Relationship between Changes in Cerebral Blood Flow with Symptoms of Acute Mountain Sickness in Men Repeatedly Exposed to Simulated High Altitude (original) (raw)
Related papers
Brain and Behavior, 2016
Introduction: We hypothesized that cerebral alterations in edema, perfusion, and/or intracranial pressure (ICP) are related to the development of acute mountain sickness (AMS). Methods: To vary AMS, we manipulated ambient oxygen, barometric pressure, and exercise duration. Thirty-six subjects were tested before, during and after 8 h exposures in (1) normobaric normoxia (NN; 300 m elevation equivalent); (2) normobaric hypoxia (NH; 4400 m equivalent); and (3) hypobaric hypoxia (HH; 4400 m equivalent). After a passive 15 min ascent, each subject participated in either 10 or 60 min of cycling exercise at 50% of heart rate reserve. We measured tissue absorption and scattering via radio-frequency near-infrared spectroscopy (NIRS), optic nerve sheath diameter (ONSD) via ultrasound, and AMS symptoms before, during, and after environmental exposures. Results: We observed significant increases in NIRS tissue scattering of 0.35 AE 0.11 cm À1 (P = 0.001) in subjects with AMS (i.e., AMS+), consistent with mildly increased cerebral edema. We also noted a small, but significant increase in total hemoglobin concentrations with AMS+, 3.2 AE 0.8 lmolL À1 (P < 0.0005), consistent with increased cerebral perfusion. No effect of exercise duration was found, nor did we detect differences between NH and HH. ONSD assays documented a small but significant increase in ONSD (0.11 AE 0.02 mm; P < 0.0005) with AMS+, suggesting mildly elevated ICP, as well as further increased ONSD with longer exercise duration (P = 0.005). Conclusion: In AMS+, we found evidence of cerebral edema, elevated cerebral perfusion, and elevated ICP. The observed changes were small but consistent with the reversible nature of AMS.
Wilderness & Environmental Medicine, 2012
Objective.-Rapid ascent to altitude can result in the development of high altitude illnesses such as acute mountain sickness (AMS). This study aimed to investigate AMS symptoms in adolescents and study basic cardiopulmonary measurements at altitude. Methods.-Thirty-eight adolescents aged 16 to 19 years flew to 3500 m from 215 m and continued over a 23-day period to ascend to a maximum altitude of 5200 m. Each member of the expedition completed a Lake Louise Self-Assessment Questionnaire (LLSAQ) on a daily basis, and AMS was defined as a score of Ն3, with an associated headache. Physiology measurements included a step test, and both before and after exercise pulse oximetry, blood pressure, and pulse rate. Results.-Oxygen saturation inversely correlated with altitude (P ϭ .001). Mean pulse rate increased from 70 beats/min (Ϯ6.5) at 215 m to 83 beats/min (Ϯ2.2) at 3500 m (P ϭ .01), and a rise in blood pressure with ascent was highlighted (P ϭ .004). The majority of subjects (84%) had an LLSAQ of 3 or more on at least 1 occasion, and they tended to record higher pulse rates (P ϭ .005) and lower oxygen saturations (P ϭ .001). Exercise-induced drops in oxygen saturation and raised pulse rates were more prolonged in subjects with severe AMS compared with subjects not having AMS (P ϭ .046 and P ϭ .005, respectively). Conclusions.-The LLSAQ scoring system appeared to be a simple and effective technique to aid the diagnosis of adolescents who have AMS, and it may help improve the safety of large groups traveling to altitude. The AMS subjects tended to have low oxygen saturations and high pulse rates, highlighting potential areas for further research.
Acute mountain sickness: Is there a lag period before symptoms?
