Altitude Exposure Research Articles

The Effect of Altitude on the Anaerobic Energy System During a Maximal 60 Second Sprint on a Cycle Ergometer

Introduction: The purpose of this study is to examine the effect of altitude on the anaerobic performance during a maximal 60s sprint on a cycle ergometer. Methods: Seven female and 12 male college students volunteered to participate in the study. Each participant performed two separate 60s Wingate tests, once at an elevation of 90 m (~300 ft), and once at an altitude of 2,438 m (8,000 ft). Testing at altitude was simulated by an Everett Summit II Hypoxic Generator. Each subject was given a minimum of seven days between each test to ensure that they were well rested and recovered from the previous bout. Peak power, mean power, relative peak power, relative mean power, and fatigue index were measured. Data were analyzed via a paired sample t-test. Results: Significant differences were noted for both mean power (p = 0.012) and relative mean power (p = 0.008) for the sprint at 2,438 m (8,000 ft) of altitude. All other measured variables were not statistically significant (p > 0.05). Conclusion: This study, found no effect on peak power, relative peak power, or fatigue index in 2,438 m (8,000 ft) of altitude during a 60s maximal effort bout. However, mean power was reduced in altitude conditions. These results highlight that altitude exposure may reduce mean power during an acute, maximal bout of exercise.

Altitude exposure in pediatric pulmonary hypertension-are we ready for (flight) recommendations?

Patients with congenital heart disease are surviving further into adulthood and want to participate in multiple activities. This includes exposure to high altitude by air travel or recreational activities, such as hiking and skiing. However, at an altitude of about 2,500 m, the barometric environmental pressure is reduced and the partial pressure of inspired oxygen drops from 21% to 15% (hypobaric hypoxia). In physiologic response to high-altitude-related hypoxia, pulmonary vasoconstriction is induced within minutes of exposure followed by compensatory hyperventilation and increased cardiac output. Even in healthy children and adults, desaturation can be profound and lead to a significant rise in pulmonary pressure and resistance. Individuals with already increased pulmonary pressure may be placed at risk during high-altitude exposure, as compensatory mechanisms may be limited. Little is known about the physiological response and risk of developing clinically relevant events on altitude exposure in pediatric pulmonary hypertension (PAH). Current guidelines are, in the absence of clinical studies, mainly based on expert opinion. Today, healthcare professionals are increasingly faced with the question, how best to assess and advise on the safety of individuals with PAH planning air travel or an excursion to mountain areas. To fill the gap, this article summarises the current clinical knowledge on moderate to high altitude exposure in patients with different forms of pediatric PAH.

The effects of acute incremental hypocapnia on the magnitude of neurovascular coupling in healthy participants.

The high metabolic demand of cerebral tissue requires that local perfusion is tightly coupled with local metabolic rate (neurovascular coupling; NVC). During chronic altitude exposure, where individuals are exposed to the antagonistic cerebrovascular effects of hypoxia and hypocapnia, pH is maintained through renal compensation and NVC remains stable. However, the potential independent effect of acute hypocapnia and respiratory alkalosis on NVC remains to be determined. We hypothesized that acute steady‐state hypocapnia via voluntary hyperventilation would attenuate the magnitude of NVC. We recruited 17 healthy participants and insonated the posterior cerebral artery (PCA) with transcranial Doppler ultrasound. NVC was elicited using a standardized strobe light stimulus (6 Hz; 5 × 30 s on/off) where absolute delta responses from baseline (BL) in peak, mean, and total area under the curve (tAUC) were quantified. From a BL end‐tidal (PET)CO2 level of 36.7 ± 3.2 Torr, participants were coached to hyperventilate to reach steady‐state hypocapnic steps of Δ‐5 Torr (31.6 ± 3.9) and Δ‐10 Torr (26.0 ± 4.0; p < 0.001), which were maintained during the presentation of the visual stimuli. We observed a small but significant reduction in NVC peak (ΔPCAv) from BL during controlled hypocapnia at both Δ‐5 (−1.58 cm/s) and Δ‐10 (−1.37 cm/s), but no significant decrease in mean or tAUC NVC response was observed. These data demonstrate that acute respiratory alkalosis attenuates peak NVC magnitude at Δ‐5 and Δ‐10 Torr PETCO2, equally. Although peak NVC magnitude was mildly attenuated, our data illustrate that mean and tAUC NVC are remarkably stable during acute respiratory alkalosis, suggesting multiple mechanisms underlying NVC.

