Maria Wille

Prevalence of acute mountain sickness in the Eastern Alps.

Little information is available on the prevalence of acute mountain sickness (AMS) in the Eastern Alps compared with the Western Alps. Because of differences regarding the populations of mountaineers, we hypothesized that the prevalence differs between the Eastern and Western Alps. Thus, we determined the prevalence and risk factors of AMS at four different altitudes in the Eastern Alps of Austria. Four hundred and thirty-one recreational hikers were studied using questionnaires on the morning of their first night at high altitude. A diagnosis of AMS was based on a Lake Louise Score > or =4, the presence of headache, and at least one additional symptom. Overall 16.2% of the subjects met the criteria for AMS, and the prevalence of AMS increased significantly with altitude (2200 m: 6.9%; 2500 m: 9.1%; 2800 m: 17.4%; 3500 m: 38.0%). Heavy perceived exertion, a history of migraine, the absolute altitude reached, little mountaineering experience, and inadequate water intake (< or =2 L) were independent AMS risk factors. The reported altitude-related AMS prevalence in the Western Alps is 4% to 8% lower compared with that found in this study for the Eastern Alps. In conclusion, the prevalence of AMS is higher in the tourist population of the Eastern Alps compared to the more experienced mountaineers of the Western Alps. Consideration of easily modifiable risk factors such as individual exertion and water intake could markedly reduce AMS and contribute to the enjoyment of mountaineering.

The prevalence of and risk factors for acute mountain sickness in the Eastern and Western Alps.

Acute mountain sickness (AMS) is the most common condition of high altitude illnesses. Its prevalence varies between 15% and 80% depending on the speed of ascent, absolute altitude reached, and individual susceptibility. Additionally, we assumed that the more experienced mountaineers of the Western Alps are less susceptible to developing AMS than recreational mountaineers of the Eastern Alps or tourist populations. Therefore, the main goals of the present study were the collection of data regarding the AMS prevalence and triggers in both the Eastern and Western Alps using identical methods. A total of 162 mountaineers, 79 in the Eastern Alps (3454 m) and 83 in the Western Alps (3817 m) were studied on the morning after their first night at high altitude. A diagnosis of AMS was based on a Lake Louise Score (LLS) ≥4, the presence of headache, and at least one additional symptom. Thirty of 79 subjects (38.0%) suffered from AMS at 3454 m in the Eastern Alps as did 29 of 83 (34.9%) at 3817 m in the Western Alps. After adjustment for altitude, the prevalence in the Western Alps constituted 24.5%, which differed significantly (p = 0.04) from that found in the Eastern Alps. The lower mountaineering experience of mountaineers in the Eastern Alps turned out to be the only factor for explaining their higher AMS prevalence. Thus, expert advice by mountain guides or experienced colleagues could help to reduce the AMS risk in these subjects.

Risk factors for high-altitude headache in mountaineers.

Aim: The aim was to identify most relevant risk factors of high-altitude headache within a broad mountaineering population through a prospective, observational, rater-blinded study. Methods: A total of 506 mountaineers were enrolled after their first overnight stay in one of seven alpine huts between 2200–3817 m. Structured interview including information on mountaineering histories, caffeine intake, smoking habits, alcohol consumption, intake of medication, rate of ascent, physical fitness, the level of exertion and the amount of fluids intake at the day of ascent were recorded along with a standardized medical examination. Results: High-altitude headache occurred in 31% of study participants. Logistic regression analysis revealed a migraine history, low arterial oxygen saturation, high ratings of perceived exertion and fluid intake below 2 l to be independent risk factors for the development of high-altitude headache. Conclusion: Given the high prevalence, high-altitude headache is a relevant medical condition and a better understanding of risk factors has important impact and may facilitate patient behaviour and future study design.

Cardiac Troponins in Young Marathon Runners

Cardiac troponin increases are common in adult marathon finishers. However, data on troponin values for young marathon runners are scarce. Forty young runners (20 healthy male and 20 female) 13 to 17 years old participated in this study. Blood samples were taken before, immediately after, and 24 hours after the race for determination of cardiac troponin T (cTnT) and troponin I (cTnI). Thirty-seven runners completed the race with a mean finishing time of 4 hours 53 minutes. No participant developed an adverse medical event during or after the race. In 30 of 37 participants, levels of cTnT and/or cTnI exceeded upper reference limits of 0.01 and 0.1 ng/ml immediately after the race, and in 3 participants these levels were even higher than the reference range for acute myocardial infarction (>0.1 and >0.5 ng/ml for cTnT and cTnI, respectively). Twenty-four hours after the race no participant had troponin levels exceeding the upper reference limits. Average increases of troponin levels did not differ between sexes. In conclusion, this is the first study to show that cardiac troponin levels increase to a similar extent in male and female adolescent marathon runners as observed in adults. Rapid recovery of troponin levels after a race is indicative of a physiologic rather than a pathologic response.

