Objectives To investigate the efficacy of pink noise and earplugs in mitigating sleep fragmentation induced by intermittent environmental noise. Methods Twenty-five healthy adults (mean ± SD age 28.5 ± 5.9 years, 7 male) participated in a polysomnographic laboratory study with intermittent exposure to environmental noise (93 events; maximum sound pressure level 45 to 65 dBA), pink noise (40 or 50 dBA), foam earplugs, and their combination. Results Pink noise mitigated aircraft noise induced arousals and awakenings in a dose-response manner but was outperformed by earplugs. Awakening and arousal probability were highest for a crying baby and a fire alarm sound, followed by helicopter, low sonic boom, drone, rail, jet, and road noise. Conclusions Earplugs emerged as a more efficacious option for mitigating environmental noise effects on sleep disruption compared to pink noise. Noise legislation relying on jet noise studies likely underestimate the effects of helicopter noise and other emerging aircraft sounds on sleep. Clinical Trial Registration ClinicalTrials.gov, NCT05774977.

Despite pressurization of airliner cabins, some passengers experience in-flight hypobaric hypoxia with blood oxygen saturation dropping below 90%, potentially causing discomfort and increasing the risk of medical events. Enrichment of the cabin air with carbon dioxide (CO2) may augment passengers' blood and tissue oxygenation by stimulating respiratory drive, thereby increasing health and safety during air travel. In a randomized double-blind crossover study, we exposed 17 healthy adults (8 women; age range: 18-40 yr) on separate days to two ambient CO2 levels (0.1% vs. 1.0% indoor sea-level equivalents; 0.76 vs. 7.60 mmHg partial pressure) during 6 h of hypobaric hypoxia (∼565 mmHg total barometric pressure; corresponding to 2,438 m altitude) in an altitude chamber simulating long-haul flight conditions. We measured oxygen saturation of the blood ([Formula: see text]), brain, and muscle (tissue saturation index derived from near-infrared spectroscopy), respiration, and cognitive function (sustained attention, working memory, and hand-eye coordination) hourly. In addition, we conducted capillary blood gas analyses at baseline, 15 min, and 6 h after hypoxia onset. During hypobaric hypoxia, ambient CO2 enrichment on average increased Pco2 from 36.3 to 38.3 mmHg, Po2 from 60.9 to 68.3 mmHg, and minute ventilation from 9.7 to 10.4 L/min, whereas reducing the time fraction of [Formula: see text] < 90% from 18.8% to 2.5%. Tissue oxygenation increased in the brain from 62.8% to 63.9%, whereas no change was found in the muscle. High ambient CO2 had no effect on cognitive performance. Taken together, enrichment of cabin air with CO2 during hypobaric hypoxia may improve blood and brain oxygenation.NEW & NOTEWORTHY Elevating ambient CO2 can improve blood and brain oxygenation in healthy individuals during moderate hypoxia as experienced in an airliner cabin. The findings offer a new approach potentially benefiting the health and safety of airline passengers and support investigating CO2 enrichment in broader passenger populations, especially in those at risk of hypoxemia. Exploration of CO2-based interventions to enhance passenger oxygenation may also prompt regulatory reassessment of cabin CO2 limits and technological innovations in ventilation systems.

STUDY OBJECTIVES:The cerebral adenosinergic system is involved in sleep-wake regulation and presumably represents a neuro-molecular correlate of homeostatic sleep pressure. For acute sleep deprivation, it has been shown that increased cerebral A1 adenosine receptor (A1AR) availability was related to impairments in cognitive performance. The present study examined A1AR availability in response to chronic sleep restriction and recovery. METHODS:To quantify A1AR availability we used 8-Cyclopentyl-3-(3-[18F]fluoropropyl)-1-propylxanthine ([18F] CPFPX) positron emission tomography in 21 volunteers after 5 nights with 5-h sleep opportunities followed by 8 h recovery sleep. Data were compared to a control group of 15 volunteers who slept 8 h each night. In addition, polysomnography, cognitive performance, and alertness were recorded. RESULTS:Chronic sleep restriction did not increase the A1AR availability. Slow wave sleep (SWS) and EEG slow-wave-activity (SWA) in the first 5 h of sleep did not differ from baseline (BL), but SWA in the last 3 h of sleep was increased and cognitive performance and alertness were impaired. While SWA returned to BL in the last 3 h of recovery sleep, performance, and alertness remained impaired. CONCLUSION:The results indicate that chronic sleep loss likely induces parallel upregulations of extracellular adenosine and A1AR resulting in no net gain in receptor availability. The results contrast with findings from acute sleep deprivation in which we found impaired performance and increased A1AR availability that were restored to rested levels after recovery sleep. The findings reveal fundamental differences in the mechanisms through which acute and chronic sleep loss affect adenosinergic regulation and cognitive performance.