Transcriptional landscape in rat intestines under hypobaric hypoxia.

Oxygen metabolism is closely related to the intestinal homeostasis environment, and the occurrence of many intestinal diseases is as a result of the destruction of oxygen gradients. The hypobaric hypoxic environment of the plateau can cause dysfunction of the intestine for humans, such as inflammation. The compensatory response of the small intestine cells to the harsh environment definitely changes their gene expression. How the small intestine cells response the hypobaric hypoxic environment is still unclear. We studied the rat small intestine under hypobaric hypoxic conditions to explore the transcriptional changes in rats under acute/chronic hypobaric hypoxic conditions. We randomly divided rats into three groups: normal control group (S), acute hypobaric hypoxia group, exposing to hypobaric hypoxic condition for 2 weeks (W2S) and chronic hypobaric hypoxia group, exposing to hypobaric hypoxic condition for 4 weeks (W4S). The RNA sequencing was performed on the small intestine tissues of the three groups of rats. The results of principal component analysis showed that the W4S and W2S groups were quite different from the control group. We identified a total of 636 differentially expressed genes, such as ATP binding cassette, Ace2 and Fabp. KEGG pathway analysis identified several metabolic and digestive pathways, such as PPAR signaling pathway, glycerolipid metabolism, fat metabolism, mineral absorption and vitamin metabolism. Cogena analysis found that up-regulation of digestive and metabolic functions began from the second week of high altitude exposure. Our study highlights the critical role of metabolic and digestive pathways of the intestine in response to the hypobaric hypoxic environment, provides new aspects for the molecular effects of hypobaric hypoxic environment on intestine, and raises further questions about between the lipid metabolism disorders and inflammation.

Effect of acute altitude exposure on ventilatory thresholds in recreational athletes

PurposeHigh altitude (HA) training is frequently used in endurance sports and recreational athletes increasingly participate in cross mountain competitions. At high altitude aerobic physiology changes profoundly. Ventilatory thresholds (VTs) are measures for endurance performance but the impact of exposure to acute altitude (AA) on VTs in recreational athletes has been insufficiently explored to date and most studies investigated effects under normobaric hypoxia. MethodsIn this cross-sectional study we investigated the effects of AA exposure at 2650 m/715 mbar on anerobic threshold (VT1) and respiratory compensation point (VT2) in a graded cycling test in 14 recreational athletes (4 female, 10 male) compared to baseline levels (521 m, 949 mbar). ResultsAt VT1, a decline in power output (PO) from median 115.5 W to 105.0 W (median -12.3 %, p = 0.032; Wilcoxon test) during exposure to HA was observed. VO2/body weight and VO2/heart rate decreased markedly (- 9.5 %, p = 0.016; -10.5 %, p = 0.012). At VT2 we found a significant decline of PO from 184.5–170.5 W (-13.1 %, p = 0.0014), of VO2/body weight and of VO2/heart rate (-10.1 %, p = 0.0015; -8.7 %, p = 0.002) compared to baseline values. Absolute VO2 decreased (-9.5 %, p = 0.0014 and -10.1 %, p = 0.0002) while minute ventilation and heart rates remained unchanged at both thresholds. ConclusionOur data allows a quantification of performance loss at HA in recreational athletes and demonstrates that VT-guided training intensities and workloads need to be adapted for training at HA.

Effects of altitude and recombinant human erythropoietin on iron metabolism: a randomized controlled trial.