Short-term intermittent hypoxia reduces the severity of acute mountain sickness.

Intermittent hypoxia (IH) is a promising approach to induce acclimatization and hence lower the risk of developing acute mountain sickness (AMS). We hypothesized that a short‐term IH protocol in normobaric hypoxia (7 × 1 h to 4500 m) effectively increases the hypoxic ventilatory response (HVR) and reduces the incidence and severity of AMS. Therefore, 26 men (25.5 ± 4.4 years), assigned in a double‐blinded fashion to the hypoxia group (HG) or placebo group (PG), spent 8 h at 5300 m before (PRE) and 2 days after cessation of the IH protocol (POST). Measurements included the evaluation of the Lake Louise Score (LLS) and the HVR. The severity of AMS decreased from PRE to POST in the HG (from 6.0 ± 2.7 at PRE to 4.1 ± 2.1 at POST), whereas the LLS in the PG stayed high (from 5.7 ± 2.9 to 5.5 ± 2.8, respectively). The HVR in the HG increased from 0.73 ± 0.4 L/min/% at PRE to 1.10 ± 0.5 L/min/% at POST and did not increase in the PG. The reduction of the LLS was inversely related to the changes in the HVR (r = −0.434), but the AMS incidence was not different between the HG and the PG at POST. In conclusion, short‐term IH reduced the severity of AMS development during a subsequent 8‐h exposure to normobaric hypoxia.

Changes in cardiac autonomic activity during a passive 8 hour acute exposure to 5 500 m normobaric hypoxia are not related to the development of acute mountain sickness.

Alterations in the autonomic nervous system after ascent to high altitude may be related to the development of acute mountain sickness (AMS). So far, the time course of cardiac autonomic modulation in relation to AMS development during the early hours at altitude is not well established. As AMS develops sometimes as early as 1 h and typically within 6 to 10 h at altitude, evaluating this time period provides information on cardiac autonomic responses with regard to AMS development. Prior studies exclusively investigated autonomic modulations in hypobaric hypoxia. Because barometric pressure per se might influence autonomic nervous system activity, the evaluation of cardiac autonomic alterations caused by hypoxia alone might give new insights on the role of the autonomic nervous system in AMS development. To assess the early responses of acute hypoxia on cardiac autonomic modulation and its association to the development of AMS, 48 male subjects were exposed for 8 h to acute normobaric hypoxia (FiO2 11.0%, 5 500 m respectively). Heart rate variability (HRV) was determined by 5-min recordings of successive NN-intervals in normoxia and after 2, 4, 6 and 8 h in hypoxia. Compared with normoxia, acute exposure to hypoxia decreased total power (TP), high frequency (HF) and low frequency (LF) components as well as the standard deviation of all NN intervals (SDNN), the root mean square of differences of successive NN intervals (rMSSD) and the proportion of differences between adjacent NN intervals of more than 50 ms (pNN50). LF:HF ratio, heart rate (HR) and blood lactate (LA) were augmented, indicating an increase in cardiac sympathetic activity. No differences were found between those who developed AMS and those who did not. Our results confirm reduced HRV with a shift towards sympathetic predominance during acute exposure to hypoxia. However, changes in cardiac autonomic modulations are not related to AMS development in acute normobaric hypoxia.

Association between body water status and acute mountain sickness.

Purpose The present study determined the association between body fluid variation and the development of acute mountain sickness (AMS) in adults. Methods Forty-three healthy participants (26 males and 17 females, age: 26±6 yr, height: 174±9 cm, weight: 68±12 kg) were passively exposed at a FiO2 of 12.6% (simulated altitude hypoxia of 4500 m, PiO2 = 83.9 mmHg) for 12-h. AMS severity was assessed using the Lake Louise Score (LLS). Food and drink intakes were consumed ad libitum and measured; all urine was collected. Before and after the 12-h exposure, body weight and plasma osmolality were measured and whole-body bioimpedance analysis was performed. Results The overall AMS incidence was 43% (38% males, 50% females). Participants who developed AMS showed lower fluid losses (3.0±0.9 vs. 4.5±2.0 ml/kg/h, p = 0.002), a higher fluid retention (1.9±1.5 vs. 0.6±0.8 ml/kg/h, p = 0.022), greater plasma osmolality decreases (−7±7 vs. −2±5 mOsm/kg, p = 0.028) and a larger plasma volume expansion (11±10 vs. 1±15%, p = 0.041) compared to participants not developing AMS. Net water balance (fluid intake – fluid loss) and the amount of fluid loss were strong predictors whether getting sick or not (Nagelkerkes r2 = 0.532). The LLS score was related to net water balance (r = 0.358, p = 0.018), changes in plasma osmolality (r = −0.325, p = 0.033) and sodium concentration (r = −0.305, p = 0.047). Changes in the impedance vector length were related to weight changes (r = −0.550, p<0.001), fluid intake (r = −0.533, p<0.001) and net water balance (r = −0.590, p<0.001). Conclusions Participants developing AMS within 12 hours showed a positive net water balance due to low fluid loss. Thus measures to avoid excess fluid retention are likely to reduce AMS symptoms.