STUDY OBJECTIVES:Nighttime environmental noise (EN) exposure disturbs sleep and increases morbidity and mortality. Affordable and effective countermeasures are needed, but rigorous research is scarce. This study investigates the efficacy of pink noise (PN) and earplugs for mitigating the effects of intermittent EN on sleep. METHODS:Twenty-five healthy adults (mean ± SD age 28.5 ± 5.9 years, seven male) participated in a seven-night polysomnographic laboratory study with different noise conditions including exposure to EN (93 events; maximum sound pressure level 45 to 65 dBA), PN (40 or 50 dBA), earplugs, and their combination. In the morning, participants completed cognitive tests, cardiovascular measurements, hearing tests, and surveys. RESULTS:Compared to a noise-free control night, EN reduced N3 deep sleep (p < .0001) while PN reduced REM sleep (p < .001). Adding PN to EN worsened sleep structure, despite minor dose-dependent improvements of EN-induced sleep fragmentation and N3 sleep increases. Earplugs mitigated nearly all EN effects on sleep but started failing at the highest EN level (65 dBA). Morning cognition, cardiovascular measures, and hearing were not affected by nighttime noise, but subjective assessments of sleep, alertness and mood were significantly worse after EN and PN exposure. CONCLUSIONS:In contrast to PN, earplugs proved efficacious in mitigating the effects of EN on sleep. Considering the importance of REM sleep for memory, emotion regulation, and neurodevelopment, the negative effects of PN on REM sleep caution against the widespread and indiscriminate use of broadband noise (BN). Additional research on optimal BN color/level and long-term use is needed, especially in vulnerable populations. CLINICAL TRIAL REGISTRATION:Registered at clinicaltrials.gov under "Broadband Sound and Sleep"; https://clinicaltrials.gov/study/NCT05774977; registration # NCT05774977.

STUDY OBJECTIVES:Although teamwork under fatigue is highly common in the workplace, the effects of sleep loss on group performance have rarely been studied. Here, we examined whether cooperative teamwork in a control room setting has a protective effect by attenuating performance impairment caused by sleep loss. METHODS:Sixty-six healthy volunteers (32 females, 26 ± 5 [SD] years) were randomly assigned to teams of three to undergo a laboratory study for five consecutive days. They completed tasks in a simulated control room setting calling on different cognitive domains (sustained attention during monitoring, logical reasoning during problem diagnosis) once after 19 hours awake (sleep deprivation, circadian low) and once following 8 hours of scheduled sleep (control) in counterbalanced order. Participants completed the tasks on their own (solo work) and in teams with each member instructed to work to their own advantage (competitive work) or to the team's advantage (cooperative work). Performance, communication, decision behavior, and team cohesion were analyzed. RESULTS:Findings showed during monitoring longer reaction times and more errors under sleep deprivation compared to control, but no interaction between sleep condition and work mode. During diagnosis, sleep-deprived participants were slower, whereas the error rate depended on the work mode: contrary to solo and competitive work, the error rate decreased during cooperative work compared to control. Transcripts revealed that sleep-deprived participants shared fewer incorrect information and reported higher team cohesion than when rested. CONCLUSIONS:We conclude that in a control room, teams can compensate for some effects of fatigue on logical reasoning by working cooperatively and adapting their communication behavior.

ABSTRACTCircadian clocks in the body drive daily cycles in physiology and behavior. A master clock in the brain maintains synchrony with the environmental day–night cycle and uses internal signals to keep clocks in other tissues aligned. Work in cell cultures uncovered cyclic changes in tissue oxygenation that may serve to reset and synchronize circadian clocks. Here we show in healthy humans, following a randomized controlled single‐blind counterbalanced crossover study design, that one‐time exposure to moderate ambient hypoxia (FiO2 ~15%, normobaric) for ~6.5 h during the early night advances the dim‐light onset of melatonin secretion by 9 min (95% CI: 1–16 min). Exposure to moderate hypoxia may thus be strong enough to entrain circadian clocks to a 24‐h cycle in the absence of other entraining cues. Together, the results provide direct evidence for an interaction between the body's hypoxia‐sensing pathway and circadian clocks. The finding offers a mechanism through which behaviors that change tissue oxygenation (e.g., exercise and fasting/eating) can affect circadian timing and through which hypoxia‐related diseases (e.g., obstructive sleep apnea and chronic obstructive pulmonary disease) can result in circadian misalignment and associated pathologies.Trial Registration: Registration number: DRKS00023387; German Clinical Trials Register: http://www.drks.de

