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The study was aimed at determining cardiorespiratory coordination under the influence of acute hypoxia in athletes with different levels of sports qualifications. Eighteen runners aged 17 to 25 were exposed to acute (10% O2) hypoxia for 10 min. Respiration, gas exchange, and heart rate were measured during normoxia and hypoxia. The principal component (PC) analysis was used to assess cardiorespiratory coordination; the stability of PCs under the influence of hypoxia was evaluated by the Tucker’s Congruence Coefficient. The analysis was performed on a time series of 10 min of normoxia and hypoxia with the inclusion of heart rate, minute ventilation, the expired fraction of O2 and CO2. According to the level of qualification, athletes were divided into two groups: highly trained (HT, no less than category I, n = 9) and medium-trained (MT, category II, n = 9). Under normoxia, cardiorespiratory coordination in athletes of both groups was higher than in normobaric hypoxia (p = 0.001): during normoxia, the model included one PC from coordinated variables according to the Kaiser criterion in 44% of the athletes; during hypoxia, the model consisted of two PCs in 100% of the athletes. During hypoxia, the percentage of total variance explained by PC2 increased significantly (p < 0.001), regardless of the level of qualification. In hypoxia, there was a change in the variable contributions to PC1 and PC2, more pronounced in the MT group: the contribution of heart rate to PC1 increased, and the expired fraction of CO2 decreased (p < 0.001). The congruence coefficient of the first PC between normoxia and hypoxia in the HT group showed a high level of similarity (median = 0.88; 25/75% = 0.84/0.93) and was significantly (p < 0.05) higher than in MT (0.82; 0.46/0.94). Thus, highly qualified athletes have the higher cardio-respiratory stability under hypoxic exposure. This can be an additional predictive sign of good athletic performance.

Idiopathic acute eosinophilic pneumonia (IAEP) is characterized by febrile hypoxic respiratory failure with diffuse radiographic infiltrates and peripheral and pulmonary eosinophilia in a previously healthy child. Diagnosis is by exclusion, but promptness is imperative, as IAEP can lead to life-threatening acute lung injury and acute respiratory distress syndrome. Prognosis is usually good after steroid treatment with total recovery and absence of relapse in reported cases. We report a case of a previously healthy 14-year-old boy with this diagnosis who presented with acute hypoxia and characteristic radiographic and bronchoalveolar lavage findings. He had full recovery after corticosteroid treatment. This case report highlights the diagnostic approach to a patient with IAEP, an uncommon diagnosis, and one of the exclusions, in children.

The availability of oxygen (O2) is vital for maintaining neurological function during exercise. This is clear when performing exercise in low oxygen environments, such as high altitude, where reductions in O2 availability result in limitations in motor performance. However, the ongoing contribution of central and peripheral mechanisms to hypoxia-related limitations in motor performance is yet to be fully understood. A wide variety of experimental designs have been used to test motor pathways during hypoxic exposure. Indeed, there is little consistency in the literature with regards to 1) the severity of hypoxic exposure, 2) the duration of hypoxic exposure, 3) the fatigue-state of the motor system, and 4) the intensity of exercise. This Thesis presents a series of controlled laboratory experiments which assess the effects of acute hypoxia (2 hr at 80% SpO2) on central and peripheral motor mechanisms. The experiments used high-density electromyography, electrical stimulation of the motor nerve (MNS), and transcranial magnetic stimulation (TMS) of the motor cortex, to clarify how motor activity is affected with hypoxia. The first experiment assessed how the firing characteristics of biceps brachii motor units (MU) were modulated by acute hypoxia when performing sustained isometric elbow flexions. Maximal voluntary contraction (MVC) toque remained unaffected during hypoxia, however, individuals exhibited specific changes in MU firing. Bidirectional changes in MU discharge were strongly correlated to the rate of desaturation and sensitivity to O2 availability during the titration phase. Differences in intrinsic properties of neurons, afferent input to motoneurones, neuromodulation, and sympathetic nerve activity may explain these differences. The second experiment assessed how corticospinal excitability, voluntary activation using motor nerve stimulation (VAMNS) and perception of fatigue (RPF) during brief and sustained MVCs were modulated by acute hypoxia. RPF and corticospinal excitability increased, while VAMNS decreased across the hypoxia protocol. Changes in the motor evoked potential (MEP) area and VAMNS were only seen during the brief MVCs and not the sustained MVCs. This may be due to redirection of blood flow to active areas of the motor system during prolonged contraction. The third experiment assessed how acute hypoxia altered neural mechanisms of muscle activation during, and following recovery from, a sustained submaximal (20% MVC) fatiguing contraction. MVC torque, root mean square EMG (EMGRMS), VAMNS and voluntary activation using TMS (VATMS), RPF, MEP area, and silent period duration (SP) were measured to characterise muscle activation. Hypoxia effects were only seen during the recovery phase, where VAMNS and VATMS, as well as MEP area, was reduced during acute hypoxia. This was likely due to hypoxia-related mechanisms involving supraspinal motor circuits that were impaired during the recovery phase. The fourth experiment assessed how acute hypoxia altered the neural mechanisms of muscle activation across a full range of force output once fatigued. MVC torque, EMGRMS, VAMNS and VATMS, MEP area, and SP were assessed following the sustained MVC. VATMS was reduced during hypoxia, which was not reflected in VAMNS. This indicates that acute hypoxia significantly impaired the ability of the motor cortex to voluntarily activate the fatigued muscle. This was partly due to suboptimal output from the motor cortex. Collectively, the findings of the four experiments in this Thesis provide novel evidence that a moderate acute hypoxic stimulus 1) reduces VA of a muscle during maximal and submaximal contraction due to suboptimal output from the motor cortex, 2) modulates the excitability of the corticospinal pathway, and 3) enhances perceptions of muscle fatigue during maximal, but not submaximal, fatiguing contractions. For these findings to occur, the elbow flexor muscle group needed to be sufficiently fatigued during at least 2 hr of prolonged exposure to a moderate hypoxic stimulus.

