weeks of holiday). Pulmonary hemodynamics has been investigated by Doppler echocardiography in 26 healthy Caucasian males, mean age 42 +/- 9 yr. First at lowland (760 m) and next during the fourth week of work at high altitude. Investigations were repeated in 21 subjects 1d year later at the end of the high-altitude exposure. The third series of investigations was performed 2 yr after the initial ones in 10 subjects who earlier had shown the strongest hypoxic vasoconstriction. At lowland, subjects presented with normal pulmonary hemodynamics. At high altitude, mean pulmonary artery pressure (PAPm) rose from 14.7 +/- 2.7 mmHg to 25.8 +/- 8.3 mmHg. One year later the PAPm remained unchanged in hypoxic conditions (25.0 +/- 7.3 mmHg). At the end of a 2-year follow-up of 10 "hyperreactors," PAPm measured at the end of the hypoxic exposure was the same as at the initial investigation, averaging 28 +/- 4.0, 28 +/- 3.5, and 29 +/- 2.5 mmHg at the beginning and at 1 and after 2 yr of intermittent exposure to high altitude. We concluded that intermittent exposure to 4000 m lasting 3 yr does not lead to development of permanent pulmonary hypertension.
When lowlanders go to high altitude, the resulting oxygen deprivation impairs mental and physical performance, quality of sleep, and general well-being. This paper compares the effects of ventilatory acclimatization and oxygen enrichment of room air on the improvement of oxygenation as judged by the increase in the alveolar P(O2) and the reduction in equivalent altitude. The results show that, on the average, complete ventilatory acclimatization at an altitude of 5000 m increases the alveolar P(O2) by nearly 8 torr, which corresponds to a reduction in equivalent altitude of about 1000 m, although there is considerable individual variability. By comparison, oxygen enrichment to 27% at 5000 m can easily reduce the equivalent altitude to 3200 m, which is generally well tolerated. Because full ventilatory acclimatization at altitudes up to about 3600 m reduces the equivalent altitude to about 3000 m, oxygen enrichment is not justified for well-acclimatized persons. At an altitude of 4200 m, where several telescopes are located on the summit of Mauna Kea, full acclimatization reduces the equivalent altitude to about 3400 m, but the pattern of commuting probably would not allow this. Therefore, at this altitude, oxygen enrichment would be beneficial but is not essential. At higher altitudes such as 5050 m, where other telescopes are located or planned, the gain in oxygenation from acclimatization is insufficient to produce an adequate mental or physical performance for most work, and oxygen enrichment is highly desirable. Full ventilatory acclimatization requires at least a week of continuous exposure, although much of the improvement is seen in the first 2 days.
We tested the hypothesis that acute hypoxia may alter the circadian pattern of body temperature in adult humans. Six healthy subjects were studied in normoxia, hypoxia (similar to13% inspired O-2), and again normoxia, each session lasting >24 h and spaced a few days apart, with a constant routine protocol of sustained wakefulness and minimal activity. Some parameters (e.g., tympanic and abdominal temperatures, heart rate) were recorded continuously; others (e.g., oxygen consumption and pulmonary ventilation) were monitored for similar to10 min every 2 h. The amplitudes of the circadian oscillation of tympanic, abdominal, and calf skin temperatures were reduced in hypoxia, averaging, respectively, 61%, 80% and 50% of the normoxic amplitude. Oxygen consumption and pulmonary ventilation, which presented a circadian pattern in normoxia had no longer significant oscillations during hypoxia, whereas the opposite was the case for heart rate and diastolic pressure. Therefore, acute hypoxia can disturb the normal circadian patterns and, specifically, depress those of body temperature. These effects, qualitatively similar to those observed in chronically hypoxic animals and humans, could contribute to sleep disturbances at high altitude.