American Journal of Human Biology, 1998
The present study was designed to determine if symptoms of acute mountain sickness are presented within six hours after arrival at high altitude. Seventeen male subjects, 23-30 years, were studied. The subjects were professional soccer players, life-long residents at low altitudes except one player who was playing soccer in a team at 3400 m (512 mm Hg of Barometric Pressure) during an entire year in 1995. The players were transported by a commercial airline from Lima (150 m) to Cusco (3400 m). The trip lasted 1 hour. Heart rate and arterial oxygen saturation were measured at rest in Lima (150 m), at the time of arrival at Cusco, and at 4 and 6 hours after arrival at 3400 m. On day 6 at high altitude, the physical performance during a soccer game was assessed. The symptoms of acute mountain sickness (AMS) were assessed 6 hours after arrival at Cusco with a selfadministered questionnaire, and thereafter each 24-hours up to 5 days of exposure to high altitude. The following symptoms were assessed: headache, gastrointestinal symptoms, dizziness, fatigue, and sleep abnormalities. AMS was defined by a Lake-Louise score ജ4 (self-assessment only). Thirty five percent of the soccer players developed AMS within 6 hours after arrival by air at 3400 m altitude. Arterial oxygen saturation at arrival was higher in those player who developed AMS within 6 hours after arrival (94.3 ± 0.94% vs 90.8 ± 2.36; P < 0.001). From arrival to 6 hours of exposure to altitude, there was a significant fall in arterial oxygen saturation in those men who developed AMS than in those who did not. Results from the stepwise multiple regression (R 2 ס 0.59; P < 0.04) and logistic regression (R 2 ס 0.48; P < 0.0019) analyses showed that the difference between arterial oxygen saturation at sea level and at arrival at Cusco was a predictor for the development of AMS within 6 hours upon arrival at altitude. This suggests that the lower the difference between arterial oxygen saturation at sea level and at arrival, the higher the probability to develop AMS within 6 hours after arrival at 3400 m.
Prediction of the susceptibility to AMS in simulated altitude
Sleep and Breathing, 2008
Acute mountain sickness (AMS) develops when rapidly ascending to high altitudes. However, some mountaineers will suffer from AMS even at 2,000 m and others not until 5,000 m. The awareness of the individual susceptibility for AMS would be helpful for preventive strategies. Thus, the main purpose of this paper is the comparison of existing studies dealing with the prediction of AMS susceptibility and to draw conclusions on presently most valuable tests. Data source: A PubMed search has been performed, and preliminary observations from our laboratory have been included. The cautious conclusion derived from the reviewed 16 studies is that values of arterial oxygen saturation (SaO 2), determined 20-30 min after exposure to simulated hypoxia equivalent to 2,300-4,200 m, seem to be the most useful predictors of AMS susceptibility (>80% correct prediction). Because the sympathetic activation during acute exposure to hypoxia may well contribute to the AMS development, parameters like heart rate variability or blood lactate could even enhance this predictability. The ventilatory response to hypoxia is easily trainable by pre-exposures to hypoxia but considers only part of the complex acclimatization process.
2012
Background. The aim of this prospective observational cohort study was to investigate relationships between acute mountain sickness (AMS) and physical and mental health during a high altitude expedition. Methods. Forty-four participants (mean age, 34 ± 13 y; body mass index, 23.6 ± 3.5 kg·m 2 ; 57% male) completed the Dhaulagiri base camp trek in Nepal, a 19-day expedition attaining 5,372 m. Participants self-reported the following daily physical and mental health: AMS (defined by Lake Louise diagnosis and individual and total symptom scores), upper respiratory symptoms, diarrhea, and anxiety, plus physiological and behavioral factors. Results. The rate of Lake Louise-defined AMS per 100 person days was 9.2 (95% CI: 7.2-11.7). All investigated illnesses except diarrhea increased with altitude (all p < 0.001 by analysis of variance). Total AMS symptom score was associated with a lower arterial oxygen saturation, higher resting heart rate, more upper respiratory and diarrhea symptoms, greater anxiety, and lower fluid intake (all p < 0.02 by longitudinal multiple regression analyses). However, only upper respiratory symptoms, heart rate, arterial oxygen saturation, and fluid intake predicted future AMS symptoms [eg, an increase in upper respiratory symptoms by 5 units predicted an increase in the following day's AMS total symptom score by 0.72 units (0.54-0.89)].
