Exercise exacerbates acute mountain  sickness at simulated high altitude

Roach, Robert C.; Maes, Damon; Sandoval, Darleen A.; Robergs, Robert A.; Icenogle, Milton V.; Hinghofer‐Szalkay, Helmut; Lium, D.; Loeppky, Jack A.

doi:10.1152/jappl.2000.88.2.581

Cited by 205 publications

(118 citation statements)

References 12 publications

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“…Avoiding overexertion following ascent is another commonly recommended measure, although studies have reported varying results about the relationship between exertion and risk of AMS [29,30,113]. Abrupt cessation of caffeine intake in chronic users of caffeinated beverages may provoke withdrawal symptoms that mimic those of AMS [114].…”

Section: Other Measuresmentioning

confidence: 99%

Acute high-altitude sickness

2017

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At any point 1-5 days following ascent to altitudes ⩾2500 m, individuals are at risk of developing one of three forms of acute altitude illness: acute mountain sickness, a syndrome of nonspecific symptoms including headache, lassitude, dizziness and nausea; high-altitude cerebral oedema, a potentially fatal illness characterised by ataxia, decreased consciousness and characteristic changes on magnetic resonance imaging; and high-altitude pulmonary oedema, a noncardiogenic form of pulmonary oedema resulting from excessive hypoxic pulmonary vasoconstriction which can be fatal if not recognised and treated promptly. This review provides detailed information about each of these important clinical entities. After reviewing the clinical features, epidemiology and current understanding of the pathophysiology of each disorder, we describe the current pharmacological and nonpharmacological approaches to the prevention and treatment of these diseases.

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Section: Other Measuresmentioning

confidence: 99%

Acute high-altitude sickness

2017

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“…Furthermore, exercise accelerates and increases the severity of AMS, which is associated with the greater arterial hypoxemia that takes place during exercise at high altitude. 40 In addition, acute hypoxia is a potent activator of the sympathetic nervous system in at least two ways. It causes relaxation of the vascular smooth muscle of the systemic circulation, which leads to hypotension that activates baroreceptor mediation in order to maintain homeostasis.…”

Section: Correlation Between Hrv Measurements In Normoxia and Spo 2 Imentioning

confidence: 99%

Cardiorespiratory parameters during submaximal exercise under acute exposure to normobaric and hypobaric hypoxia

Basualto-Alarcón

Rodas

Galilea

et al. 2012

Apunts. Medicina de l'Esport

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Seven healthy young men were submitted twice to a hypoxia tolerance test at a simulated altitude (3000 m). Their first acute exposure was in a hypobaric chamber; and the second, in a hypoxic tent. Cardiorespiratory parameters and heart rate variability measurements were obtained under each hypoxic condition. A significant decrease of 6% to 8% compared to normal oxygen conditions was observed in arterial oxygen saturation (SpO 2 ) in both hypoxic conditions at rest; whereas exercise led to decreases of 10% in SpO 2 despite an increase of 27% in respiratory minute volume. The low frequency (LF) and high frequency (HF) components of heart rate variability significantly changed from normoxia (LF: 37.1, HF: 62.9, LF/HF: 1.27) to hypobaric hypoxia (HH) (LF: 49.1, HF: 50.6, LF/HF: 1.96). However, these changes were not observed under normobaric hypoxia. Thus, heart rate variability behaved differently in the two hypoxic conditions, supporting the hypothesis that normobaric hypoxia and hypobaric hypoxia are not equal stimuli to the cardiovascular and respiratory systems. A correlation was found between sympathetic and vagal modulations in normoxia and SpO 2 at exercise under hypobaric hypoxia (HH). Individuals with higher sympathetic modulation (LF%) in normoxia had higher SpO 2 at exercise under HH (r = 0.808, P < 0.05) and individuals with higher vagal modulation (HF%) in normoxia showed a trend to lower SpO 2 in exercise under HH (r = −0.636, P = 0.125). This opens up the possibility of using this correlation as a tool for predicting the individual capacity to altitude acclimatization. © 2011 Consell Català de l'Esport. Generalitat de Catalunya. Published by Elsevier España, S.L. All rights reserved. * Corresponding author. E-mail address: gviscor@ub.edu (G. Viscor). PALABRAS CLAVEVariabilidad de la frecuencia cardiaca; Prueba de tolerancia a hipoxia; Tienda hipóxica; Cámara hipobárica; Saturación arterial de oxígeno Parámetros cardiorrespiratorios durante ejercicio submáximo en hipoxia aguda hipobárica y normobáricaResumen Siete jóvenes sanos y en buena condición física realizaron dos pruebas de tolerancia a hipoxia a una altitud simulada de 3.000 m. La primera fue en cámara hipobárica, mientras que la segunda se efectuó en una tienda hipóxica. Se registraron varios parámetros cardiorrespiratorios y la variabilidad de la frecuencia cardiaca. En comparación con las condiciones de normoxia, se observó un decremento significativo del 6% al 8% en la saturación de oxígeno arterial (SpO 2 ) en reposo en ambas condiciones de hipoxia. El ejercicio desencadenó descensos de un 10% en SpO 2 pese a un incremento del 27% del volumen minuto ventilatorio. Tanto los componentes de baja (LF) como alta frecuencia (HF) de la variabilidad del ritmo cardiaco cambiaron significativamente en hipoxia hipobárica (LF: 49,1, HF: 50,6, LF/HF: 1,96) respecto a normoxia (LF: 37,1, HF: 62,9, LF/HF: 1,27). Estos cambios no se apreciaron en condiciones de hipoxia normobárica, lo cual apoya la hipótesis de que la hipoxia hipobárica y norm...