MRI evidence: acute mountain sickness is not associated with cerebral edema formation during simulated high altitude.

Acute mountain sickness (AMS) is a common condition among non-acclimatized individuals ascending to high altitude. However, the underlying mechanisms causing the symptoms of AMS are still unknown. It has been suggested that AMS is a mild form of high-altitude cerebral edema both sharing a common pathophysiological mechanism. We hypothesized that brain swelling and consequently AMS development is more pronounced when subjects exercise in hypoxia compared to resting conditions. Twenty males were studied before and after an eight hour passive (PHE) and active (plus exercise) hypoxic exposure (AHE) (FiO2 = 11.0%, PiO2∼80 mmHg). Cerebral edema formation was investigated with a 1.5 Tesla magnetic resonance scanner and analyzed by voxel based morphometry (VBM), AMS was assessed using the Lake Louise Score. During PHE and AHE AMS was diagnosed in 50% and 70% of participants, respectively (p>0.05). While PHE slightly increased gray and white matter volume and the apparent diffusion coefficient, these changes were clearly more pronounced during AHE but were unrelated to AMS. In conclusion, our findings indicate that rest and especially exercise in normobaric hypoxia are associated with accumulation of water in the extracellular space, however independent of AMS development. Thus, it is suggested that AMS and HACE do not share a common pathophysiological mechanism.

Hypoxia triggers high-altitude headache with migraine features: A prospective trial

Background Given the high prevalence and clinical impact of high-altitude headache (HAH), a better understanding of risk factors and headache characteristics may give new insights into the understanding of hypoxia being a trigger for HAH or even migraine attacks. Methods In this prospective trial, we simulated high altitude (4500 m) by controlled normobaric hypoxia (FiO2 = 12.6%) to investigate acute mountain sickness (AMS) and headache characteristics. Clinical symptoms of AMS according to the Lake Louise Scoring system (LLS) were recorded before and after six and 12 hours in hypoxia. O2 saturation was measured using pulse oximetry at the respective time points. History of primary headache, especially episodic or chronic migraine, was a strict exclusion criterion. Findings In total 77 volunteers (43 (55.8%) males, 34 (44.2%) females) were enrolled in this study. Sixty-three (81.18%) and 40 (71.4%) participants developed headache at six or 12 hours, respectively, with height and SpO2 being significantly different between headache groups at six hours (p < 0.05). Binary logistic regression model revealed a significant association of SpO2 and headache development (p < 0.05, OR 1.123, 95% CI 1.001–1.259). In a subgroup of participants, with history of migraine being a strict exclusion criterion, hypoxia triggered migraine-like headache according to the International Classification of Headache Disorders (ICHD-3 beta) in n = 5 (8%) or n = 6 (15%), at six and 12 hours, respectively. Interpretation Normobaric hypoxia is a trigger for HAH and migraine-like headache attacks even in healthy volunteers without any history of migraine. Our study confirms the pivotal role of hypoxia in the development of AMS and beyond that suggests hypoxia may be involved in migraine pathophysiology.

Effects of massage under hypoxic conditions on exercise-induced muscle damage and physical strain indices in professional soccer players.

Reports based on experiences from masseurs and players, mostly without any scientific background, suggest that the combination of a classical regeneration method (i.e. massage) with exposure to hypoxia may enhance regeneration in soccer. The aim of this study was to evaluate whether this specific combination could affect blood parameters related to muscle damage and physical strain after a soccer game. Approximately 15 hours after two separate championship games, 10 professional male outfield players of the first Austrian division were exposed to normobaric hypoxia (FiO2 13.5% ∼ 4000m) or normoxia for 1 hour (30 minutes rest followed by 30 min massage) (cross-over design). Creatine kinase (CK), urea and uric acid (UA) were measured 4 days before the first game, and 15 and 63 hours after the two games. Match play increased CK values independently of the intervention. No effect of the massage in combination with hypoxia was seen. A trend was found between Δ UA ([UA] 48 hours after exposure minus [UA] before exposure) in response to hypoxia and SaO2 measured in hypoxia (r=0.612, p=0.06). Results show that massage under hypoxic conditions had no additional positive effect on the measured parameters compared to massage alone. Solely the trend of a relationship for Δ UA and SaO2 might indicate that redox alterations are a potential consequence of hypoxic exposure.