High Altitude Medicine & Biology, 2004
Prediction of susceptibility to acute mountain sickness by Sa O 2 values during short-term exposure to hypoxia. High Alt. Med. Biol. 5:335-340, 2004-Prediction of the development of acute mountain sickness (AMS) in individuals going to high altitudes is still a matter of debate. Whereas some studies found that subjects with a blunted hypoxic ventilatory response (HVR) are predisposed to AMS, others did not. However, the HVR has often been determined under very acute (5 to 10 min) isocapnic hypoxia without consideration of the subsequent hypoxic ventilatory decline (HVD), and the assessment of AMS susceptibility was based on a single altitude exposure. Therefore, the aim of the present study was to evaluate the relationship between the individual arterial oxygen saturation (Sa O 2) after a 20-to 30-min exposure to poikilocapnic hypoxia and the AMS susceptibility based on repeated observations. A total of 150 healthy male and female mountaineers (ages: 42 Ϯ 13 yr), 63 of whom had known susceptibility to AMS and 87 of whom never suffered from AMS, were exposed to various degrees of normobaric and hypobaric hypoxia. Sa O 2 values were taken by finger pulseoximetry after 20 to 30 min of hypoxic exposure. Sa O 2 values after 20 to 30 min of hypoxia were on average 4.9% lower in subjects susceptible to AMS than in those who were not. Logistic regression analysis revealed altitude-dependent Sa O 2 values to be predictive for AMS susceptibility. Based on the derived model, AMS susceptibility was correctly predicted in 86% of the selected individuals exposed to short-term hypoxia. In conclusion, Sa O 2 values after 20 to 30 min of exposure to normobaric or hypobaric hypoxia represent a useful tool to detect subjects highly susceptible to AMS.
Acute mountain sickness, inflammation, and permeability: new insights from a blood biomarker study
Journal of Applied Physiology, 2011
Julian CG, Subudhi AW, Wilson MJ, Dimmen AC, Pecha T, Roach RC. Acute mountain sickness, inflammation, and permeability: new insights from a blood biomarker study. The pathophysiology of acute mountain sickness (AMS) is unknown. One hypothesis is that hypoxia induces biochemical changes that disrupt the blood-brain barrier (BBB) and, subsequently, lead to the development of cerebral edema and the defining symptoms of AMS. This study explores the relationship between AMS and biomarkers thought to protect against or contribute to BBB disruption. Twenty healthy volunteers participated in a series of hypobaric hypoxia trials distinguished by pretreatment with placebo, acetazolamide (250 mg), or dexamethasone (4 mg), administered using a randomized, doubleblind, placebo-controlled, crossover design. Each trial included peripheral blood sampling and AMS assessment before (Ϫ15 and 0 h) and during (0.5, 4, and 9 h) a 10-h hypoxic exposure (barometric pressure ϭ 425 mmHg). Anti-inflammatory and/or anti-permeability [interleukin (IL)-1 receptor agonist (IL-1RA), heat shock protein (HSP)-70, and adrenomedullin], proinflammatory (IL-6, IL-8, IL-2, IL-1, and substance P), angiogenic, or chemotactic biomarkers (macrophage inflammatory protein-1, VEGF, TNF-␣, monocyte chemotactic protein-1, and matrix metalloproteinase-9) were assessed. AMS-resistant subjects had higher IL-1RA (4 and 9 h and overall), HSP-70 (0 h and overall), and adrenomedullin (overall) compared with AMS-susceptible subjects. Acetazolamide raised IL-1RA and HSP-70 compared with placebo in AMS-susceptible subjects. Dexamethasone also increased HSP-70 and adrenomedullin in AMSsusceptible subjects. Macrophage inflammatory protein-1 was higher in AMS-susceptible than AMS-resistant subjects after 4 h of hypoxia; dexamethasone minimized this difference. Other biomarkers were unrelated to AMS. Resistance to AMS was accompanied by a marked anti-inflammatory