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“…Accentuation of arterial deoxygenation and cardiorespiratory responses during exercise are two mechanisms potentially underlying the exacerbation of AMS and cerebral edema when hypoxic exposure is associated with exercise. 13,14 Whether larger cerebral changes during hypoxia when exercise is performed compared with resting condition as reported by Mairer et al 14 are the consequences of exercise-induced accentuation of hypoxemia (and therefore due to greater hypoxic stress) or cardiorespiratory responses to exercise (e.g., hemodynamic changes) remains to be determined to further clarify the mechanisms of cerebral changes associated with hypoxic exposure.…”

Section: Introductionmentioning

confidence: 92%

“…3,4,[8][9][10] Some reports suggest that performing physical activity during the first hours of hypoxic exposure may accentuate symptoms of AMS. [11][12][13] Only one recent study compared the effects of hypoxic exposure for 8 hours associated or not with physical exercise (3 times 30 minutes of moderate intensity exercise) on brain volume and cerebral edema. 14 The authors reported greater increase in gray-and white-matter volumes and higher ADC after hypoxic exposure when subjects performed physical exercise but these changes did not correlate with AMS severity.…”

Section: Introductionmentioning

confidence: 99%

“…[11][12][13][14][15]27 Rupp et al 15 showed that when conditions of hypoxic exposure with and without physical exercise are matched for SpO 2 level (i.e., taking into account the exercise-induced desaturation and therefore the larger hypoxic stress during exercise), AMS score and prevalence are not significantly increased by prolonged moderate intensity exercise. This suggests that hypoxemia, whether exercise is performed, is the main mechanism underlying AMS.…”

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confidence: 99%

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Cerebral Volumetric Changes Induced by Prolonged Hypoxic Exposure and Whole-Body Exercise

Rupp

Jubeau

Lamalle

et al. 2014

J Cereb Blood Flow Metab

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The present study assessed the isolated and synergetic effects of hypoxic exposure and prolonged exercise on cerebral volume and subedema and symptoms of acute mountain sickness (AMS). Twelve healthy males performed three semirandomized blinded 11-hour sessions with (1) an inspiratory oxygen fraction (FiO 2 ) of 12% and 4-hour cycling, (2) FiO 2 = 21% and 4-hour cycling, and (3) FiO 2 = 8.5% to 12% at rest (matching arterial oxygen saturation measured during the first hypoxic session). Volumetric, apparent diffusion coefficient (ADC), and arterial spin labelling 3T magnetic resonance imaging sequences were performed after 30 minutes and 10 hours in each session. Thirty minutes of hypoxia at rest induced a significant increase in white-matter volume (+0.8 ± 1.0% compared with normoxia) that was exacerbated after 10 hours of hypoxia at rest (+1.5 ± 1.1%) or with cycling (+1.6 ± 1.1%). Total brain parenchyma volume increased significantly after 10 hours of hypoxia with cycling only (+1.3 ± 1.1%). Apparent diffusion coefficient was significantly reduced after 10 hours of hypoxia at rest or with cycling. No significant change in cerebral blood flow was observed. These results demonstrate changes in white-matter volume as early as after 30 minutes of hypoxia that worsen after 10 hours, probably due to cytotoxic edema. Exercise accentuates the effect of hypoxia by increasing total brain volume. These changes do not however correlate with AMS symptoms.

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Exercise exacerbates acute mountain sickness at simulated high altitude

Cited by 205 publications

References 12 publications

Acute high-altitude sickness

Acute high-altitude sickness

Cardiorespiratory parameters during submaximal exercise under acute exposure to normobaric and hypobaric hypoxia

Cerebral Volumetric Changes Induced by Prolonged Hypoxic Exposure and Whole-Body Exercise

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