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Purpose: We compared the effects of hypobaric and normobaric hypoxia on select cardio-respiratory responses, oxidative stress and acute mountain sickness (AMS) severity in prematurely born individuals, known to exhibit blunted hypoxic ventilatory response.Methods: Sixteen prematurely born but otherwise healthy males underwent two 8-h hypoxic exposures under: (1) hypobaric hypoxic [HH; terrestrial altitude 3840 m; PiO2:90.2 (0.5) mmHg; BP: 478 (2) mmHg] and (2) normobaric hypoxic [NH; PiO2:90.6 (0.9) mmHg; FiO2:0.142 (0.001)] condition. Resting values of capillary oxyhemoglobin saturation (SpO2), heart rate (HR) and blood pressure were measured before and every 2 h during the exposures. Ventilatory responses and middle cerebral artery blood flow velocity (MCAv) were assessed at rest and during submaximal cycling before and at 4 and 8 h. Plasmatic levels of selected oxidative stress and antioxidant markers and AMS symptoms were also determined at these time points.Results: HH resulted in significantly lower resting (P = 0.010) and exercise (P = 0.004) SpO2 as compared to NH with no significant differences in the ventilatory parameters, HR or blood pressure. No significant differences between conditions were found in resting or exercising MCAv and measured oxidative stress markers. Significantly lower values of ferric-reducing antioxidant power (P = 0.037) were observed during HH as opposed to NH. AMS severity was higher at 8 h compared to baseline (P = 0.002) with no significant differences between conditions.Conclusion: These data suggest that, in prematurely born adults, 8-h exposure to hypobaric, as opposed to normobaric hypoxia, provokes greater reductions in systemic oxygenation and antioxidant capacity. Further studies investigating prolonged hypobaric exposures in this population are warranted.Registration: NCT02780908 (ClinicalTrials.gov). [ABSTRACT FROM AUTHOR]

Purpose: Through time- and frequency-domain analysis, we compared the effects of acute hypobaric hypoxia on the changes in heart rate variability (HRV) following night sleeping and morning awakening in individuals with and without acute mountain sickness (AMS).Method: Thirty-nine nonacclimatised healthy individuals were transported by bus from sea level to 3150 m within 3 h. Short-term HRV was measured two times a day-before sleeping (BS) and after awakening (AA)- at 3 days before ascent (T0), two consecutive nights at 3150 m (T1 and T2), and 2 days after descent (T3). AMS was diagnosed using the self-reported Lake Louise score questionnaire.Result: AMS developed in 19 of 39 participants (48.7%). At sea level, individuals had higher HRV at AA than at BS, and the trend of increased HRV at AA remained unchanged at high altitude, irrespective of AMS. At T1 BS, low-frequency power in normalised unit was significantly lower in participants with AMS than in those without AMS. Compared with those at T1 BS, the square root of the mean squared differences of successive normal-normal (NN) intervals, the number of interval differences of successive NN intervals more than 50 ms (NN50), and the proportion derived by dividing NN50 by the total number of NN intervals at T1 AA significantly increased in participants without AMS but nonsignificantly decreased in those with AMS.Conclusion: After rapid ascent, individuals with AMS did not demonstrate sympathetic hyperactivity but did exhibit withdrawal of cardiac vagal modulation in the morning following the first night's sleep. [ABSTRACT FROM AUTHOR]

Purpose: A diuresis is a key part of acclimatisation to high altitude (HA). Arginine vasopressin (AVP) is a hormone involved in salt and water balance and may potentially have a role in the development of altitude illness. ProAVP (copeptin) is more stable than AVP and is assayed by a straightforward, automated method. We investigated the relationship of AVP to copeptin and the copeptin response to exercise and altitude illness in a large cohort during a field study at HA. Methods: 48 subjects took part in a 10-day trek at HA. Venous blood samples were taken at 3,833, 4,450 and 5,129 m post-trek (exercise) and the following day at rest. Daily recordings of symptoms of altitude illness, oxygen saturations and perceived exertion were carried out. Results: AVP and copeptin levels increased with exercise and correlated closely ( ρ 0.621 p < 0.001), this was strongest in the stressed state when AVP secretion was highest, at 5,129 m post-exercise ( ρ 0.834 p < 0.001). On two-way ANOVA, both altitude ( F = 3.5; p = 0.015) and exercise ( F = 10.2; p = 0.002) influenced copeptin levels (interaction F = 2.2; p = 0.08). AVP levels were influenced by exercise ( F = 14.4; p = 0.0002) but not altitude ( F = 2.0; p = 0.12) with no overall group interactions ( F = 1.92.6; p = 0.06). There was no association between copeptin or arginine vasopressin and altitude illness. Copeptin correlated with the Borg RPE score and was significantly higher in the group with a Borg score ≥15 (7.9 vs. 3.7 p < 0.001). Conclusion: We have shown that arginine vasopressin and copeptin levels correlate and are suppressed below 5,129 m. Furthermore, we have demonstrated that exertion, rather than altitude illness or increasing osmolality, is the stimulus for increases in copeptin. [ABSTRACT FROM AUTHOR]