Current markers of iron deficiency (ID), such as ferritin and hemoglobin, have shortcomings, and hepcidin and erythroferrone (ERFE) could be of clinical relevance in relation to early assessment of ID. Here, we evaluate whether exposure to altitude-induced hypoxia (2,320 m) alone, or in combination with recombinant human erythropoietin (rHuEPO) treatment, affects hepcidin and ERFE levels before alterations in routine ID biomarkers and stress erythropoiesis manifest. Two interventions were completed, each comprising a 4-wk baseline, a 4-wk intervention at either sea level or altitude, and a 4-wk follow-up. Participants (n = 39) were randomly assigned to 20 IU·kg body wt-1 rHuEPO or placebo injections every second day for 3 wk during the two intervention periods. Venous blood was collected weekly. Altitude increased ERFE (P ≤ 0.001) with no changes in hepcidin or routine iron biomarkers, making ERFE of clinical relevance as an early marker of moderate hypoxia. rHuEPO treatment at sea level induced a similar pattern of changes in ERFE (P < 0.05) and hepcidin levels (P < 0.05), demonstrating the impact of accelerated erythropoiesis and not of other hypoxia-induced mechanisms. Compared with altitude alone, concurrent rHuEPO treatment and altitude exposure induced additive changes in hepcidin (P < 0.05) and ERFE (P ≤ 0.001) parallel with increases in hematocrit (P < 0.001), demonstrating a relevant range of both hepcidin and ERFE. A poor but significant correlation between hepcidin and ERFE was found (R2 = 0.13, P < 0.001). The findings demonstrate that hepcidin and ERFE are more rapid biomarkers of changes in iron demands than routine iron markers. Finally, ERFE and hepcidin may be sensitive markers in an antidoping context.

Effect of moderate altitude on human cerebral metabolite levels: A preliminary, multi-site, proton magnetic resonance spectroscopy investigation

Epidemiological studies show that altitude-of-residence is an independent risk factor for worsening rates of mood disorders, substance abuse, and suicide. Proton (1H) magnetic resonance spectroscopy (MRS) studies in rodent models of moderate-to-high altitude exposure have documented significant alterations in total creatine, glutamate, and myo-inositol, neurometabolites involved in bioenergetic homeostasis and neuronal/glial cell function. This preliminary study utilized 3 Tesla 1H MRS to study anterior cingulate cortex (ACC) and parietal-occipital cortex (POC) neurochemistry in healthy subjects residing in Utah (n = 19), Massachusetts (n = 10), and South Carolina (n = 10), to test the hypothesis that individuals residing at moderate altitude (Utah; 1,372 m) would show neurometabolite alterations vs. subjects living at sea level. Expressed as ratios to total N-acetyl aspartate (NAA), Utah participants showed lower ACC (p = 0.03) and POC (p < 0.01) total creatine, a trend towards lower ACC glutamate (p = 0.06), and lower POC myo-inositol (p = 0.02). Study limitations include small sample sizes and uncorrected multiple comparisons. To our knowledge, this is the first MRS investigation to identify potential neurochemical differences in individuals residing at moderate altitudes vs. sea level, warranting future 1H MRS studies in larger cohorts and across a range of altitudes-of-residence.

The Effects of Acute High Altitude Exposure and Arterial Blood Gas Manipulation on Neurovascular Coupling in Healthy Humans

The Effects of Acute High Altitude Exposure and Arterial Blood Gas Manipulation on Neurovascular Coupling in Healthy Humans

The Effects of Hypoxia‐Induced Central Sleep Apnea on Splenic Contraction and Oxygen Carrying Capacity

