Mild hypobaric hypoxia influences splenic proliferation during the later phase of stress erythropoiesis

Tissue trauma and hemorrhagic shock are common battlefield injuries that can induce hypoxia, inflammation, and/or anemia. Inflammation and hypoxia can initiate adaptive mechanisms, such as stress erythropoiesis in the spleen, to produce red blood cells and restore the oxygen supply. In a military context, mild hypobaric hypoxia—part of the environmental milieu during aeromedical evacuation or en route care—may influence adaptive mechanisms, such as stress erythropoiesis, and host defense. In the present study, healthy (control), muscle trauma, and polytrauma (muscle trauma and hemorrhagic shock) mice were exposed to normobaric normoxia or hypobaric hypoxia for ∼17.5 h to test the hypothesis that hypobaric hypoxia exposure influences splenic erythropoiesis and splenic inflammation after polytrauma. This hypothesis was partially supported. The polytrauma + hypobaric hypoxia group exhibited more splenic neutrophils, fewer total spleen cells, and fewer splenic proliferating cells than the polytrauma+normobaric normoxia group; however, no splenic erythroid cell differences were detected between the two polytrauma groups. We also compared splenic erythropoiesis and myeloid cell numbers among control, muscle trauma, and polytrauma groups. More reticulocytes at 1.7 days (40 h) post-trauma (dpt) and neutrophils at 4 dpt were produced in the muscle trauma mice than corresponding control mice. In contrast to muscle trauma, polytrauma led to a reduced red blood cell count and elevated serum erythropoietin levels at 1.7 dpt. There were more erythroid subsets and apoptotic reticulocytes in the polytrauma mice than muscle trauma mice at 4 and 8 dpt. At 14 dpt, the red blood cell count of the polytrauma + normobaric normoxia mice was 12% lower than that of the control + normobaric normoxia mice; however, no difference was observed between polytrauma + hypobaric hypoxia and control + hypobaric hypoxia mice. Our findings suggest muscle trauma alone induces stress erythropoiesis; in a polytrauma model, hypobaric hypoxia exposure may result in the dysregulation of splenic cells, requiring a treatment plan to ensure adequate immune functioning.

Cognitive Impairment During Combined Normobaric vs. Hypobaric and Normoxic vs. Hypoxic Acute Exposure

INTRODUCTION: Exposure to hypoxia has a deleterious effect on cognitive function; however, the putative effect of hypobaria remains unclear. The present study aimed to evaluate cognitive performance in pilot trainees who were exposed to acute normobaric (NH) and hypobaric hypoxia (HH). Of relevance for military pilots, we also aimed to assess cognitive performance in hypobaric normoxia (HN).METHODS: A total of 16 healthy pilot trainees were exposed to 4 randomized conditions (i.e., normobaric normoxia, NN, altitude level of 440 m; HH at 5500 m; NH, altitude simulation of 5500 m; and HN). Subjects performed a cognitive assessment (KLT-R test). Cerebral oxygen delivery (cDO2) was estimated based middle cerebral artery blood flow velocity (MCAv) and pulse oxygen saturation (Spo2) monitored during cognitive assessment.RESULTS: Percentage of errors increased in NH (14.3 9.1%) and HH (12.9 6.4%) when compared to NN (6.5 4.1%) and HN (6.0 4.0%). Number of calculations accomplished was lower only in HH than in NN and HN. When compared to NN, cDO2 decreased in NH and HH.DISCUSSION: Cognitive performance was decreased similarly in acute NH and HH. The cDO2 reduction in NH and HH implies insufficient MCAv increase to ensure cognitive performance maintenance. The present study suggests negligible hypobaric influence on cognitive performance in hypoxia and normoxia.Aebi MR, Bourdillon N, Noser P, Millet GP, Bron D. Cognitive impairment during combined normobaric vs. hypobaric and normoxic vs. hypoxic acute exposure. Aerosp Med Hum Perform. 2020; 91(11):845851.

