scholarly journals Altitude Cardiomyopathy Is Associated With Impaired Stress Electrocardiogram and Increased Circulating Inflammation Makers

2021 ◽  
Vol 12 ◽  
Author(s):  
Ya-Jun Shi ◽  
Jin-Li Wang ◽  
Ling Gao ◽  
Dong-Lin Wen ◽  
Qing Dan ◽  
...  
Keyword(s):  
Blood Pressure ◽  
High Altitude ◽  
Sea Level ◽  
Exercise Intensity ◽  
Exercise Tolerance ◽  
Acute Mountain Sickness ◽  
Young Men ◽  
Acute Exposure ◽  
Physiological Variables ◽  
Metabolic Equivalents

Many sea-level residents suffer from acute mountain sickness (AMS) when first visiting altitudes above 4,000 m. Exercise tolerance also decreases as altitude increases. We observed exercise capacity at sea level and under a simulated hypobaric hypoxia condition (SHHC) to explore whether the response to exercise intensity represented by physiological variables could predict AMS development in young men. Eighty young men from a military academy underwent a standard treadmill exercise test (TET) and biochemical blood test at sea level, SHHC, and 4,000-m altitude, sequentially, between December 2015 and March 2016. Exercise-related variables and 12-lead electrocardiogram parameters were obtained. Exercise intensity and AMS development were investigated. After exposure to high altitude, the count of white blood cells, alkaline phosphatase and serum albumin were increased (P < 0.05). There were no significant differences in exercise time and metabolic equivalents (METs) between SHHC and high-altitude exposures (7.05 ± 1.02 vs. 7.22 ± 0.96 min, P = 0.235; 9.62 ± 1.11 vs. 9.38 ± 1.12, P = 0.126, respectively). However, these variables were relatively higher at sea level (8.03 ± 0.24 min, P < 0.01; 10.05 ± 0.31, P < 0.01, respectively). Thus, subjects displayed an equivalent exercise tolerance upon acute exposure to high altitude and to SHHC. The trends of cardiovascular hemodynamics during exercise under the three different conditions were similar. However, both systolic blood pressure and the rate–pressure product at every TET stage were higher at high altitude and under the SHHC than at sea level. After acute exposure to high altitude, 19 (23.8%) subjects developed AMS. Multivariate logistic regression analysis showed that METs under the SHHC {odds ratio (OR) 0.355 per unit increment [95% confidence intervals (CI) 0.159−0.793], P = 0.011}, diastolic blood pressure (DBP) at rest under SHHC [OR 0.893 per mmHg (95%CI 0.805−0.991), P = 0.030], and recovery DBP 3 min after exercise at sea level [OR 1.179 per mmHg (95%CI 1.043−1.333), P = 0.008] were independently associated with AMS. The predictive model had an area under the receiver operating characteristic curve of 0.886 (95%CI 0.803−0.969, P < 0.001). Thus, young men have similar exercise tolerance in acute exposure to high altitude and to SHHC. Moreover, AMS can be predicted with superior accuracy using characteristics easily obtainable with TET.

scholarly journals Risk factors underlying high-altitude pulmonary edema in the Ecuadorian Andes

2021 ◽  
Author(s):  
Karen Sánchez ◽  
Wilfre Machado ◽  
Anita Villafuerte ◽  
Santiago Ballaz
Keyword(s):  
Blood Pressure ◽  
Logistic Regression ◽  
Pulmonary Edema ◽  
High Altitude ◽  
Sea Level ◽  
Acute Mountain Sickness ◽  
Vital Signs ◽  
Blood Analysis ◽  
High Altitude Pulmonary Edema ◽  
Simple Logistic