Central sleep apnea (CSA) begins developing above 3000m due to respiratory control system instability in hypoxia, and represents a series of short-duration, end-expiratory apneas during sleep. Previous studies demonstrate that splenic contraction is induced by both sustained hypoxia and apnea, ejecting of a store of red blood cells (RBCs) into the systemic circulation, with associated elevations in [hemoglobin] ([Hb]) and arterial oxygen content (CaO2). Therefore, we aimed to assess whether the apneas associated with CSA in the context of high altitude ascent elicit splenic contraction, contributing to hematological acclimatization early in ascent to high altitude. We recruited two groups of participants for two protocols, one lab-based (1045m; Part A) and one during rapid ascent and residence at high altitude (3800m; Part B). For Part A, 15 participants (6 females) performed five intermittent voluntary end-expiratory apneas (15-sec; separated by 1-min) in normobaric hypoxia (FIO2 0.15-0.16) in a seated position. Splenic volume was measured via ultrasonography prior to and immediately following apneas. Capillary blood samples for [Hb] and peripheral pulse oximetry (SpO2) was collected before and immediately following apneas. For Part B, 21 participants (8 females) ascended rapidly by car to 3800m over 5-6 hours, and CSA was assessed via portable polysomnography on night two, with capillary [Hb] samples and SpO2 collected before sleep (pm) and after waking (am). In Part A, splenic volume decreased from normoxia (201±83 mL) to hypoxia (172±62 mL; Δ29±30 mL, 95% CI [11.7–46.1 mL], P=0.003), and decreased further following apneas (151±61 mL, Δ21±17 mL, 95% CI [5.3–36.4], P=0.005) compared to hypoxia baseline. However, [Hb] and CaO2 were unchanged following apneas. At 3800m, the apnea-hypopnea index increased from 3.4±3.5 before ascent (1045m) to 12.3±14.5 events/hour at 3800m (P=0.002), suggesting CSA. [Hb] was elevated from 143±11 g L-1 (night 2) to 152±12 g L-1 (morning 3; Δ9±15 g L-1, 95% CI [2.6–16.2 g L-1] P=0.01), which resulted in increases in CaO2 from 16.9±1.3 to 18.5±1.5 ml dl-1 (Δ1.6±2 ml dl-1, 95% CI [0.6–2.6 ml dl-1], P=0.003). Our data suggest that CSA-mediated intermittent apneas in the context of early high altitude ascent results in functional splenic contraction and ejection of RBCs into the systemic circulation, increasing [Hb] and CaO2. This is the first demonstration that CSA-induced splenic contraction may contribute to hematological acclimatization and increased oxygen carrying capacity early in ascent to high altitude, before the known time-course of erythropoietin-induced increases in [Hb] with sustained high altitude exposure.

A Prospective Evaluation of the Acute Effects of High Altitude on Cognitive and Physiological Functions in Lowlanders.

Cognitive function impairment due to high altitude exposure has been reported with some contradictory results regarding the possible selective cognitive domain involvement. We prospectively evaluated in 36 lowlanders, exposed for 3 consecutive days to an altitude of 3,269 m, specific cognitive abilities (attention, processing speed, and decision-making) required to safely explore the mountains, as well as to work at altitude. We simultaneously monitored the physiological parameters. Our study provides evidence of a reduced processing speed in lowlanders when exposed to altitude in the first 24 h. There was a fairly quick recovery since this impairment was no more detectable after 36 h of exposure. There were no clinically relevant effects on decision-making, while psychomotor vigilance was unaffected at altitude except for individuals with poor sleep. Significant changes were seen in physiological parameters (increased heart rate and reduced peripheral oxygen saturation). Our results may have practical implications, suggesting that individuals should practice prudence with higher ascent when performing risky activities in the first 24–36 h, even at altitudes below 3,500 m, due to an impairment of the cognitive performance that could worsen and lead to accidents.

Exercise-Induced Hypoxemia in Endurance Athletes: Consequences for Altitude Exposure.