Purpose: We aimed at identifying the cerebral hemodynamic characteristics of acute mountain sickness (AMS). Methods: Transcranial Doppler (TCD) sonography examinations were performed between 18 and 24 h after arrival at 3,700 m via plane from 500 m ( n = 454). A subgroup of 151 subjects received TCD examinations at both altitudes. Results: The velocities of the middle cerebral artery, vertebral artery (VA) and basilar artery (BA) increased while the pulsatility indexes (PIs) and resistance indexes (RIs) decreased significantly (all p < 0.05). Velocities of BA were higher in AMS (AMS+) individuals when compared with non-AMS (AMS−) subjects (systolic velocity: 66 ± 12 vs. 69 ± 15 cm/s, diastolic velocity: 29 ± 7 vs. 31 ± 8 cm/s and mean velocity, 42 ± 9 vs. 44 ± 10 cm/s). AMS was characterized by higher diastolic velocity [ V (26 ± 4 vs. 25 ± 4, p = 0.013)] with lower PI and RI (both p = 0.004) in VA. Furthermore, the asymmetry index (AI) of VAs was significantly lower in the AMS + group [−5.7 % (21.0 %) vs. −2.5 % (17.8 %), p = 0.016]. The AMS score was closely correlated with the hemodynamic parameters of BA and the V, PI, RI and AI of VA. Conclusion: AMS is associated with alterations in cerebral hemodynamics in the posterior circulation rather than the anterior one, and is characterized by higher blood velocity with lower resistance. In addition, the asymmetry of VAs may be involved in AMS. [ABSTRACT FROM AUTHOR]

The impact of acute altitude exposure on pulmonary function is variable. A large inter-individual variability in the changes in forced expiratory flows (FEFs) is reported with acute exposure to altitude, which is suggested to represent an interaction between several factors influencing bronchial tone such as changes in gas density, catecholamine stimulation, and mild interstitial edema. This study examined the association between FEF variability, acute mountain sickness (AMS) and various blood markers affecting bronchial tone (endothelin-1, vascular endothelial growth factor (VEGF), catecholamines, angiotensin II) in 102 individuals rapidly transported to the South Pole (2835 m). The mean FEF between 25 and 75% (FEF(25-75)) and blood markers were recorded at sea level and after the second night at altitude. AMS was assessed using Lake Louise questionnaires. FEF(25-75) increased by an average of 12% with changes ranging from -26 to +59% from sea level to altitude. On the second day, AMS incidence was 36% and was higher in individuals with increases in FEF(25-75) (41 vs. 22%, P = 0.05). Ascent to altitude induced an increase in endothelin-1 levels, with greater levels observed in individuals with decreased FEF(25-75). Epinephrine levels increased with ascent to altitude and the response was six times larger in individuals with decreased FEF(25-75). Greater levels of endothelin-1 in individuals with decreased FEF(25-75) suggest a response consistent with pulmonary hypertension and/or mild interstitial edema, while epinephrine may be upregulated in these individuals to clear lung fluid through stimulation of β(2)-adrenergic receptors. [ABSTRACT FROM AUTHOR]

The levels of distortion product otoacoustic emissions (DPOAEs) change at frequencies between 0.75 and 1.5 kHz along with intracranial pressure (ICP) and DPOAEs are suggested for monitoring ICP changes. Elevated ICP plays a major role in high-altitude disease, but direct measurement is unlikely to be feasible at high altitudes. The aim of the presented study was to measure DPOAEs at extreme altitudes in order to determine whether information about elevated ICP can be obtained. Data are presented from DPOAE measurements at the frequencies 1, 1.5, 2, 3 and 4 kHz in 13 climbers during an ascent to Gasherbrum II (8,035 m) up to an altitude of 7,400 m. Valid DPOAE measurements could be obtained in all climbers. DPOAE levels exhibited great variability concerning both the affected frequency range and the change. As expected due to elevated ICP, DPOAE levels decreased in some of the climbers at 1 kHz. However, an even more pronounced decline of DPOAE levels was observed at 3 and 4 kHz, which cannot be explained by intracranial hypertension. Possible other reasons for DPOAE level changes at extreme altitude are hypoxia, increased serum osmolarity and unbalanced middle ear pressure. Only one climber developed severe acute mountain sickness with clinical signs of intracranial hypertension. The most pronounced decline of DPOAEs at 1 kHz was seen on that occasion, which suggests a possible use of DPOAEs for detection of intracranial hypertension and early detection of high-altitude cerebral edema. [ABSTRACT FROM AUTHOR]