Substantial numbers of children are exposed to moderate altitude while traveling to mountain resorts with their families. Although there has been extensive study of the adult physiologic response to altitude exposure, few studies of infants and young children exist. This investigation examines the acute physiologic responses to moderate altitude exposure among young children and the relationship of these responses to the development of acute mountain sickness (AMS). Children 3 to 36 months old participated in the prospective observational study, which included baseline measurements at 1610 m and measurements after a 24-h exposure to 3109 In. Measurements included pulse and respiratory rate, end-tidal CO2, arterial oxygen saturation (pulse oximetry), cerebral tissue oxygenation (St(o2)) by near-infrared spectroscopy, middle cerebral artery resistive index by transcranial Doppler, lateral ventricle volumes (ultrasound), and clinical evaluation for the presence of acute mountain sickness (Children's Lake Louise Score). Twenty-four children (13 girls and 11 boys, age 14.5 +/- 10.2 months) participated. After acute exposure to 3109 In, these children showed an increase in respiratory rate from 45 +/- 13 to 51.9 +/- 15 breaths/min (p < 0.008), accompanied by a decrease of end-tidal CO2 from 31 +/- 3 to 28 +/- 2 mm Hg (p < 0.001) and a reduction of arterial oxygen saturation from 95 +/- 2 to 91 +/- 2% (p < 0.001). St(o2) also decreased from 78 +/- 8 to 67 +/- 13% (p < 0.001), and this reduction appeared to be related to age (r = 0.58, p < 0.05), with lower saturations found in younger children. No evidence of increased intracranial pressure, as assessed by middle cerebral artery resistive index, was seen during ascent. Seven subjects developed symptoms of AMS; however, no relationship was found between the physiologic changes observed and the presence of symptoms. Ascent from 1610 to 3109 m resulted in tachypnea, relative hypoxia, hypocapnia, and a reduction in cerebral tissue oxygenation (St(o2)). The reduction in St(o2) appeared to be related to age, with infants appearing to be the most susceptible to cerebral tissue oxygen desaturation at high altitude. No relationship appears to exist between the presence of AMS and the physiologic measurements.
When lowlanders go to high altitude, the resulting oxygen deprivation impairs mental and physical performance, quality of sleep, and general well-being. This paper compares the effects of ventilatory acclimatization and oxygen enrichment of room air on the improvement of oxygenation as judged by the increase in the alveolar P-O2 and the reduction in equivalent altitude. The results show that, on the average, complete ventilatory acclimatization at an altitude of 5000 m increases the alveolar P-O2 by nearly 8 torr, which corresponds to a reduction in equivalent altitude of about 1000 m, although there is considerable individual variability. By comparison, oxygen enrichment to 27% at 5000 m can easily reduce the equivalent altitude to 3200 m, which is generally well tolerated. Because full ventilatory acclimatization at altitudes up to about 3600 m reduces the equivalent altitude to about 3000 m, oxygen enrichment is not justified for well-acclimatized persons. At an altitude of 4200 In, where several telescopes are located on the summit of Mauna Kea, full acclimatization reduces the equivalent altitude to about 3400 m, but the pattern of commuting probably would not allow this. Therefore, at this altitude, oxygen enrichment would be beneficial but is not essential. At higher altitudes such as 5050 m, where other telescopes are located or planned, the gain in oxygenation from acclimatization is insufficient to produce an adequate mental or physical performance for most work, and oxygen enrichment is highly desirable. Full ventilatory acclimatization requires at least a week of continuous exposure, although much of the improvement is seen in the first 2 days.