Abstract Background Ascent to high altitude (> 2500 m) exposes people to hypobaric atmospheric pressure and blood hypoxemia. It provokes a syndrome whose symptoms vary from the mild acute mountain sickness (AMS) to the life-threatening, high-altitude pulmonary edema (HAPE). This study analyzed the risk for developing high-altitude sickness in a group of HAPE patients (n = 59), which was contrasted against a group of AMS patients (n = 240) as the NO HAPE group, after sojourning above 4,000 m height. The objective of this retrospective was to analyse the factors contributing to the HAPE prevalence among travellers and dwellers of the Ecuadorian Andes. Methods AMS and HAPE groups were compared through demographic (ethnicity, sex, and age), environmental (permanent residence altitude and recent stay at sea-level), health status (vital signs), and blood analysis variables. The Cramer´s V, simple logistic regression(SLR), and multiple logistic regression(MLR) analyses revealed patterns of significant associations. Results Analyses revealed that high-altitude indigenous residents were HAPE-prone, while mestizos living at sea level only had AMS. Blood pressure played a role in HAPE risk. Women were more tolerant to HAPE than men. Among indigenes, HAPE prevalence significantly rose after sojourning at sea level, a phenomenon called “reentry HAPE”. Conclusions In Andean indigenes, HAPE could be produced by a poor adaptation to high altitude, a high haemoglobin, and a blunted reactivity of blood pressure to environmentally-induced hypoxia. All the above gives support to the complex gene-environment interactions in the progress of HAPE, which may give some clues about of the etiopathogenesis of non-cardiogenic edema.

A STUDY OF VARIOUS INDICES OF ADRENOCORTICAL ACTIVITY DURING 23 DAYS AT HIGH ALTITUDE

1963 ◽  
Vol 26 (4) ◽  
pp. 555-566 ◽  
Author(s):  
P. C. B. MACKINNON ◽  
M. E. MONK-JONES ◽  
K. FOTHERBY
Keyword(s):  
Length Of Stay ◽  
High Altitude ◽  
Sea Level ◽  
Acute Exposure ◽  
Adrenocorticotrophic Hormone ◽  
Adrenocortical Activity

SUMMARY 1. Four men and three women ascended by télépherique and helicopter from 1000 to 4333 m. where they remained for 23 days. 2. Measurements of urinary 17-hydroxycorticosteroids, 17-oxosteroids, pregnanediol and pregnanetriol and circulating eosinophils were made at sea level and at high altitude. 3. An attempt was also made to measure changes in emotional activity by means of the palmar sweat index (PSI). This index was assessed at intervals throughout the day at sea level and at high altitude, and in response to adrenocorticotrophic hormone (ACTH) and a self-imposed stress. 4. Within 24 hr. of acute exposure to high altitude urinary 17-hydroxycorticosteroids increased whilst circulating eosinophils decreased; by the 5th day both were returning to sea-level values. The output of 17-oxosteroids was lower by the 5th day at high altitude and subsequently increased; pregnanediol and pregnanetriol levels remained unchanged. 5. PSIs throughout the day become progressively lower as the length of stay at altitude increased. The response to ACTH at sea level and high altitude appeared to be similar but the response to a self-imposed stress was longer in duration at high altitude than at sea level.

Effect of beta-adrenoceptor blockade on renin-aldosterone and alpha-ANF during exercise at altitude

1989 ◽  
Vol 67 (1) ◽  
pp. 141-146 ◽  
Author(s):  
P. Bouissou ◽  
J. P. Richalet ◽  
F. X. Galen ◽  
M. Lartigue ◽  
P. Larmignat ◽  
...  
Keyword(s):  
High Altitude ◽  
Sea Level ◽  
Acute Mountain Sickness ◽  
Plasma Renin ◽  
Barometric Pressure ◽  
Suppressive Effect ◽  
Beta Blockade ◽  
Plasma Norepinephrine ◽  
Plasma Aldosterone Concentration ◽  
Ergometer Exercise