Exercise-induced hypoxemia (EIH) is well-described in endurance-trained athletes during both maximal and submaximal exercise intensities. Despite the drop in oxygen (O2) saturation and provided that training volumes are similar, athletes who experience EIH nevertheless produce the same endurance performance in normoxia as athletes without EIH. This lack of a difference prompted trainers to consider that the phenomenon was not relevant to performance but also suggested that a specific adaptation to exercise is present in EIH athletes. Even though the causes of EIH have been extensively studied, its consequences have not been fully characterized. With the development of endurance outdoor activities and altitude/hypoxia training, athletes often train and/or compete in this stressful environment with a decrease in the partial pressure of inspired O2 (due to the drop in barometric pressure). Thus, one can reasonably hypothesize that EIH athletes can specifically adapt to hypoxemic episodes during exercise at altitude. Although our knowledge of the interactions between EIH and acute exposure to hypoxia has improved over the last 10 years, many questions have yet to be addressed. Firstly, endurance performance during acute exposure to altitude appears to be more impaired in EIH vs. non-EIH athletes but the corresponding physiological mechanisms are not fully understood. Secondly, we lack information on the consequences of EIH during chronic exposure to altitude. Here, we (i) review research on the consequences of EIH under acute hypoxic conditions, (ii) highlight unresolved questions about EIH and chronic hypoxic exposure, and (iii) suggest perspectives for improving endurance training.

Nocturnal cerebral tissue oxygenation in lowlanders with chronic obstructive pulmonary disease travelling to an altitude of 2,590m: Data from a randomised trial.

Altitude exposure induces hypoxaemia in patients with chronic obstructive pulmonary disease (COPD), particularly during sleep. The present study tested the hypothesis in patients with COPD staying overnight at high altitude that nocturnal arterial hypoxaemia is associated with impaired cerebral tissue oxygenation (CTO). A total of 35 patients with moderate-to-severe COPD, living at <800m (mean [SD] age 62.4[12.3]years, forced expiratory volume in 1s [FEV1 ] 61[16]% predicted, awake pulse oximetry ≥92%) underwent continuous overnight monitoring of pulse oximetry (oxygen saturation [SpO2 ]) and near-infrared spectroscopy of prefrontal CTO, respectively, at 490m and 2,590m. Regression analysis was used to evaluate whether nocturnal arterial desaturation (COPDDesat , SpO2 <90% for >30% of night-time) at 490m predicted CTO at 2,590m when controlling for baseline variables. At 2,590m, mean nocturnal SpO2 and CTO were decreased versus 490m, mean change -8.8% (95% confidence interval [CI] -10.0 to -7.6) and -3.6% (95% CI -5.7 to -1.6), difference in change ΔCTO-ΔSpO2 5.2% (95% CI 3.0 to 7.3; p<.001). Moreover, frequent cyclic desaturations (≥4% dips/hr) occurred in SpO2 and CTO, mean change from 490m 35.3/hr (95% CI 24.9 to 45.7) and 3.4/hr (95% CI 1.4 to 5.3), difference in change ΔCTO-ΔSpO2 -32.8/hr (95% CI -43.8 to -21.8; p<.001). Regression analysis confirmed an association of COPDDesat with lower CTO at 2,590m (coefficient -7.6%, 95% CI -13.2 to -2.0; p=.007) when controlling for several confounders. We conclude that lowlanders with COPD staying overnight at 2,590m experience altitude-induced hypoxaemia and periodic breathing in association with sustained and intermittent cerebral deoxygenation. Although less pronounced than the arterial deoxygenation, the altitude-induced cerebral tissue deoxygenation may represent a risk of brain dysfunction, especially in patients with COPD with nocturnal hypoxaemia at low altitude.

Hyperoxic Effects on Decompression Strain During Alternating High and Moderate Altitude Exposures.

