Real-Time Electrocardiogram Transmission from Mount Everest during Continued Ascent

The feasibility of a real-time electrocardiogram (ECG) transmission via satellite phone from Mount Everest to determine a climber’s suitability for continued ascent was examined. Four Taiwanese climbers were enrolled in the 2009 Mount Everest summit program. Physiological measurements were taken at base camp (5300 m), camp 2 (6400 m), camp 3 (7100 m), and camp 4 (7950 m) 1 hour after arrival and following a 10 minute rest period. A total of 3 out of 4 climbers were able to summit Mount Everest successfully. Overall, ECG and global positioning system (GPS) coordinates of climbers were transmitted in real-time via satellite phone successfully from base camp, camp 2, camp 3, and camp 4. At each camp, Resting Heart Rate (RHR) was transmitted and recorded: base camp (54–113 bpm), camp 2 (94–130 bpm), camp 3 (98–115 bpm), and camp 4 (93–111 bpm). Real-time ECG and GPS coordinate transmission via satellite phone is feasible for climbers on Mount Everest. Real-time RHR data can be used to evaluate a climber’s physiological capacity to continue an ascent and to summit.     

The effect of high altitude on saliva aldosterone and glucocorticoid concentrations

Saliva was collected from six healthy young men at hourly intervals at sea level and after 1-2, 8-9 and 15-16 days at 4450 m on Mount Kenya for measurement of aldosterone (SA) and glucocorticoid (SGC, cortisol + cortisone) concentrations. Blood samples were collected simultaneously with some of the saliva samples and analysis of these showed that plasma and saliva concentrations of aldosterone and glucocorticoids were highly correlated (r = 0.91 and 0.75 respectively; p less than 0.01 for both hormones). Mean SA for the group was reduced to approximately 50% of the sea-level value (p less than 0.05) by the time the first saliva samples were collected at altitude, and remained at this depressed level throughout the 2-week period on Mount Kenya, although there was considerable inter-subject variation. SGC concentration also tended to be lower on Mount Kenya than at sea level. Though SA was lower throughout the day at altitude compared to sea level, the principal difference in the temporal pattern of SA was the reduction or complete absence of the marked rise in SA that normally occurs in the first few hours after rising. SA and SGC responses to exercise, which consisted of stepping on and off and 0.4-m high stool 60 times/min for 25 min, were assessed at sea level and after various periods at 4450 m.(ABSTRACT TRUNCATED AT 250 WORDS)     

Microbial community structure in moraine lakes and glacial meltwaters, Mount Everest

The bacterial diversity and abundance in two moraine lakes and two glacial meltwaters (5140, 5152, 5800 and 6350 m above sea level, respectively) in the remote Mount Everest region were examined through 16S rRNA gene clone library and flow cytometry approaches. In total, 247 clones were screened by RFLP and 60 16S rRNA gene sequences were obtained, belonging to the following groups: Proteobacteria (8% alpha subdivision, 21% beta subdivision, and 1% gamma subdivision), Cytophaga-Flavobacteria-Bacteroides (CFB) (54%), Actinobacteria (4%), Planctomycetes (2%), Verrucomicrobia (2%), Fibrobacteres (1%) and Eukaryotic chroloplast (3%), respectively. The high dominance of CFB distinguished the Mount Everest waters from other mountain lakes. The highest bacterial abundance and diversity occurred in the open moraine lake at 5152 m, and the lowest in the glacial meltwater at 6350 m. Low temperature at high altitude is considered to be critical for component dominancy. At the same altitude, nutrient availability plays a role in regulating population structure. Our results also show that the bacteria in Mount Everest may be derived from different sources.     

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.     

Ventilatory chemosensitive adaptations to intermittent hypoxic exposure with endurance training and detraining.

