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PurposeStanding balance control is important for everyday function and often goes unnoticed until impairments appear. Presently, more than 200 million people live at altitudes > 2500 m above sea level, and many others work at or travel to these elevations. Thus, it is important to understand how hypoxia alters balance owing to implications for occupations and travelers. Herein, the influence of normobaric and hypobaric hypoxia on standing balance control is reviewed and summarized. As postural control relies on the integration of sensorimotor signals, the potential hypoxic-sensitive neurophysiological factors that contribute to balance impairments are also reviewed. Specifically, we examine how hypoxia impairs visual, vestibular, and proprioceptive cues, and their integration within subcortical or cortical areas.MethodsThis systematic review included a literature search conducted via multiple databases with keywords related to postural balance, hypoxia, and altitude. Articles (n = 13) were included if they met distinct criteria.ResultsCompared to normoxia, normobaric hypoxia worsened parameters of standing balance by 2–10% and up to 83 and 240% in hypobaric hypoxia (high-altitude and lab-based, respectively). Although balance was only disrupted during normobaric hypoxia at FIO2 <  ~ 0.15, impairments consistently occurred during hypobaric hypoxia at altitudes > 1524 m (~ FIO2 < 0.18).ConclusionHypoxia, especially hypobaric, impairs standing balance. The mechanisms underpinning postural decrements likely involve alterations to processing and integration of sensorimotor signals within subcortical or cortical structures involving visual, vestibular, and proprioceptive pathways and subsequent motor commands that direct postural adjustments. Future studies are required to determine the sensorimotor factors that may influence balance control in hypoxia.

Cold temperatures (<−15°C) increase exercise‐induced bronchoconstriction (EIB), while hypoxic‐induced hyperventilation exacerbates respiratory muscle fatigue for a given exercising task. This study aimed to determine the individual and combined effects of cold and normobaric hypoxia on the respiratory system responses to high‐intensity exercise. Fourteen trained male runners (V̇O2max ${{\\dot{V}}_{{{\\mathrm{O}}}_2}{\\mathrm{max}}}$ : 64 ± 5 mL/kg/min) randomly performed an incremental cardiopulmonary exercise test (CPET) to volitional exhaustion under four environmental conditions: normothermic (18°C) normoxia (FIO2 ${{F}_{{\\mathrm{I}}{{{\\mathrm{O}}}_2}}}$ : 20.9%) and hypoxia (FIO2 ${{F}_{{\\mathrm{I}}{{{\\mathrm{O}}}_2}}}$ : 13.5%), and cold (−20°C) normoxia and hypoxia. Ventilatory responses during exercise and lung function (LF), maximal inspiratory (MIP) and expiratory (MEP) pressure measurements before and after exercise were evaluated. Volume of air forcefully exhaled in 1 s (FEV1), FEV1/forced vital capacity (FVC), peak expiratory flow, forced expiratory flow during the mid (25–75%) portion of the FVC, and maximal expiratory flow at 50% of FVC were affected by cold exposure. No significant pre‐ to post‐exercise change in MIP and MEP was found, independent of environmental conditions. Greater LF impairments in cold‐normoxia and coldhypoxia were associated with the lowest peak ventilatory responses during exercise. Cold exposure was found to negatively impact peak ventilatory responses and post‐exercise LF, further highlighting a relationship between EIB presence and the blunted ventilatory response in the cold. Respiratory muscle strength remained unchanged after exercise regardless of the environmental condition, suggesting no detrimental effect of hypoxia on this parameter when intermittent short‐duration high‐intensity exercises are performed. Future studies should investigate the combined cold‐hypoxic effect on longer exercise durations at a sustained high intensity, accounting for differences between normobaric and hypobaric hypoxia exposures. What is the central question of this study? What are the independent and combined effects of cold and normobaric hypoxia on respiratory responses to high‐intensity exercise? What is the main finding and its importance? Cold exposure impaired lung function and peak ventilatory responses during high‐intensity exercise, with greater impairments observed under combined cold‐hypoxia condition. The findings highlight a link between exercise‐induced bronchoconstriction and reduced ventilatory capacity in cold environments. Respiratory muscle strength remained unaffected post‐exercise across all conditions, suggesting no detrimental impact of hypoxia during short‐duration high‐intensity tasks.