The renin-aldosterone system may be depressed in subjects exercising at high altitude, thereby preventing excessive angiotensin I (ANG I) and aldosterone levels, which could favor the onset of acute mountain sickness. The role of beta-adrenoceptors in hormonal responses to hypoxia was investigated in 12 subjects treated with a nonselective beta-blocker, pindolol. The subjects performed a standardized maximal bicycle ergometer exercise with (P) and without (C) acute pindolol treatment (15 mg/day) at sea level, as well as during a 5-day period at high altitude (4,350 m, barometric pressure 450 mmHg). During sea-level exercise, pindolol caused a reduction in plasma renin activity (PRA, 2.83 +/- 0.35 vs. 5.13 +/- 0.7 ng ANG I.ml-1.h-1, P less than 0.01), an increase in plasma alpha-atrial natriuretic factor (alpha-ANF) level (23.1 +/- 2.9 (P) vs. 10.4 +/- 1.5 (C) pmol/1, P less than 0.01), and no change in plasma aldosterone concentration [0.50 +/- 0.04 (P) vs. 0.53 +/- 0.03 (C) nmol/1]. Compared with sea-level values, PRA (3.45 +/- 0.7 ng ANG I.ml-1.h-1) and PA (0.39 +/- 0.03 nmol/1) were significantly lower (P less than 0.05) during exercise at high altitude. alpha-ANF was not affected by hypoxia. When beta-blockade was achieved at high altitude, exercise-induced elevation in PRA was completely abolished, but no additional decline in PA occurred. Plasma norepinephrine and epinephrine concentrations tended to be lower during maximal exercise at altitude; however, these differences were not statistically significant. Our results provide further evidence that hypoxia has a suppressive effect on the renin-aldosterone system. However, beta-adrenergic mechanisms do not appear to be responsible for inhibition of renin secretion at high altitude.

scholarly journals Benzolamide improves oxygenation and reduces acute mountain sickness during a high-altitude trek and has fewer side effects than acetazolamide at sea level

2016 ◽  
Vol 4 (3) ◽  
pp. e00203 ◽  
Author(s):  
David J. Collier ◽  
Chris B. Wolff ◽  
Anne-Marie Hedges ◽  
John Nathan ◽  
Rod J. Flower ◽  
...  
Keyword(s):  
Side Effects ◽  
High Altitude ◽  
Sea Level ◽  
Acute Mountain Sickness ◽  
Mountain Sickness

Cardiovascular autonomic modulation and activity of carotid baroreceptors at altitude

1998 ◽  
Vol 95 (5) ◽  
pp. 565-573 ◽  
Author(s):  
Luciano BERNARDI ◽  
Claudio PASSINO ◽  
Giammario SPADACINI ◽  
Alessandro CALCIATI ◽  
Robert ROBERGS ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Systolic Blood Pressure ◽  
High Altitude ◽  
Sea Level ◽  
Skin Blood Flow ◽  
Low Frequency ◽  
Sympathetic Activation ◽  
High Altitude Natives

1.To assess the effects of acute exposure to high altitude on baroreceptor function in man we evaluated the effects of baroreceptor activation on R–R interval and blood pressure control at high altitude. We measured the low-frequency (LF) and high-frequency (HF) components in R–R, non-invasive blood pressure and skin blood flow, and the effect of baroreceptor modulation by 0.1-Hz sinusoidal neck suction. Ten healthy sea-level natives and three high-altitude native, long-term sea-level residents were evaluated at sea level, upon arrival at 4970 ;m and 1 week later. 2.Compared with sea level, acute high altitude decreased R–R and increased blood pressure in all subjects [sea-level natives: R–R from 1002±45 to 775±57 ;ms, systolic blood pressure from 130±3 to 150±8 ;mmHg; high-altitude natives: R–R from 809±116 to 749±47 ;ms, systolic blood pressure from 110±12 to 125±11 ;mmHg (P< 0.05 for all)]. One week later systolic blood pressure was similar to values at sea level in all subjects, whereas R–R remained elevated in sea-level natives. The low-frequency power in R–R and systolic blood pressure increased in sea-level natives [R–R-LF from 47±8 to 65±10% (P< 0.05), systolic blood pressure-LF from 1.7±0.3 to 2.6±0.4 ln-mmHg2 (P< 0.05)], but not in high-altitude natives (R–R-LF from 32±13 to 38±19%, systolic blood pressure-LF from 1.9±0.5 to 1.7±0.8 ln-mmHg2). The R–R-HF decreased in sea-level natives but not in high-altitude natives, and no changes occurred in systolic blood pressure-HF. These changes remained evident 1 week later. Skin blood flow variability and its spectral components decreased markedly at high altitude in sea-level natives but showed no changes in high-altitude natives. Neck suction significantly increased the R–R- and systolic blood pressure-LF in all subjects at both sea level and high altitude. 3.High altitude induces sympathetic activation in sea-level natives which is partially counteracted by active baroreflex. Despite long-term acclimatization at sea level, high-altitude natives also maintain active baroreflex at high altitude but with lower sympathetic activation, indicating a persisting high-altitude adaptation which may be genetic or due to baroreflex activity not completely lost by at least 1 year's sea-level residence.