INTRODUCTION: In fighter aircraft, long-duration high-altitude sorties are typically interrupted by refueling excursions to lower altitude. In normoxia, excursions to moderate cabin altitude may increase the occurrence of venous gas emboli (VGE) at high cabin altitude. The aim was to investigate the effect of hyperoxia on VGE and decompression sickness (DCS) during alternating high and moderate altitude exposure.METHODS: In an altitude chamber, 13 healthy men were exposed to three different conditions: A) 90 min at 24,000 ft (7315 m) breathing normoxic gas (54% O₂; H-NOR); B) 90 min at 24,000 ft breathing hyperoxic gas (90% O₂; H-HYP); and C) three 30-min exposures to 24,000 ft interspersed by two 30-min exposures to 18,000 ft (5486 m) breathing 90% O₂ (ALT-HYP). VGE occurrence was evaluated from cardiac ultrasound imaging. DCS symptoms were rated using a scale.RESULTS: DCS occurred in all conditions and altogether in 6 of the 39 exposures. The prevalence of VGE was similar in H-NOR and H-HYP throughout the exposures. During the initial 30 min at 24,000 ft, the prevalence of VGE was similar in ALT-HYP as in the other two conditions, whereas, after the first excursion to 18,000 ft, the VGE score was lower in ALT-HYP than in H-NOR and H-HYP.DISCUSSION: Hyperoxic excursions from 24,000 to 18,000 ft reduces VGE occurrence, presumably by facilitating diffusive gas exchange across the bubble surfaces, increasing the share of bubble content contributed by oxygen. Still, the excursions did not abolish the DCS risk.Ånell R, Grönkvist M, Gennser M, Eiken O. Hyperoxic effects on decompression strain during alternating high and moderate altitude exposures. Aerosp Med Hum Perform. 2021; 92(4):223230.

Sex-Dependent Association Between Early Morning Ambulatory Blood Pressure Variations and Acute Mountain Sickness.

BackgroundAcute high altitude (HA) exposure elicits blood pressure (BP) responses in most subjects, and some of them suffer from acute mountain sickness (AMS). However, a 24-h ambulatory BP (ABP) change and the correlation with the occurrence of AMS in different sexes are still unclear.ObjectivesThis prospective study aimed to investigate HA induced BP responses in males and females and the relationship between AMS and 24-h ABP.MethodsForty-six subjects were matched according to demographic parameters by propensity score matching with a ratio of 1:1. All the subjects were monitored by a 24-h ABP device; the measurement was one period of 24 h BP. 2018 Lake Louise questionnaire was used to evaluate AMS.ResultsBoth the incidence of AMS (14 [60.9%] vs. 5 [21.7%], P = 0.007) and headache (18 [78.3%] vs. 8 [34.8%], P = 0.003) were higher in females than in males. All subjects showed an elevated BP in the early morning [morning systolic BP (SBP), 114.72 ± 13.57 vs. 120.67 ± 11.10, P = 0.013]. The elevation of morning SBP variation was more significant in females than in males (11.95 ± 13.19 vs. −0.05 ± 14.49, P = 0.005), and a higher morning BP surge increase (4.69 ± 18.09 vs. −9.66 ± 16.96, P = 0.005) was observed after acute HA exposure in the female group. The increase of morning SBP was associated with AMS occurrence (R = 0.662, P < 0.001) and AMS score (R = 0.664, P = 0.001). Among the AMS symptoms, we further revealed that the incidence (R = 0.786, P < 0.001) and the severity of headache (R = 0.864, P < 0.001) are closely correlated to morning SBP.ConclusionsOur study demonstrates that females are more likely to suffer from AMS than males. AMS is closely associated with elevated BP in the early morning period, which may be correlated to higher headache incidence in subjects with higher morning SBP.

Pro-Oxidant/Antioxidant Balance during a Prolonged Exposure to Moderate Altitude in Athletes Exhibiting Exercise-Induced Hypoxemia at Sea-Level.