This study aimed to investigate the effects of a 4-week live high train low (LHTL; FiO2 ~ 13.5%), intervention, followed by a tapering phase, on muscle glycogen concentration. Fourteen physically active males (28 ± 6 years, 81.6 ± 15.4 kg, 179 ± 5.2 cm) were divided into a control group (CON; n = 5), and the group that performed the LHTL, which was exposed to hypoxia (LHTL; n = 9). The subjects trained using a one-legged knee extension exercise, which enabled four experimental conditions: leg training in hypoxia (TLHYP); leg control in hypoxia (CLHYP, n = 9); leg trained in normoxia (TLNOR, n = 5), and leg control in normoxia (CLNOR, n = 5). All participants performed 18 training sessions lasting between 20 and 45 min [80–200% of intensity corresponding to the time to exhaustion (TTE) reached in the graded exercise test]. Additionally, participants spent approximately 10 h day−1 in either a normobaric hypoxic environment (14.5% FiO2; ~ 3000 m) or a control condition (i.e., staying in similar tents on ~ 530 m). Thereafter, participants underwent a taper protocol consisting of six additional training sessions with a reduced training load. SpO2 was lower, and the hypoxic dose was higher in LHTL compared to CON (p < 0.001). After 4 weeks, glycogen had increased significantly only in the TLNOR and TLHYP groups and remained elevated after the taper (p < 0.016). Time to exhaustion in the LHTL increased after both the 4-week training period and the taper compared to the baseline (p < 0.001). Although the 4-week training promoted substantial increases in muscle glycogen content, TTE increased in LHTL condition.

Much hypoxia research has been carried out at high altitude in a hypobaric hypoxia (HH) environment. Many research teams seek to replicate high-altitude conditions at lower altitudes in either hypobaric hypoxic conditions or normobaric hypoxic (NH) laboratories. Implicit in this approach is the assumption that the only relevant condition that differs between these settings is the partial pressure of oxygen (PO 2 ), which is commonly presumed to be the principal physiological stimulus to adaptation at high altitude. This systematic review is the first to present an overview of the current available literature regarding crossover studies relating to the different effects of HH and NH on human physiology. After applying our inclusion and exclusion criteria, 13 studies were deemed eligible for inclusion. Several studies reported a number of variables (e.g. minute ventilation and NO levels) that were different between the two conditions, lending support to the notion that true physiological difference is indeed present. However, the presence of confounding factors such as time spent in hypoxia, temperature, and humidity, and the limited statistical power due to small sample sizes, limit the conclusions that can be drawn from these findings. Standardisation of the study methods and reporting may aid interpretation of future studies and thereby improve the quality of data in this area. This is important to improve the quality of data that is used for improving the understanding of hypoxia tolerance, both at altitude and in the clinical setting.

PurposeTo investigate the influence of acute normobaric hypoxia on standing balance under single and dual-task conditions, both with and without visual input.Methods20 participants (7 female, 20–31 years old) stood on a force plate for 16, 90-s trials across four balance conditions: single-task (quiet stance) or dual-task (auditory Stroop test), with eyes open or closed. Trials were divided into four oxygen conditions where the fraction of inspired oxygen (FIO2) was manipulated (normoxia: 0.21 and normobaric hypoxia: 0.16, 0.145 and 0.13 FIO2) to simulate altitudes of 1100, 3,400, 4300, and 5200 m. Participants breathed each FIO2 for ~ 3 min before testing, which lasted an additional 7–8 min per oxygen condition. Cardiorespiratory measures included heart rate, peripheral blood oxygen saturation, and pressure of end tidal (PET) CO2 and O2. Center of pressure measures included total path length, 95% ellipse area, and anteroposterior and mediolateral velocity. Auditory Stroop test performance was measured as response accuracy and latency.ResultsSignificant decreases in oxygen saturation and PETO2, and increased heart rate were observed between normoxia and normobaric hypoxia (P < 0.0001). Total path length was higher at 0.13 compared to 0.21 FIO2 for the eyes closed no Stoop test condition (P = 0.0197). No other significant differences were observed.ConclusionThese findings suggest that acute normobaric hypoxia has a minimal impact on standing balance and does not influence auditory Stroop test or dual-task performance. Further investigation with longer exposure is required to understand the impact and time course of normobaric hypoxia on standing balance.

The ability of operators to integrate visual and auditory information places a high demand on their attention when monitoring instruments and systems. In this context, physiological constraints such as reduced oxygen levels alone or combined with restricted sleep are known to impair attention capacities. However, it is not known whether EEG markers of visual attention are affected differently from those of auditory attention in a situation combining both constraints. This study aimed to investigate the effects of prolonged moderate hypoxia exposure (4 h at fraction of inspired oxygen FiO 2 = 13.6%, ≃ 3500 m), sleep restriction (3 h of time-in-bed) and their combination on the evoked potential P300 and the alpha rhythm in 17 healthy participants. We first found that visually and auditory evoked P300 amplitude were reduced by sleep restriction and the combination of hypoxia plus sleep restriction, but not by hypoxia alone, reproducing previous findings regarding sleep restriction. We also found less efficient alpha event-related desynchronization (α-ERD) and alpha inter-trial phase coherence (α-ITPC) as it has already been observed during sleep restriction, while also providing novel insights into the effects of acute moderate and prolonged hypoxia exposure. Furthermore, our results confirm that certain neural aspects of visual and auditory attentional processes are differentially affected by hypoxia and sleep restriction, and also suggest that sleep restriction plays a primary role in driving the effects observed under combined constraints.