Acute Mountain Sickness Symptoms Depend on Normobaric versus Hypobaric Hypoxia

Acute mountain sickness (AMS), characterized by headache, nausea, fatigue, and dizziness when unacclimatized individuals rapidly ascend to high altitude, is exacerbated by exercise and can be disabling. Although AMS is observed in both normobaric (NH) and hypobaric hypoxia (HH), recent evidence suggests that NH and HH produce different physiological responses. We evaluated whether AMS symptoms were different in NH and HH during the initial stages of exposure and if the assessment tool mattered. Seventy-two 8 h exposures to normobaric normoxia (NN), NH, or HH were experienced by 36 subjects. The Environmental Symptoms Questionnaire (ESQ) and Lake Louise Self-report (LLS) were administered, resulting in a total of 360 assessments, with each subject answering the questionnaire 5 times during each of their 2 exposure days. Classification tree analysis indicated that symptoms contributing most to AMS were different in NH (namely, feeling sick and shortness of breath) compared to HH (characterized most by feeling faint, appetite loss, light headedness, and dim vision). However, the differences were not detected using the LLS. These results suggest that during the initial hours of exposure (1) AMS in HH may be a qualitatively different experience than in NH and (2) NH and HH may not be interchangeable environments.

Acute mountain sickness, chemosensitivity, and cardiorespiratory responses in humans exposed to hypobaric and normobaric hypoxia

We examined the control of breathing, cardiorespiratory effects, and the incidence of acute mountain sickness (AMS) in humans exposed to hypobaric hypoxia (HH) and normobaric hypoxia (NH), and under two control conditions [hypobaric normoxia (HN) and normobaric normoxia (NN)]. Exposures were 6 h in duration, and separated by 2 wk between hypoxic exposures and 1 wk between normoxic exposures. Before and after exposures, subjects ( n = 11) underwent hyperoxic and hypoxic Duffin CO2 rebreathing tests and a hypoxic ventilatory response test (HVR). Inside the environmental chamber, minute ventilation (V̇e), tidal volume (Vt), frequency of breathing ( fB), blood oxygenation, heart rate, and blood pressure were measured at 5 and 30 min and hourly until exit. Symptoms of AMS were evaluated using the Lake Louise score (LLS). Both the hyperoxic and hypoxic CO2 thresholds were lower after HH and NH, whereas CO2 sensitivity was increased after HH and NH in the hypoxic test and after NH in the hyperoxic test. Values for HVR were similar across the four exposures. No major differences were observed for V̇e or any other cardiorespiratory variables between NH and HH. The LLS was greater in AMS-susceptible than in AMS-resistant subjects; however, LLS was alike between HH and NH. In AMS-susceptible subjects, fB correlated positively and Vt negatively with the LLS. We conclude that 6 h of hypoxic exposure is sufficient to lower the peripheral and central CO2 threshold but does not induce differences in cardiorespiratory variables or AMS incidence between HH and NH.

Relationship between resting ventilatory chemosensitivity and maximal oxygen uptake in moderate hypobaric hypoxia

This study tested the hypothesis that the extent of the decrement in V̇o2max and the respiratory response seen during maximal exercise in moderate hypobaric hypoxia (H; simulated 2,500 m) is affected by the hypoxia ventilatory and hypercapnia ventilatory responses (HVR and HCVR, respectively). Twenty men (5 untrained subjects, 7 long distance runners, 8 middle distance runners) performed incremental exhaustive running tests in H and normobaric normoxia (N) condition. During the running test, V̇o2, pulmonary ventilation (V̇e) and arterial oxyhemoglobin saturation (SaO2) were measured, and in two ventilatory response tests performed during N, a rebreathing method was used to evaluate HVR and HCVR. Mean HVR and HCVR were 0.36 ± 0.04 and 2.11 ± 0.2 l·min−1·mmHg−1, respectively. HVR correlated significantly with the percent decrements in V̇o2max (%dV̇o2max), SaO2 [%dSaO2 = (N−H)·N−1·100], and V̇e/V̇o2 seen during H condition. By contrast, HCVR did not correlate with any of the variables tested. The increment in maximal V̇e between H and N significantly correlated with %dV̇o2max. Our findings suggest that O2 chemosensitivity plays a significant role in determining the level of exercise hyperventilation during moderate hypoxia; thus, a higher O2 chemosensitivity was associated with a smaller drop in V̇o2max and SaO2 under those conditions.