Infections and acute mountain sickness (AMS) are common at high altitude, yet their precise etiologies remain elusive and the potential for differential diagnosis is considerable. The present study was therefore designed to compare clinical nonspecific symptoms associated with these pathologies and basic changes in free radical and amino-acid metabolism. Nineteen males were examined at rest and after maximal exercise at sea level before (SL1/SL2) and following a 20 +/- 5 day ascent to Kanchenjunga base camp located at 5100 m (HA). Four subjects with symptoms consistent with an ongoing respiratory and recent gastrointestinal infection were also diagnosed with clinical AMS on the evening of day I at HA. These and six other subjects recovering from symptoms consistent with a respiratory infection presented with a greater increase (HA minus SL1) in AMS scores and resting venous concentration of lipid hydroperoxides (LH) and in total creatine phosphokinase and ratio of free tryptophan/branched chain amino acids, and greater decrease in glutamine (Gln) compared to healthy controls (n = 9, p < 0.05). The decrease in Gln was consistently related to the altitude/exercise-induced increase in LH (r = -0.69/r = -0.45; p < 0.05) and altitude-induced increase in myoglobin (r = -0.73, p < 0.05). These findings highlight the potential for the misdiagnosis of altitude illness due to the similarity of nonspecific constitutional symptoms associated with infection and AMS. Both conditions were characterized by parallel changes in peripheral biomarkers related to free-radical, skeletal muscle damage and amino acid metabolism. While clearly not establishing cause and effect, free radical-mediated changes in peripheral amino acid metabolism known to influence immune and cerebral serotoninergic function may enhance susceptibility to and/or delay recovery from altitude illness.
The aim of this study was to investigate the effect of mountain living conditions and high altitude hiking activities on glucose tolerance. In study 1, we performed an oral glucose tolerance test on nine untrained subjects before and after 3 days of mountain living. In study II, the same measurement was used to determine the effect of high altitude hiking in two distinct geographic environments; participants included 19 professionally trained mountaineers. We found that trained mountaineers displayed significantly better sea-level glucose tolerance than sedentary subjects of a similar age (p < 0.05). This result suggests that mountaineering training could produce a beneficial effect on glucose tolerance. More importantly, in study I we demonstrated that 3 days of high altitude living (altitude approximately 2400 in) was sufficient to improve glucose tolerance. Furthermore, hiking in a relatively flat plateau area (Pamirs highland area, China, altitude approximately 4000 in) generated significantly better improvement in glucose tolerance than hiking in a mountain that contained many rough hills at a similar altitude (Mountain Snow, Taiwan, altitude approximately 3800 in). In conclusion, we found that living at a high altitude for the short term can significantly improve glucose tolerance. Additionally, the improving effect of hiking at high altitudes on glucose tolerance appears to be influenced by the geographic environment. These preliminary results suggest that high altitude living conditions and activities may possibly be developed as potential natural medicines for the prevention and treatment of type II diabetes in the future.
Kleinsasser, Axel; David Levin; Alex Loeckinger, Susan Hopkins. A pig model of high altitude pulmonary edema. High Alt. Med. Biol. 4:465-474, 2003. High altitude pulmonary edema (HAPE) affects unacclimatized individuals ascending rapidly to high altitude. The pathogenesis of HAPE is not fully elucidated, and many investigative techniques that could provide valuable information are not suitable for use in humans; thus, an animal model is desirable. Rabbits, sheep, dogs, and ferrets have been shown not to consistently develop HAPE, and studies in rats are limited by the animal's small size and inconsistent response. Pigs develop a marked pulmonary vasoconstrictive response to hypoxia, and preliminary studies of HAPE in pigs have been promising. To determine the suitability of pigs as an animal model of HAPE, we exposed six subadult (20 to 25 kg) pigs to normobaric hypoxia (10% oxygen) for 48 hr. One week before, and immediately after exposure to hypoxia, under anesthesia, arterial blood gases were obtained and bronchoalveolar lavage (BAL) and chest x-ray were performed. Hypoxia increased alveolar-arterial pressure difference for oxygen from 22 +/- 9 to 38 +/- 5 torr, p < 0.01) and red cell (from 12.3 +/- 5.9 to 27.4 +/- 5.3 cells x 10(5)/mL(-1), p < 0.001) and white cell (from 1.59 +/- 0.90 to 7.88 +/- 3.36 cells x 10(5)/mL(-1), p < 0.05) concentrations in BAL in all animals. Total BAL protein concentration increased by 64% and fractional albumin by 38% (both p < 0.05) posthypoxia. One animal had evidence of pulmonary edema on X ray. Some pigs develop findings consistent with early HAPE when exposed to normobaric hypoxia. Increasing the duration of hypoxic exposure or exercising the animals in hypoxia may better model the disease process observed in humans with clinically significant HAPE.