PURPOSE: To study the effect of amtizol, 2-aminobenzthiazole (2-ABT) and 2-amino-4-acetylthiazolo[5,4-b]indole (BM-606) on the resistance of male outbred mice to acute hypoxia with hypercapnia under conditions of isolated functioning of one from the hemispheres, as well as both hemispheres of the brain. METHODS: A model of acute hypoxia with hypercapnia (canned hypoxia) was used in mice of the same mass, the lifespan of all animals was determined. Temporary shutdown of the cortex of one of the hemispheres or both hemispheres was achieved by epidural application of filter paper moistened with 25% potassium chloride solution, creating a spreading depression according to Leao. Amtizol, 2-aminobenzthiazole (2-ABT) and 2-amino-4-acetylthiazolo[5,4-b]indole (BM-606) at equimolar doses of 25, 32.5, and 50 mg/kg, respectively were used as pharmacological analyzers, the compounds were injected intraperitoneally 30 min before the hypoxic episode. RESULTS: It was shown that, in contrast to amtizol, 2-ABT and VM-606 increase the life time of experimental animals when any hemisphere is turned off. The use of drugs when both hemispheres were turned off revealed that amtizol has approximately equal effect on the brain and the rest of the body, in 2-ABT antihypoxic activity is 1/3 associated with the brain, in VM-606 exclusively with the brain. CONCLUSION: The experimental model used in this work makes it possible to quite easily evaluate the effect of either one drug or compare several drugs, their role in the functioning of the cerebral hemispheres, on which part of the sample highly resistant or low resistant to hypoxia they have the greatest effect.

Labor and vaginal delivery cause acute ischemic/hypoxic insult to the placenta. Previous studies demonstrate that placentas from high altitude non-natives showed blunted responses to ischemic/hypoxic insult caused by labor and vaginal birth, and there were some differences in the ATP/ADP production ratio. We hypothesized that adapted highlanders would not have a stress response to the acute hypoxia/ischemia of labor. Tibetan laboring (n = 10) and non-laboring (n = 5) and European descendants laboring (n = 10) and non-laboring (n = 5) high-altitude placentas were analyzed using genome-wide expression array analysis. There was no evidence for ischemic/hypoxic stress in high-altitude Tibetan laboring as compared with non-laboring placentas, while there were differences in gene expression between laboring and non-laboring placentas from high-altitude European descendants. Our results provide evidence for adaptation to acute hypoxic ischemic insult caused by labor and vaginal birth in placentas in a high-altitude native Tibetan population.