The present study was performed to clarify the effects of intermittent exposure to an altitude of 4,500 m with endurance training and detraining on ventilatory chemosensitivity. Seven subjects (sea-level group) trained at sea level at 70% maximal oxygen uptake (VO2 max) for 30 min/day, 5 days/wk for 2 wk, whereas the other seven subjects (altitude group) trained at the same relative intensity (70% altitude VO2 max) in a hypobaric chamber. VO2 max, hypoxic ventilatory response (HVR), and hypercapnic ventilatory response, as an index of central hypercapnic chemosensitivity (HCVR) and as an index of peripheral chemosensitivity (HCVRSB), were measured. In both groups VO2 max increased significantly after training, and a significant loss of VO2 max occurred during 2 wk of detraining. HVR tended to increase in the altitude group but not significantly, whereas it decreased significantly in the sea-level group after training. HCVR and HCVRSB did not change in each group. After detraining, HVR returned to the pretraining level in both groups. These results suggest that ventilatory chemosensitivity to hypoxia is more variable by endurance training and detraining than that to hypercapnia.     

Lactate during exercise at extreme altitude

Maximal exercise at extreme altitude results in profound arterial hypoxemia and, presumably, extreme tissue hypoxia. The best evidence available indicates that the resting arterial PO2 on the summit of Mount Everest is about 28 torr and that it falls even further during exercise. Nevertheless, some 10 climbers have now reached the summit without supplementary oxygen. Paradoxically, blood lactate for a given work rate at high altitude in acclimatized subjects is essentially the same as at sea level. Because work capacity decreases markedly with increasing altitude, maximal blood lactate also falls. Extrapolation of available data up to 6300 m indicates that a climber who reaches the Everest summit will have no increase in blood lactate. The cause of the low blood lactate during exercise at extreme altitude is not fully understood. One possibility is depletion of plasma bicarbonate in acclimatized subjects, which reduces buffering and results in large increases in H+ concentration for a given release of lactate. The consequent local fall in pH may inhibit enzymes, e.g., phosphofructokinase (EC 2.7.1.56), in the glycolytic pathway.     

George I. Finch and his pioneering use of oxygen for climbing at extreme altitudes.

George Ingle Finch (1888-1970) was the first person to prove the great value of supplementary oxygen for climbing at extreme altitudes. He did this during the 1922 Everest expedition when he and his companion, Geoffrey Bruce, reached an altitude of 8,320 m, higher than any human had climbed before. Finch was well qualified to develop the oxygen equipment because he was an eminent physical chemist. Many of the features of the 1922 design are still used in modern oxygen equipment. Finch also demonstrated an extraordinary tolerance to severe acute hypoxia in a low-pressure chamber experiment. Remarkably, despite Finch's desire to participate in the first three Everest expeditions in 1921-1924, he was only allowed to be a member of one. His rejection from the 1921 expedition was based on medical reports that were apparently politically biased. Then, following his record ascent in 1922, he was refused participation in the 1924 expedition for complex reasons related to his Australian origin, his forthright and unconventional views, and the fact that some people in the climbing establishment in Britain saw Finch as an undesirable outsider.     

Effect of beta-adrenergic blockade on plasma lactate concentration during exercise at high altitude

When unacclimatized lowlanders exercise at high altitude, blood lactate concentration rises higher than at sea level, but lactate accumulation is attenuated after acclimatization. These responses could result from the effects of acute and chronic hypoxia on beta-adrenergic stimulation. In this investigation, the effects of beta-adrenergic blockade on blood lactate and other metabolites were studied in lowland residents during 30 min of steady-state exercise at sea level and on days 3, 8, and 20 of residence at 4300 m. Starting 3 days before ascent and through day 15 at high altitude, six men received propranolol (80 mg three times daily) and six received placebo. Plasma lactate accumulation was reduced in propranolol- but not placebo-treated subjects during exercise on day 3 at high altitude compared to sea-level exercise of the same percentage maximal oxygen uptake (VO2max). Plasma lactate accumulation exercise on day 20 at high altitude was reduced in both placebo- and propranolol-treated subjects compared to exercise of the same percentage VO2max performed at sea level. The blunted lactate accumulation during exercise on day 20 at high altitude was associated with reduced muscle glycogen utilization. Thus, increased plasma lactate accumulation in unacclimatized lowlanders exercising at high altitude appears to be due to increased beta-adrenergic stimulation. However, acclimatization-induced changes in muscle glycogen utilization and plasma lactate accumulation are not adaptations to chronically increased beta-adrenergic activity.     