and/or anti-permeability response that may have prevented downstream pathophysiological events leading to AMS. Conversely, AMS susceptibility does not appear to be related to an exaggerated inflammatory response. high altitude; headache; hypoxia; cerebral edema; inflammatory ACUTE MOUNTAIN SICKNESS (AMS) is a transient syndrome primarily defined by a headache developing within hours after ascent to high altitude (12). The pathophysiology of AMS remains unclear (21, 39), as do the processes responsible for resistance to the condition. A popular theory, the "tight-fit hypothesis," suggests that increased brain volume with hypobaric hypoxia elevates intracranial pressure and, when accompanied by impaired or diminished intracranial buffering capacity, contributes to the development of the symptoms that define AMS (50). Brain imaging studies show evidence of cerebral vasogenic edema in moderate to
Endurance Athletes Are at Increased Risk for Early Acute Mountain Sickness at 3450 m
Medicine & Science in Sports & Exercise, 2019
Introduction Acute mountain sickness (AMS) may develop in nonacclimatized individuals after exposure to altitudes ≥2500 m. Anecdotal reports suggest that endurance-trained (ET) athletes with a high maximal oxygen uptake (V˙O2max) may be at increased risk for AMS. Possible underlying mechanisms include a training-induced increase in resting parasympathetic activity, higher resting metabolic rate (RMR), and lower hypoxic ventilatory response (HVR). Methods In 38 healthy, nonacclimatized men (19 ET and 19 untrained controls [UT], V˙O2max 66 ± 6 mL·min−1·kg−1 vs 45 ± 7 mL·min−1·kg−1; P < 0.001) peripheral oxygen saturation (SpO2), heart rate variability, RMR, and poikilocapnic HVR were assessed at 424 m and during 48 h at 3450 m after passive ascent by train (~2 h). Acute mountain sickness was evaluated by AMS cerebral (AMS-C) score. Results On day 1 at altitude, ET presented with a higher AMS incidence (42% vs 11%; P < 0.05) and severity (AMS-C score: ET, 0.48 ± 0.5 vs UT, 0.21 ±...
Research Square (Research Square), 2021
AMS Acute mountain sickness AMSc Environmental symptom questionnaire, cerebral score ARI Cerebral autoregulation index CA Cerebral autoregulation CVCi Cerebrovascular conductance index CVRi Cerebrovascular resistance index MAP Mean arterial blood pressure MCA Middle cerebral artery MCAv Middle cerebral artery peak blood flow velocity P ET CO 2 End-tidal partial pressure of carbon dioxide SpO 2 Arterial oxygen saturation measured by pulse oximetry 3 ABSTRACT Cerebral autoregulation (CA) is impaired during acute high-altitude (HA) exposure and effects of acclimatization and re-exposure on CA are unknown. In 18 healthy lowlanders (11 women), we hypothesized that the cerebral autoregulation index (ARI) assessed by the percentage change in middle cerebral artery peak blood flow velocity (Δ%MCAv)/percentage change in mean arterial blood pressure (Δ%MAP) induced by a sit-to-stand maneuver, is i) reduced on Day1 at 5050m compared to 520m, ii) is improved after 6 days at 5050m, and iii) is less impaired during re-exposure to 5050m after 7 days at 520m compared to Cycle1. Participants spent 4-8h/day at 5050m and slept at 2900m similar to real-life working shifts. High/low ARI indicate impaired/intact CA, respectively. With the sit-to-stand at 520m, mean(95%CI) in ΔMAP and ΔMCAv were-26%(-41 to-10) and-13%(-19 to-7); mean±SE in ARI was 0.58±0.63Δ%/Δ%, respectively. On Day1 at 5050m, ARI worsened compared to 520m (3.29±0.70Δ%/Δ%), but improved with acclimatization (1.44±0.65Δ%/Δ%, P<0.05 for both). ARI was less affected during re-exposure to 5050m (1.22±0.70Δ%/Δ%, P<0.05 acute altitude-induced change between sojourns). This study showed that CA i) is impaired during acute HA exposure, ii) improves with acclimatization and iii) is ameliorated during re-exposure to HA a week later.