scholarly journals Adenosine receptor-dependent signaling is not obligatory for normobaric and hypobaric hypoxia-induced cerebral vasodilation in humans

2017 ◽  
Vol 122 (4) ◽  
pp. 795-808 ◽  
Author(s):  
Ryan L. Hoiland ◽  
Anthony R. Bain ◽  
Michael M. Tymko ◽  
Mathew G. Rieger ◽  
Connor A. Howe ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
High Altitude ◽  
Sea Level ◽  
Adenosine Receptor ◽  
Hypobaric Hypoxia ◽  
End Tidal ◽  
Double Blinded

Hypoxia increases cerebral blood flow (CBF) with the underlying signaling processes potentially including adenosine. A randomized, double-blinded, and placebo-controlled design, was implemented to determine if adenosine receptor antagonism (theophylline, 3.75 mg/Kg) would reduce the CBF response to normobaric and hypobaric hypoxia. In 12 participants the partial pressures of end-tidal oxygen ([Formula: see text]) and carbon dioxide ([Formula: see text]), ventilation (pneumotachography), blood pressure (finger photoplethysmography), heart rate (electrocardiogram), CBF (duplex ultrasound), and intracranial blood velocities (transcranial Doppler ultrasound) were measured during 5-min stages of isocapnic hypoxia at sea level (98, 90, 80, and 70% [Formula: see text]). Ventilation, [Formula: see text] and [Formula: see text], blood pressure, heart rate, and CBF were also measured upon exposure (128 ± 31 min following arrival) to high altitude (3,800 m) and 6 h following theophylline administration. At sea level, although the CBF response to hypoxia was unaltered pre- and postplacebo, it was reduced following theophylline ( P < 0.01), a finding explained by a lower [Formula: see text] ( P < 0.01). Upon mathematical correction for [Formula: see text], the CBF response to hypoxia was unaltered following theophylline. Cerebrovascular reactivity to hypoxia (i.e., response slope) was not different between trials, irrespective of [Formula: see text]. At high altitude, theophylline ( n = 6) had no effect on CBF compared with placebo ( n = 6) when end-tidal gases were comparable ( P > 0.05). We conclude that adenosine receptor-dependent signaling is not obligatory for cerebral hypoxic vasodilation in humans. NEW & NOTEWORTHY The signaling pathways that regulate human cerebral blood flow in hypoxia remain poorly understood. Using a randomized, double-blinded, and placebo-controlled study design, we determined that adenosine receptor-dependent signaling is not obligatory for the regulation of human cerebral blood flow at sea level; these findings also extend to high altitude.

ACETAZOLAMIDE COUNTERACTS AMBULATORY BLOOD PRESSURE INCREASE UNDER ACUTE EXPOSURE TO HIGH ALTITUDE

2011 ◽  
Vol 29 ◽  
pp. e34
Author(s):  
G. BILO ◽  
C. Lombardi ◽  
M. Revera ◽  
E. Diazzi ◽  
A. Giuliano ◽  
...  
Keyword(s):  
Blood Pressure ◽  
High Altitude ◽  
Ambulatory Blood Pressure ◽  
Pressure Increase ◽  
Acute Exposure ◽  
Blood Pressure Increase

scholarly journals Baseline psychological traits contribute to Lake Louise Acute Mountain Sickness score at high altitude

2021 ◽  
Author(s):  
Benjamin James Talks ◽  
Catherine Campbell ◽  
Stephanie J Larcombe ◽  
Lucy Marlow ◽  
Sarah Louise Finnegan ◽  
...  
Keyword(s):  
High Altitude ◽  
Sea Level ◽  
Acute Mountain Sickness ◽  
Symptom Burden ◽  
Control Group ◽  
Physiological Changes ◽  
Symptom Experience ◽  
Psychological Traits ◽  
Bodily Sensations ◽  
Mountain Sickness