Implications of moderate altitude training for sea-level endurance in elite distance runners

Elite distance runners participated in one of two studies designed to investigate the effects of moderate altitude training (inspiratory partial pressure of oxygen ≈115–125 mmHg) on submaximal, maximal and supramaximal exercise performance following return to sea-level. Study 1 (New Mexico, USA) involved 14 subjects who were assigned to a 4-week altitude training camp (1500–2000 m) whilst 9 performance-matched subjects continued with an identical training programme at sea-level (CON). Ten EXP subjects who trained at 1640 m and 19 CON subjects also participated in study 2 (Krugersdorp, South Africa). Selected metabolic and cardiorespiratory parameters were determined with the subjects at rest and during exercise 21 days prior to (PRE) and 10 and 20 days following their return to sea-level (POST). Whole blood lactate decreased by 23% (P < 0.05 vs PRE) during submaximal exercise in the EXP group only after 20 days at sea-level (study 1). However, the lactate threshold and other measures of running economy remained unchanged. Similarly, supramaximal performance during a standardised track session did not change. Study 2 demonstrated that hypoxia per se did not alter performance. In contrast, in the EXP group supramaximal running velocity decreased by 2% (P < 0.05) after 20 days at sea-level. Both studies were characterised by a 50% increase in the frequency of upper respiratory and gastrointestinal tract infections during the altitude sojourns, and two male subjects were diagnosed with infectious mononucleosis following their return to sea-level (study 1). Group mean plasma glutamine concentrations at rest decreased by 19% or 143 (74) μM (P < 0.001) after 3 weeks at altitude, which may have been implicated in the increased incidence of infectious illness. Accepted: 19 March 1998     

Operation Everest II: elevated high-altitude pulmonary resistance unresponsive to oxygen

High altitude increases pulmonary arterial pressure (PAP), but no measurements have been made in humans above 4,500 m. Eight male athletic volunteers were decompressed in a hypobaric chamber for 40 days to a barometric pressure (PB) of 240 Torr, equivalent to the summit of Mt. Everest. Serial hemodynamic measurements were made at PB 760 (sea level), 347 (6,100 m), and 282/240 Torr (7,620/8,840 m). Resting PAP and pulmonary vascular resistance (PVR) increased from sea level to maximal values at PB 282 Torr from 15 +/- 0.9 to 34 +/- 3.0 mmHg and from 1.2 +/- 0.1 to 4.3 +/- 0.3 mmHg.l-1 X min, respectively. During near maximal exercise PAP increased from 33 +/- 1 mmHg at sea level to 54 +/- 2 mmHg at PB 282 Torr. Right atrial and wedge pressures were not increased with altitude. Acute 100% O2 breathing lowered cardiac output and PAP but not PVR. Systemic arterial pressure and resistance did not rise with altitude but did increase with O2 breathing, indicating systemic control differed from the lung circulation. We concluded that severe chronic hypoxia caused elevated pulmonary resistance not accompanied by right heart failure nor immediately reversed by O2 breathing.     

Peripheral chemoreflex function in hyperoxia following ventilatory acclimatization to altitude.

After a period of ventilatory acclimatization to high altitude (VAH), a degree of hyperventilation persists after relief of the hypoxic stimulus. This is likely, in part, to reflect the altered acid-base status, but it may also arise, in part, from the development during VAH of a component of carotid body (CB) activity that cannot be entirely suppressed by hyperoxia. To test this hypothesis, eight volunteers undergoing a simulated ascent of Mount Everest in a hypobaric chamber were acutely exposed to 30 min of hyperoxia at various stages of acclimatization. For the second 10 min of this exposure, the subjects were given an infusion of the CB inhibitor, dopamine (3 microg. kg(-1). min(-1)). Although there was both a significant rise in ventilation (P < 0.001) and a fall in end-tidal PCO(2) (P < 0.001) with VAH, there was no progressive effect of dopamine infusion on these variables with VAH. These results do not support a role for CB in generating the persistent hyperventilation that remains in hyperoxia after VAH.     

