This study is the first to investigate the mechanisms underlying plasma volume (PV) contraction in response to hypoxia in women while strictly controlling for confounders. PV contraction in women has a similar time course and magnitude as in men and is driven by the same mechanism, namely, oncotically driven redistribution rather than loss of fluid. We further report that hypoxia facilitates an increase in diuresis, that is, however, short-lived and of little relevance for PV regulation.

Cardiopulmonary resuscitation (CPR) is considered an aerosol-generating procedure. Consequently, COVID-19 resuscitation guidelines recommend the use of personal protective equipment (PPE) during resuscitation. In this simulation of randomised crossover trials, we investigated the influence of PPE on the quality of chest compressions (CCs). Thirty-four emergency medical service BLS-providers performed two 20 min CPR sequences (five 2 min cycles alternated by 2 min of rest) on manikins, once with and once without PPE, in a randomised order. The PPE was composed of a filtering facepiece 3 FFP3 mask, safety glasses, gloves and a long-sleeved gown. The primary outcome was defined as the difference between compression depth with and without PPE; secondary outcomes were defined as differences in CC rate, release and the number of effective CCs. The participants graded fatigue and performance, while generalised estimating equations (GEE) were used to analyse data. There was no significant difference in CC quality between sequences without and with PPE regarding depth (mean depth 54 ± 5 vs. 54 ± 6 mm respectively), rate (mean rate 119 ± 9 and 118 ± 6 compressions per minute), release (mean release 2 ± 2 vs. 2 ± 2 mm) and the number of effective CCs (43 ± 18 vs. 45 ± 17). The participants appraised higher fatigue when equipped with PPE in comparison to when equipped without PPE (p < 0.001), and lower performance was appraised when equipped with PPE in comparison to when equipped without PPE (p = 0.031). There is no negative effect of wearing PPE on the quality of CCs during CPR in comparison to not wearing PPE.

During acute hypoxic exposure, cerebral blood flow (CBF) increases to compensate for the reduced arterial oxygen content (CaO₂). Nevertheless, as exposure extends, both CaO₂ and CBF progressively normalize. Haemoconcentration is the primary mechanism underlying the CaO₂ restoration and may therefore explain, at least in part, the CBF normalization. Accordingly, we tested the hypothesis that reversing the haemoconcentration associated with extended hypoxic exposure returns CBF towards the values observed in acute hypoxia. Twenty‐three healthy lowlanders (12 females) completed two identical 4‐day sojourns in a hypobaric chamber, one in normoxia (NX) and one in hypobaric hypoxia (HH, 3500 m). CBF was measured by ultrasound after 1, 6, 12, 48 and 96 h and compared between sojourns to assess the time course of changes in CBF. In addition, CBF was measured at the end of the HH sojourn after hypervolaemic haemodilution. Compared with NX, CBF was increased in HH after 1 h (P = 0.001) but similar at all later time points (all P > 0.199). Haemoglobin concentration was higher in HH than NX from 12 h to 96 h (all P < 0.001). While haemodilution reduced haemoglobin concentration from 14.8 ± 1.0 to 13.9 ± 1.2 g·dl⁻¹ (P < 0.001), it did not increase CBF (974 ± 282 to 872 ± 200 ml·min⁻¹; P = 0.135). We thus conclude that, at least at this moderate altitude, haemoconcentration is not the primary mechanism underlying CBF normalization with acclimatization. These data ostensibly reflect the fact that CBF regulation at high altitude is a complex process that integrates physiological variables beyond CaO₂. image Key points: Acute hypoxia causes an increase in cerebral blood flow (CBF). However, as exposure extends, CBF progressively normalizes. We investigated whether hypoxia‐induced haemoconcentration contributes to the normalization of CBF during extended hypoxia. Following 4 days of hypobaric hypoxic exposure (corresponding to 3500 m altitude), we measured CBF before and after abolishing hypoxia‐induced haemoconcentration by hypervolaemic haemodilution. Contrary to our hypothesis, the haemodilution did not increase CBF in hypoxia. Our findings do not support haemoconcentration as a stimulus for the CBF normalization during extended hypoxia.

Altitude exposure may suppress appetite and hence provide a viable weight-loss strategy. While changes in food intake and availability as well as physical activity may contribute to altered appetite at altitude, herein we aimed to investigate the isolated effects of hypobaric hypoxia on appetite regulation and sensation. Twelve healthy women (age: 24.0±4.2 years, body mass: 60.6±7.0 kg) completed two 4-day sojourn in a hypobaric chamber, one in normoxia (P_B=761 mmHg, 262 m, NX) and one in hypobaric hypoxia (P_B=493 mmHg, HH) equivalent to 3,500 m altitude. Energy intake was standardized 4 days prior and throughout both sojourns. Plasma concentrations of leptin, acylated ghrelin, cholecystokinin (CCK) and cytokine growth differentiation factor 15 (GDF15) were determined every morning. Before and after breakfast, lunch and dinner, appetite was assessed using visual analogue scales. Body mass was significantly decreased following HH but not NX (-0.71±0.32 kg vs. -0.05±0.54 kg, condition: p<0.001). Compared to NX, acylated ghrelin decreased throughout the HH sojourn (condition x time: p=0.020), while leptin was higher throughout the entire HH sojourn (condition: p<0.001). No differences were observed in CCK and GDF15 between the sojourns. Feelings of satiety and fullness were higher (condition: p<0.001 and p=0.013, respectively), whereas prospective food consumption was lower in HH than in NX (condition: p<0.001). Our findings suggest that hypoxia exerts an anorexigenic effect on appetite regulating hormones, suppresses subjective appetite sensation and can induce weight loss in young healthy women. Among the investigated hormones, acylated ghrelin and leptin most likely explain the observed HH-induced appetite suppression.

We sought to determine the effects of prolonged moderate hypobaric hypoxia (HH) on cardiac baroreflex sensitivity (cBRS) in young women, and whether these effects are a consequence of the reduced arterial oxygen (O₂) tension and/or increased pulmonary ventilation in HH. We hypothesised that HH would reduce cBRS and that this effect would be counteracted by acute restoration of the inspiratory partial pressure of O₂ (PiO₂) and/or voluntary attenuation of pulmonary ventilation. Twelve healthy women (24.0±4.2 years) were studied before (DAY 0) and twice during a sojourn in a hypobaric chamber (~8 hours, DAY 1; 4 days, DAY 4) where barometric pressure corresponded to ~3,500 m altitude. Minute ventilation (V̇_E; pneumotachometer), heart rate (electrocardiogram), and arterial pressure (finger volume clamp method) were recorded. cBRS was calculated using transfer function analysis between systolic pressure and RR interval. Assessments were made during i. spontaneous breathing, and (in HH only) ii. controlled breathing (reducing V̇_E by ~1 L·min^-1), and iii. breathing a hyperoxic gas mixture that normalized PiO₂. During spontaneous breathing HH decreased cBRS (12.5±7.1, 8.9±4.4 and 7.4±3.0 ms·mmHg^-1 on DAY 0, DAY 1 and DAY 4, respectively; P=0.018). The normalization of PiO₂ increased cBRS (10.6±3.3 and 10.7±6.1 ms·mmHg^-1 on DAY 1 and DAY 4) in HH compared to values observed during spontaneous breathing (P<0.001), whereas controlled breathing had no effect on cBRS (P=0.708). These findings indicate that ongoing arterial chemoreflex activation by the reduced arterial O₂ tension, independently of the hypoxic ventilatory response, reduces cBRS in young women exposed to extended HH.