In rats, acute normobaric hypoxia depressed left ventricular (LV) inotropic function. After 24 h of hypoxic exposure, a slight recovery of LV function occurred. We speculated that prolonged hypoxia (72 h) would induce acclimatization and, hence, recovery of LV function. Moreover, we investigated biomarkers of nitrosative stress and apoptosis as possible causes of hypoxic LV depression. To elucidate the role of hypoxic sympathetic activation, we studied whether adrenergic blockade would further deteriorate the general state of the animals and their cardiac function. Ninety-four rats were exposed over 72 h either to normal room air (N) or to normobaric hypoxia (H). The rodents received infusion (0.1 mL/h) with 0.9% NaCl or with different adrenergic blockers. Despite clear signs of acclimatization to hypoxia, the LV depression continued persistently after 72 h of hypoxia. Immunohistochemical analyses revealed significant increases in markers of nitrosative stress, adenosine triphosphate deficiency and apoptosis in the myocardium, which could provide a possible explanation for the absence of LV function recovery. Adrenergic blockade had a slightly deteriorative effect on the hypoxic LV function compared to the hypoxic group with maintained sympathetic efficacy. These findings show that hypoxic sympathetic activation compensates, at least partially, for the compromised function in hypoxic conditions, therefore emphasizing its importance for hypoxia adaptation.

Exposure to acute normobaric hypoxia (NH) elicits reactive oxygen species (ROS) accumulation, whose production kinetics and oxidative damage were here investigated. Nine subjects were monitored while breathing an NH mixture (0.125 FIO2 in air, about 4100 m) and during recovery with room air. ROS production was assessed by Electron Paramagnetic Resonance in capillary blood. Total antioxidant capacity, lipid peroxidation (TBARS and 8-iso-PFG2α), protein oxidation (PC) and DNA oxidation (8-OH-dG) were measured in plasma and/or urine. The ROS production rate (μmol·min−1) was monitored (5, 15, 30, 60, 120, 240 and 300 min). A production peak (+50%) was reached at 4 h. The on-transient kinetics, exponentially fitted (t1/2 = 30 min r2 = 0.995), were ascribable to the low O2 tension transition and the mirror-like related SpO2 decrease: 15 min: −12%; 60 min: −18%. The exposure did not seem to affect the prooxidant/antioxidant balance. Significant increases in PC (+88%) and 8-OH-dG (+67%) at 4 h in TBARS (+33%) one hour after hypoxia offset were also observed. General malaise was described by most of the subjects. Under acute NH, ROS production and oxidative damage resulted in time and SpO2-dependent reversible phenomena. The experimental model could be suitable for evaluating the acclimatation level, a key element in the context of mountain rescues in relation to technical/medical workers who have not had enough time for acclimatization—as, for example, during helicopter flights.

Purpose: This study aimed to investigate the differences between normobaric (NH) and hypobaric hypoxia (HH) on supine heart rate variability (HRV) during a 24-h exposure. We hypothesized a greater decrease in parasympathetic-related parameters in HH than in NH. Methods: A pooling of original data from forty-one healthy lowland trained men was analyzed. They were exposed to altitude either in NH (F I O 2 = 15.7 ± 2.0%; PB = 698 ± 25 mmHg) or HH (F I O 2 = 20.9%; PB = 534 ± 42 mmHg) in a randomized order. Pulse oximeter oxygen saturation (S p O 2 ), heart rate (HR), and supine HRV were measured during a 7-min rest period three times: before (in normobaric normoxia, NN), after 12 (H12), and 24 h (H24) of either NH or HH exposure. HRV parameters were analyzed for time- and frequency-domains. Results: S p O 2 was lower in both hypoxic conditions than in NN and was higher in NH than HH at H24. Subjects showed similarly higher HR during both hypoxic conditions than in NN. No difference in HRV parameters was found between NH and HH at any time. The natural logarithm of root mean square of the successive differences (LnRMSSD) and the high frequency spectral power (HF), which reflect parasympathetic activity, decreased similarly in NH and HH when compared to NN. Conclusion: Despite S p O 2 differences, changes in supine HRV parameters during 24-h exposure were similar between NH and HH conditions indicating a similar decrease in parasympathetic activity. Therefore, HRV can be analyzed similarly in NH and HH conditions.