Nutritional alterations at high altitude in man

During the French 1980 Mount Pabil (7,102 m) Expedition, a study was made of four altitude-acclimatised climbers (age 36.5 +/- 3.6 years; VO2max 50.5 +/- 3.1 ml X kg-1). Intake of various nutrients, body weight, skinfold thicknesses as indices of body composition, and water and nitrogen balances, were recorded before, and during high altitude exposure, and again after the return to low altitude. There was a significant (35-57%) reduction in total caloric intake at high altitude. Body weight decreased progressively, mainly due to a reduction in body fat. The subjects apparently remained in water balance, while the nitrogen balance was always negative during high altitude exposure. The significant nutritional alterations were mainly observed above 6,000 m. They are discussed with respect to changes in feeding patterns and in hormonal status of the climbers accompanying hypoxia and other stressors proper to high altitude.     

Propranolol does not impair exercise oxygen uptake in normal men at high altitude

Decreased maximal O2 uptake (VO2max) and stimulation of the sympathetic nervous system have been previously shown to occur at high altitude. We hypothesized that tachycardia mediated by beta-adrenergic stimulation acted to defend VO2max at high altitude. Propranolol treatment beginning before high-altitude (4,300 m) ascent reduced heart rate during maximal and submaximal exercise in six healthy men treated with propranolol (80 mg three times daily) compared with five healthy subjects receiving placebo (lactose). Compared with sea-level values, the VO2max fell on day 2 at high altitude, but the magnitude of fall was similar in the placebo and propranolol treatment groups (26 +/- 6 vs. 32 +/- 5%, P = NS) and VO2max remained similar at high altitude in both groups once treatment was discontinued. During 30 min of submaximal (80% of VO2max) exercise, propranolol-treated subjects maintained O2 uptake levels that were as large as those in placebo subjects. The maintenance of maximal or submaximal levels of O2 uptake in propranolol-treated subjects at 4,300 m could not be attributed to increased minute ventilation, arterial O2 saturation, or hemoglobin concentration. Rather, it appeared that propranolol-treated subjects maintained O2 uptake by transporting a greater proportion of the O2 uptake with each heartbeat. Thus, contrary to our hypothesis, beta-adrenergic blockade did not impair maximal or submaximal O2 uptake at high altitude due perhaps to compensatory mechanisms acting to maintain stroke volume and cardiac output.     

Ferrum metabolism after permanence at extreme altitude on Mount Everest

High altitude has always intrigued physiologists because of the remarkable ability of man to adapt to the hostile environment. Despite numerous studies examining the physiological alterations occurring during exercise after exposure to hypoxia and the adaptative effects of sustained residence at altitude, several issues remain unresolved. The aim of investigation of the Spanish Medical Research Expedition to Mount Everest in 1992 was an extensive study on the physiological adaptations to the hypobaric environment at extreme altitude. We are presenting advance results the gasometry, acid-base parameters and ferrum metabolism.     

A strategy for determining arterial blood gases on the summit of Mt. Everest

Background  

Climbers on the summit of Mt. Everest are exposed to extreme hypoxia, and the physiological implications are of great interest. Inferences have been made from alveolar gas samples collected on the summit, but arterial blood samples would give critical information. We propose a plan to insert an arterial catheter at an altitude of 8000 m, take blood samples above this using an automatic sampler, store the samples in glass syringes in an ice-water slurry, and analyze them lower on the mountain 4 to 6 hours later.     

Greater free plasma VEGF and lower soluble VEGF receptor-1 in acute mountain sickness.