This study examined to what extent athletes exhibiting exercise-induced hypoxemia (EIH) possess an altered redox status at rest, in response to exercise at sea level (SL) and during moderate altitude exposure. EIH was defined as a fall in arterial O2 saturation of at least 4% during exercise. Nine endurance athletes with EIH and ten without (NEIH) performed a maximal incremental test under three conditions: SL, one (H1) and five (H2) days after arrival to 2400 m. Gas exchange and peripheral capillary oxygen saturation (SpO2) were continuously monitored. Blood was sampled before exercise and after exercise cessation. Advanced oxidation protein products (AOPP), catalase, ferric-reducing antioxidant power, glutathione peroxidase, superoxide dismutase (SOD) and nitric oxide metabolites (NOx) were measured in plasma by spectrophotometry. EIH athletes had higher AOPP and NOx concentrations at pre- and post-exercise stages compared to NEIH at SL, H2 but not at H1. Only the EIH group experienced increased SOD activity between pre- and post-exercise exercise at SL and H2 but not at H1. EIH athletes had exacerbated oxidative stress compared to the NEIH athletes at SL and H2. These differences were blunted at H1. Oxidative stress did not alter the EIH groups’ aerobic performance and could lead to higher minute ventilation at H2. These results suggest that higher oxidative stress response EIH athletes could be involved in improved aerobic muscle functionality and a greater ventilatory acclimatization during prolonged hypoxia.

Respiratory muscle training and exercise ventilation while diving at altitude

Introduction: Pre-dive altitude exposure may increase respiratory fatigue and subsequently augment exercise ventilation at depth. This study examined pre-dive altitude exposure and the efficacy of resistance respiratory muscle training (RMT) on respiratory fatigue while diving at altitude. Methods: Ten men (26±5 years; V̇ O2peak: 39.8±3.3 mL• kg-1•min-1) performed three dives; one control (ground level) and two simulated altitude dives (3,658 m) to 17 msw, relative to ground level, before and after four weeks of resistance RMT. Subjects performed pulmonary function testing (e.g., inspiratory [PI] and expiratory [PE] pressure testing) pre- and post-RMT and during dive visits. During each dive, subjects exercised for 18 minutes at 55% V̇ O2peak, and ventilation (V̇ E), breathing frequency (ƒb,), tidal volume (VT) and rating of perceived exertion (RPE) were measured. Results: Pre-dive altitude exposure reduced PI before diving (p=0.03), but had no effect on exercise V̇ E, ƒb, or VT at depth. At the end of the dive in the pre-RMT condition, RPE was lower (p=0.01) compared to control. RMT increased PI and PE (p&lt;0.01). PE was reduced from baseline after diving at altitude (p&lt;0.03) and this was abated after RMT. RMT did not improve V̇ E or VT at depth, but decreased ƒb (p=0.01) and RPE (p=0.048) during the final minutes of exercise. Conclusion: Acute altitude exposure pre- and post-dive induces decrements in PI and PE before and after diving, but does not seem to influence ventilation at depth. RMT reduced ƒb and RPE during exercise at depth, and may be useful to reduce work of breathing and respiratory fatigue during dives at altitude.

Nodal plant materials of Valeriana jatamansi, a higher altitude-specific medicinal plant typically retained the previous lower altitude exposure and modulated above-ground probes

Nodal plant materials of Valeriana jatamansi, a higher altitude-specific medicinal plant typically retained the previous lower altitude exposure and modulated above-ground probes

Physiological and perceptual responses of exposure to different altitudes in extremely cold environment

An increasing number of people are living or working at high altitudes, which are often accompanied by cold environments. High altitude and cold exposure often result in physiological, perceptual and biochemical changes, thus affecting work efficiency and even human health. This study created different altitude conditions of 0 m, 2560 m, 3650 m, and 4290 m with an ambient temperature of −10 °C in a climate chamber. Six health subjects were recruited, and human physiological and perceptual responses during this experiment were continuously investigated, involving objective parameters such as core temperature, local skin temperature, blood oxygen saturation, heart rate, respiratory rate and subjective parameters such as overall and local thermal sensation, overall and local thermal comfort. The statistical analysis showed that blood oxygen saturation is the most sensitive parameter in short exposure to high altitude, which is consistent with previous studies and shows a close relationship with altitude. All of the mean local skin temperatures in the face, hands and feet throughout the experimental period were lowest at 0 m altitude. The overall thermal sensation decreased by 2.83 units at 0 m, whereas it decreased by only 2.00 units at an altitude of 4290 m. The local thermal sensation correlated well with the local skin temperature (R2 > 0.8) at 0 m, 2560 m and 3650 m when the subjects keep sedentary and wear clothing ensemble with total insulation of 2.16 clo. At an altitude of 4290 m, the local thermal sensations of the face, hands and feet were close to 0 (neutral). These findings indicate that higher altitude may compensate for some of the decreases in thermal sensation caused by a cold environment.