Development of methods for monitoring the functional state (FS) of people under extreme conditions is of great applied significance. The aim of this study was to investigate the dynamics of integral EEG parameters in individuals with different levels of hypoxia sensitivity and tolerance during their exposure to oxygen deficiency. Acute hypoxia was induced by a mixture of 8% oxygen in nitrogen for breathing. The study cohort was composed of 41 male participants aged from 19 to 45 years. We recorded a complex of physiological indices, as well as multichannel EEGs, based on which the structure function and the integral normalized parameters were calculated. These parameters were used as a measure of temporal (Pt) and spatial (Ps) connectivity between oscillations of brain potentials. The extreme values of parameters, 0 and 1, corresponded to the completely deterministic and “random” temporal and spatial organization of the EEG. A decrease in Pt, as hypoxia deepened, indicated a growth in the temporal connectivity and inertness in the EEG, which characterized a decrease in the physiological lability and the FS of the brain. Significant changes in Ps, which indicated an increase in the degree of EEG spatial connectivity, were recorded only in individuals with low hypoxia tolerance in a precollaptoid state. The use of the normalized Pt and Ps parameters allowed us to classify the subjects by the degree of their sensitivity to hypoxia and identify individuals with high sensitivity, under a relatively small fall in hemoglobin oxygen saturation (SaO2), and persons resistant to hypoxia even at low levels of SaO2, which is important for the selection of persons exposed to hypoxia by occupation.

The aim was to study cardiac bioelectric features across different levels of acute normobaric hypoxia (ANH) in healthy young men. Methods: We studied cardiac functions in response to exposure to ANH of mild (14.5 % O2) and medium (12.3 % O2) degrees for 20 minutes among 30 and 29 young men, respectively. Results. With mild and medium degree of ANH, SpO2 decreases to (91.6 ± 4.2) % and to (78.2 ± 5.2) %, respectively. An initial increase in the P1II wave was common for all ANH exposures. On average, during the period of mild ANH, the total BAL and BAR of the heart compartments decreased, only at the beginning the RR and QT intervals decreased, and in the end QT increased. Medium ANH was associated with more pronounced changes in ECG characteristics. On average, during the ANH period of 12.3 % O2, the RII wave (by 0.078 mV, p < 0.001), T1II (0.074 mV, p < 0.001), BAL (0.26 mV, р < 0.001) and BAR (at 0.12 mV, p < 0.001) of the heart decreased, RR intervals (at 100 ms, p < 0.001), QT (11 ms, p < 0.001), and Pc, PQc, QRSc, QTc increased. Correlations between QT deviations and SpO2, СО, SVR, VIK increased. For ANH of 14.5 % O2, the factor "positive chronotropic effect" dominated in the general structure of the ECG, while for 12.3 % O2 it was "chrono-inotropic conjugation". Conclusions. Changes in ECG parameters seem to be more pronounced in exposure to moderate than mild ANH. Possible extracardiac and myogenic regulation mechanisms in the organization of heart bioelectric processes with a mild and medium degree of hypoxia are proposed in the paper.

Okabe et al. 1 present data from animal models of acute hypoxia showing that oxygen-carrying liquid applied to the distal gut improves oxygenation and prolongs survival. This opens the possibility of recruiting the distal gut to aid when mechanical ventilation of the lungs is inadequate.

The effect of melatonin in a dose of 1 mg per 1 kg of the body mass on the intensity of lipid peroxidation and antioxidant protection in the basal ganglia of the rat brain under a combined influence of the altered photoperiod and acute hypoxia has been studied. It has been shown that melatonin administration 30 minutes before modelling acute hypoxia in animals containing under the conditions of an altered photoperiod is conducive to a normalization of the parameters of peroxidation processes in the basal ganglia., Изучено влияние мелатонина в дозе 1 мг/кг массы тела на интенсивность перекисного окисления липидов и состояние антиоксидантной защиты в базальных ядрах мозга крыс в условиях сочетанного действия измененного фотопериода и острой гипоксии. Показано, что введение мелатонина за 30 мин до моделирования острой гипоксии животным, содержавшимся в условиях измененного фотопериода, способствует нормализации показателей процессов пероксидации в базальных ядрах., Досліджено вплив мелатоніну в дозі 1 мг/кг маси тіла на інтенсивність пероксидного окиснення ліпідів та стан антиоксидантного захисту в базальних ядрах мозку щурів за поєднаного впливу зміненого фотоперіоду та гострої гіпоксії. Показано, що уведення мелатоніну за 30 хв до моделювання гострої гіпоксії тваринам, що утримувалися за умов зміненого фотоперіоду, сприяє наближенню до норми показників процесів пероксидації в базальних ядрах.