Vascular endothelial growth factor (VEGF) is a hypoxia-induced protein that produces vascular permeability, and limited evidence suggests a possible role for VEGF in the pathophysiology of acute mountain sickness (AMS) and/or high-altitude cerebral edema (HACE). Previous studies demonstrated that plasma VEGF alone does not correlate with AMS; however, soluble VEGF receptor (sFlt-1), not accounted for in previous studies, can bind VEGF in the circulation, reducing VEGF activity. In the present study, we hypothesized that free VEGF is greater and sFlt-1 less in subjects with AMS compared with well individuals at high altitude. Subjects were exposed to 4,300 m for 19-20 h (baseline 1,600 m). The incidence of AMS was determined by using a modified Lake Louise symptom score and the Environmental Symptoms Questionnaire for cerebral effects. Plasma was collected at low altitude and after 24 h at high altitude, or at time of illness, and then analyzed by ELISA for VEGF and for soluble VEGF receptor, sFlt-1. AMS subjects had lower sFlt-1 at both low and high altitude compared with well subjects and a significant rise in free plasma VEGF on ascent to altitude compared with well subjects. We conclude that increased free plasma VEGF on ascent to altitude is associated with AMS and may play a role in pathophysiology of AMS.     

Body fluid status on induction,reinduction and prolonged stay at high altitude of human volunteers

Studies on adaptation to high altitude (HA) of 3500 m in the Himalayas were conducted in three phases, each including 10 normal and healthy males normally resident at sea-level. Phase I subjects had no previous experience of HA, phase II subjects after 4–6 months at HA were airlifted to sea-level and phase III subjects stayed continuously for 6 months at 3500 m. Body fluid compartments and blood gases were determined in all three groups. Plasma volume was highly elevated in the phase II subjects on reinduction to sea-level from HA. In comparison to phase I subjects, the retention of fluid in extracellular compartment was increased at HA leading to increased susceptibility to high altitude illness. Phase III subjects were hyperhydrated with decreased plasma volume and increased PO₂ in comparison to the other two groups.     

Altitude ammonia-oxidizing bacteria and archaea in soils of Mount Everest

To determine the abundance and distribution of bacterial and archaeal ammonia oxidizers in alpine and permafrost soils, 12 soils at altitudes of 4000–6550 m above sea level (m a.s.l.) were collected from the northern slope of the Mount Everest (Tibetan Plateau), where the permanent snow line is at 5800–6000 m a.s.l. Communities were characterized by real-time PCR and clone sequencing by targeting on amo A genes, which putatively encode ammonia monooxygenase subunit A. Archaeal amo A abundance was greater than bacterial amo A abundance in lower altitude soils (≤5400 m a.s.l.), but this situation was reversed in higher altitude soils (≥5700 m a.s.l.). Both archaeal and bacterial amo A abundance decreased abruptly in higher altitude soils. Communities shifted from a Nitrosospira amo A cluster 3a-dominated ammonia-oxidizing bacteria community in lower altitude soils to communities dominated by a newly designated Nitrosospira ME and cluster 2-related groups and Nitrosomonas cluster 6 in higher altitude soils. All archaeal amo A sequences fell within soil and sediment clusters, and the proportions of the major archaeal amo A clusters changed between the lower altitude and the higher altitude soils. These findings imply that the shift in the relative abundance and community structure of archaeal and bacterial ammonia oxidizers may result from selection of organisms adapted to altitude-dependent environmental factors in elevated soils.     

Contact phase of blood coagulation is not activated in edema of high altitude

To examine whether bradykinin generated by the activation of the contact phase of blood coagulation is involved in the pathogenesis of edema occurring after acute exposure to high altitude, 15 mountaineers were examined at 490 m and 1, 3, and 5 days after arrival at 4,559 m. The clotting activity levels of factor XII, factor XI, plasma prekallikrein, and high-molecular-weight kininogen (HMWK) were measured, and plasma kallikrein-induced proteolytic cleavage of HMWK was assessed by ligand blotting by use of radiolabeled factor XI. After an ascent on foot from 1,170 to 4,559 m in 3 days, three subjects developed high-altitude pulmonary edema, and four subjects presented facial edema. There was no evidence for activation of the contact system in any subject as demonstrated by the lack of proteolytic cleavage of HMWK at high altitude. The absence of contact system activation was further supported by stable plasma levels of the individual factors of contact activation. Therefore, we conclude that bradykinin generated by plasma kallikrein-induced cleavage of HMWK is not involved in the pathogenesis of edema due to acute exposure to high altitude.