Assessment of right atrial dyssynchrony by 2D speckle-tracking in healthy young men following high altitude exposure at 4100 m.

BackgroundHigh altitude exposure induces overload of right-sided heart and may further predispose to supraventricular arrhythmia. It has been reported that atrial mechanical dyssynchrony is associated with atrial arrhythmia. Whether high altitude exposure causes higher right atrial (RA) dyssynchrony is still unknown. The aim of study was to investigate the effect of high altitude exposure on right atrial mechanical synchrony.MethodsIn this study, 98 healthy young men underwent clinical examination and echocardiography at sea level (400 m) and high altitude (4100 m) after an ascent within 7 days. RA dyssynchrony was defined as inhomogeneous timing to peak strain and strain rate using 2D speckle-tracking echocardiography.ResultsFollowing high altitude exposure, standard deviation of the time to peak strain (SD-TPS) [36.2 (24.5, 48.6) ms vs. 21.7 (12.9, 32.1) ms, p<0.001] and SD-TPS as percentage of R–R’ interval (4.6 ± 2.1% vs. 2.5 ± 1.8%, p<0.001) significantly increased. Additionally, subjects with higher SD-TPS (%) at high altitude presented decreased right ventricular global longitudinal strain and RA active emptying fraction, but increased RA minimal volume index, which were not observed in lower group. Multivariable analysis showed that mean pulmonary arterial pressure and tricuspid E/A were independently associated with SD-TPS (%) at high altitude.ConclusionOur data for the first time demonstrated that high altitude exposure causes RA dyssynchrony in healthy young men, which may be secondary to increased pulmonary arterial pressure. In addition, subjects with higher RA dyssynchrony presented worse RA contractile function and right ventricular performance.

Atrial performance in healthy subjects following high altitude exposure at 4100\xa0m: 2D speckle-tracking strain analysis

High altitude (HA) exposure has been considered as a cardiac stress and might impair ventricular diastolic function. Atrial contraction is involved in ventricular passive filling, however the atrial performance to HA exposure is poorly understood. This study aimed to evaluate the effect of short-term HA exposure on bi-atrial function. Physiological and 2D-echocardiographic data were collected in 82 healthy men at sea level (SL, 400 m) and 4100 m after an ascent within 7 days. Atrial function was measured using volumetric and speckle-tracking analyses during reservoir, conduit and contractile phases of cardiac cycle. Following HA exposure, significant decreases of reservoir and conduit function indexes were observed in bi-atria, whereas decreases of contractile function indexes were observed in right atrium (RA), estimated via RA active emptying fraction (SL 41.7 ± 13.9% vs. HA 35.4 ± 12.2%, p = 0.001), strain during the contractile phase [SL 13.5 (11.4, 17.8) % vs. HA 12.3 (9.3, 15.9) %, p = 0.003], and peak strain rate during the contractile phase [SL − 1.76 (− 2.24, − 1.48) s−1 vs. HA − 1.57 (− 2.01, − 1.23) s−1, p = 0.002], but not in left atrium (LA). In conclusion, short-term HA exposure of healthy individuals impairs bi-atrial performance, mostly observed in RA. Especially, atrial contractile function decreases in RA rather than LA, which seems not to compensate for decreased ventricular filling after HA exposure. Our findings may provide a novel evidence for right-sided heart dysfunction to HA exposure.