To test the hypothesis that the changes in hypoxic ventilatory response (HVR) of men and women mountaineers on induction to HA by trekking is not influenced by gender, isocapnic HVR as DeltaV(E)/DeltaSa(O2) was studied in eight men and eight women mountaineering trainees initially at 2100 m, then during 6 to 7 days of sojourn at 4350 m, and retested again on return to 2100 m. Results indicated that HVR at 2100 m increased significantly at 4350 In in both sexes, and the values reverted to baseline level within 4 to 5 days between leaving high altitude (4350 m) and restudy at 2100 m. No sex differences were observed at 2100- or at 4350-m altitude, indicating that men and women have a similar level of chemosensitive response as measured by HVR during induction to HA.
The aims of this study were to relate heart morphology and functions changes to heart rate variability (HRV) components after acclimatization to high altitude and to define whether preadaptation to hypoxia could modulate HRV responses to acute hypoxic stress. Doppler-echocardiographic studies of the left ventricle were performed in female Wistar rats before, during, and after a 10-week exposure to moderate hypobaric hypoxia (CH rats, similar to4000 In simulated) or normoxia (N rats, similar to55 m). Right ventricular morphology and function and pulmonary artery pressure were evaluated using heart catheterization. Spectral analysis of HRV was studied after exposure in conscious unrestrained rats in normoxia and during acute hypoxic stress. Necropsy right ventricular hypertrophy and intraventricular and pulmonary artery hypertension were found in CH rats compared with N rats. Echocardiographic left ventricular morphology and functions were similar between the groups after exposures. Compared to the control group, CH rats had similar heart rates and HRV components when measured in normoxia. During acute hypoxic stress, HRV decreased in all rats, but less in CH rats. These results support the hypothesis that long-term mild hypoxia may moderate sympathetic activation induced by acute hypoxia and that right ventricular hypertrophy cannot be the direct cause of such a shift in sympathovagal nerve interaction during acute hypoxic stress.
Faulhaber, Martin, Markus Flatz, and Martin Burtscher. beta-blockers may provoke oxygen desaturation during submaximal exercise at moderate altitudes in elderly persons. High Alt. Med. Biol. 4:475-478, 2003. Frequency of therapeutic beta-blocker use in elderly mountaineers is unknown. Therefore, the aim of this field study was to measure the regular beta-blocker intake in elderly persons visiting moderate altitudes. In a subset of mountaineers on beta-blockers, exercise response at two different altitude levels was compared to matched controls. The observed frequency of beta-blocked persons among the interviewed elderly mountaineers (age > 35) was 7%, mainly (65%) due to hypertension. In subjects taking beta-blockers, arterial oxygen saturation (84 +/- 6% vs. 90 +/- 3%, p < 0.05) was decreased and heart rate (120 +/- 17 bpm vs. 112 +/- 14 bpm, p = 0.01), rate pressure product (22,192 +/- 6459 vs. 17,576 +/- 4010, p < 0.05), and ratings of perceived exertion (14 +/- 3 vs. 12 +/- 3, p < 0.05) were increased during a submaximal step test at 2311 In compared to 1480 In. Mountaineers without beta-blocker intake showed no changes. Although the epidemiological data have to be interpreted with caution because of the small sample size and the limitation to a single geographical site, a large number of beta-blocked persons visiting high altitudes was observed. If confirmed in further studies, the increased heart work and exertion could indicate a reduced exercise tolerance of people taking beta-blockers during acute high altitude exposure.