Assessment of individual susceptibility to altitude illnesses and more particularly to acute mountain sickness (AMS) by means of tests performed in normobaric hypoxia (NH) or in hypobaric hypoxia (HH) is still debated. Eighteen subjects were submitted to HH and NH tests (PIO2=120 hPa, 30 min) before an expedition. Maximal and mean acute mountain sickness scores (AMSmax and mean) were determined using the self-report Lake Louise questionnaire scored daily. Cardio-ventilatory (f, VT, PetO2 and PetCO2, HR and finger pulse oxymetry SpO2) were measured at times 5 and 30 min of the tests. Arterial (PaO2, PaCO2, pH, SaO2) and capillary haemoglobin (Hb) measurements were performed at times 30 min. Hypoxic ventilatory (HVR) and cardiac (HCR) responses, peripheral O2 blood content (CpO2) were calculated. A significant time effect is found for ΔSpO2 ( P = 0.04). Lower PaCO2 ( P = 0.005), SaO2 ( P = 0.07) and higher pH ( P = 0.02) are observed in HH compared to NH. AMSmax varied from 3 to12 and AMSmean between 0.6 and 3.5. In NH at 30 min, AMSmax is related to PetO2 ( R = 0.61, P = 0.03), CpO2 ( R = −0.53, P = 0.02) and in HH to CpO2 ( R = −0.57, P = 0.01). In NH, AMSmean is related to Δ f ( R = 0.46, P = 0.05), HCR ( R = 0.49, P = 0.04), CpO2 ( R = −0.51, P = 0.03) and, in HH at 30 min, to VT ( R = 0.69, P = 0.01) and a tendency for CpO2 ( R = −0.43, P = 0.07). We conclude that HH and NH tests are physiologically different and they must last 30 min. CpO2 is an important variable to predict AMS. For practical considerations, NH test is proposed to quantify AMS individual susceptibility using the formulas: AMSmax = 9.47 + 0.104PetO2(hPa)–0.68CpO2 (%), ( R = 0.77, P = 0.001); and AMSmean = 3.91 + 0.059Δ f + 0.438HCR–0.135CpO2 ( R = 0.71, P = 0.017). [ABSTRACT FROM AUTHOR]

Lung oxidative stress (OS) was explored in resting and in exercising subjects exposed to moderate and high altitude. Exhaled breath condensate (EBC) was collected under field conditions in male high-competition mountain bikers performing a maximal cycloergometric exercise at 670 m and at 2,160 m, as well as, in male soldiers climbing up to 6,125 m in Northern Chile. Malondialdehyde concentration [MDA] was measured by high-performance liquid chromatography in EBC and in serum samples. Hydrogen peroxide concentration [H2O2] was analysed in EBC according to the spectrophotometric FOX2 assay. [MDA] in EBC of bikers did not change while exercising at 670 m, but increased from 30.0±8.0 to 50.0±11.0 nmol l−1 ( P<0.05) at 2,160 m. Concomitantly, [MDA] in serum and [H2O2] in EBC remained constant. On the other hand, in mountaineering soldiers, [H2O2] in EBC under resting conditions increased from 0.30±0.12 μmol l−1 at 670 m to 1.14±0.29 μmol l−1 immediately on return from the mountain. Three days later, [H2O2] in EBC (0.93 ±0.23 μmol l−1) continued to be elevated ( P<0.05). [MDA] in EBC increased from 71±16 nmol l−1 at 670 m to 128±26 nmol l−1 at 3,000 m ( P<0.05). Changes of [H2O2] in EBC while ascending from 670 m up to 3,000 m inversely correlated with concomitant variations in HbO2 saturation ( r=−0.48, P<0.05). AMS score evaluated at 5,000 m directly correlated with changes of [MDA] in EBC occurring while the subjects moved from 670 to 3,000 m ( r=0.51, P<0.05). Lung OS may constitute a pathogenic factor in AMS. [ABSTRACT FROM AUTHOR]

Vascular endothelial growth factor (VEGF) is an endothelial cell mitogen and permeability factor that is inducible by hypoxia. Its contribution to high-altitude illness in man is unknown. We measured VEGF levels in 14 mountaineers at low altitude (490 m) and 24 h after their arrival at high altitude (4,559 m). At high altitude, VEGF increased from [mean (SEM)] 32.5 (9.2) to 60.9 (18.5) pg·ml–1 (P<0.004) in the arterial blood, and from 15.9 (2.9) to 49.3 (15.9) pg·ml–1 (P=0.0001) in the mixed venous blood. Whereas at low altitude venous and arterial VEGF levels were not statistically different from each other (P=0.065), the VEGF concentration was significantly lower in venous than in arterial blood samples at high altitude (P=0.004). The pulmonary capillary VEGF concentration remained unchanged at high altitude [14.8 (2.5) vs 17.1 (5.4) pg·ml–1, P=0.85]. VEGF levels in the nine mountaineers who developed symptoms of acute mountain sickness (AMS), and in the six subjects who had radiographic evidence of high-altitude pulmonary edema were similar to those in subjects without symptoms. VEGF was not correlated with either AMS scores, mean pulmonary arterial pressures, arterial partial pressure of O2, or alveolar-arterial O2 gradients. We conclude that VEGF release is stimulated at high altitude, but that VEGF is probably not related to high-altitude illness. [ABSTRACT FROM AUTHOR]