Background: Interoception refers to an individuals ability to sense their internal bodily sensations. Acute mountain sickness (AMS) is a common feature of ascent to high altitude that is only partially explained by measures of peripheral physiology. We hypothesised that interoceptive ability may explain the disconnect between measures of physiology and symptom experience in AMS. Methods and Material: Two groups of 18 participants were recruited to complete a respiratory interoceptive task three times at two-week intervals. The control group remained in Birmingham (140m altitude) for all three tests. The altitude group completed test 1 in Birmingham, test 2 the day after arrival at 2624m, and test 3 at 2728m after an 11-day trek at high altitude (up to 4800m). Results: By measuring changes to metacognitive performance, we showed that acute ascent to altitude neither presented an interoceptive challenge, nor acted as interoceptive training. However, AMS symptom burden throughout the trek was found to relate to sea-level measures of anxiety, agoraphobia, and neuroticism. Conclusions: This suggests that the Lake Louise AMS score is not solely a reflection of physiological changes on ascent to high altitude, despite often being used as such by researchers and commercial trekking companies alike.

Acclimatization at high altitude in gradual and acute induction

1995 ◽  
Vol 79 (2) ◽  
pp. 487-492 ◽  
Author(s):  
S. S. Purkayastha ◽  
U. S. Ray ◽  
B. S. Arora ◽  
P. C. Chhabra ◽  
L. Thakur ◽  
...  
Keyword(s):  
High Altitude ◽  
Sea Level ◽  
Time Course ◽  
Physiological Responses ◽  
Acute Mountain Sickness ◽  
Blood Gases ◽  
Blood Gas ◽  
Mountain Sickness ◽  
High Altitude Illness ◽  
In Transit

The study assessed physiological responses to induction to high altitude first to 3,500 m and then to 4,200 m and compared the time course of altitude acclimatization in two groups of male volunteers. The acutely inducted group was transported by aircraft (AI) to 3,500 m in 1 h, whereas the gradually inducted group was transported by road (RI) in 4 days. Baseline recordings of basal cardiovascular, respiratory, and blood gas variables were monitored at sea level as well as at 3,500 m on days 1, 3, 5, and 7. Blood gases were measured on day 10 also. After 15 days at 3,500 m, the subjects were inducted to 4,200 m by road, and measurements were repeated on days 1, 3, and 5, except blood gas variables, which were done on day 10 only. Acute mountain sickness symptoms were recorded throughout. The responses of RI were stable by day 3 of induction at 3,500 m, whereas it took 5 days for AI. Four days in transit for RI appear equivalent to 2 days at 3,500 m for AI. Acclimatization schedules of 3 and 5 days, respectively, for RI and AI are essential to avoid malacclimatization and/or high-altitude illness. Both groups took 3 days at 4,200 m to attain stability for achieving acclimatization.

Blood pressure and plasma catecholamines in acute and prolonged hypoxia: effects of local hypothermia

1999 ◽  
Vol 87 (6) ◽  
pp. 2053-2058 ◽  
Author(s):  
Inge-Lis Kanstrup ◽  
Troels Dirch Poulsen ◽  
Jesper Melchior Hansen ◽  
Lars Juel Andersen ◽  
Morten Heiberg Bestle ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Sea Level ◽  
High Pressures ◽  
Acute Mountain Sickness ◽  
Plasma Catecholamines ◽  
Plasma Norepinephrine ◽  
Plasma Catecholamine ◽  
Local Cooling ◽  
Local Hypothermia

This study measured the pressor and plasma catecholamine response to local hypothermia during adaptation to hypobaric hypoxia. Eight healthy men were studied at rest and after 10 and 45 min of local cooling of one hand and forearm as well as after 30 min of rewarming at sea level and again 24 h and 5 days after rapid, passive transport to high altitude (4,559 m). Acute mountain sickness scores ranged from 5 to 16 (maximal attainable score: 20) on the first day but were reduced to 0–8 by the fifth day. Systolic blood pressure, heart rate, and plasma epinephrine increased on day 1 at altitude compared with sea level but declined again on day 5, whereas diastolic and mean blood pressures continued to rise in parallel with plasma norepinephrine. With local cooling, an increased vasoactive response was seen on the fifth day at altitude. Very high pressures were obtained, and the pressure elevation was prolonged. Heart rate increased twice as much on day 5 compared with the other two occasions. Thoracic fluid index increased with cooling on day 5, suggesting an increase in pulmonary vascular resistance. In conclusion, prolonged hypoxia seems to elicit an augmented pressor response to local cooling in the systemic and most likely also the pulmonary circulation.

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