It has been shown that mood is disturbed by sleep restriction (SR). We examined how mood and sleepiness after SR are impacted by the use of caffeinated coffee. Data from 72 volunteers were assessed during 3 baseline and 5 experimental (E1 to E5) days. The control group (n=15, 66.7% male, mean age ± SD 28.0 ± 5.7) had 8 h time in bed (TIB) throughout the study. The sleep restriction group (n=21, 57.1% male, 26.4 ± 3.7), the decaffeinated coffee group (DECAFF, n=17, 58.8% male, 27.9 ± 5.3) and the caffeinated coffee group (CAFF, n=19, 57.9% male, 29.9 ± 5.0) had 8 h TIB at baseline and 5 h TIB during the experimental nights. Both coffee groups consumed standardized 600 ml (E1 to E4) or 400 ml (E5) coffee. Only in the CAFF group, the coffee contained caffeine (200 ml coffee: 100 mg caffeine). Positive (PA) and negative (NA) affect (PANAS) and KSS sleepiness were rated 4 times during scheduled wakefulness. We report here results of mixed ANOVAs and Dunnett-adjusted comparisons of daytime averages during SR. At baseline, PA, NA, and sleepiness were not different between groups. Compared to baseline, PA deteriorated in the sleep restriction group on E1 through E5 (all p< 0.001), in the DECAFF group on E2 through E5 (all p< 0.001), and in the CAFF group on E3 through E5 (all p< 0.001). Compared to the control group, PA was worse in the sleep restriction group (E2 and E3, both p< 0.035), and in the DECAFF group (E1 through E5, all p< 0.03), but not in the CAFF group (all p>0.2). NA remained unchanged (group x condition: p>0.2). Compared to baseline, sleepiness increased in the sleep restriction, DECAFF, and CAFF groups on E2 through E5 (all p< 0.045). The DECAFF and CAFF groups (but not the sleep restriction group) were sleepier than the control group on E2 through E5 (all p< 0.035). PA and sleepiness, but not NA, were negatively affected by SR. The use of caffeinated coffee under chronic sleep loss may be more effective in improving mood than in counteracting sleepiness.

In animal studies it has been observed that the inhibitory neuromodulator adenosine is released into the cerebral interstitial space during hypoxic challenges. Adenosine's actions on the A1 adenosine receptor (A1AR) protect the brain from oxygen deprivation and overexertion through adjustments in cerebral blood flow, metabolism, and electric activity. Methods: Using 8-cyclopentyl-3-(3-[18F]fluoropropyl)-1-propylxanthine ([18F]CPFPX), a PET tracer for the A1AR, we tested the hypothesis that hypoxia-induced adenosine release reduces A1AR availability in the human brain. Furthermore, we investigated whether this response is associated with altered brain perfusion and psychomotor vigilance. Ten healthy volunteers completed a 110-min bolus-plus-constant-infusion [18F]CPFPX PET/MRI hybrid experiment including a 30-min interval of normobaric hypoxia with peripheral oxygen saturation between 70% and 75%. We obtained blood samples to calculate metabolite-corrected steady-state A1AR distribution volumes and measured gray matter brain perfusion via arterial spin labeling in high temporal resolution. A 3-min psychomotor vigilance test was conducted every 10 min, and heart rate and peripheral blood oxygen saturation were continuously measured. Results: In all 7 examined brain regions, hypoxia reduced A1AR availability significantly (e.g., frontal lobe, 13.5%; P = 0.0144) whereas gray matter brain perfusion increased (e.g., frontal lobe, 42.5%; P = 0.0007). Heart rate increased by 19% (P = 0.0039). Mean reaction speed decreased by 4.3% (P = 0.0021). Conclusion: Our study is the first, to our knowledge, to demonstrate that acute hypoxia, corresponding to a mean altitude of 5,500 m (18,000 ft), reduces A1AR availability in the human brain. The finding is consistent with hypoxia-induced cerebral adenosine release leading to increased A1AR occupancy.

In Nagern wurde beobachtet, dass der Neuromodulator Adenosin während Hypoxie im Gehirn freigesetzt wird und es vor Sauerstoffmangel und Überlastung schützt, indem Blutfluss, Stoffwechsel und elektrische Aktivität angepasst werden. An 10 Probanden wurde geprüft, ob durch Hypoxie – einem Sauerstoffpartialdruck auf 5500 m entsprechend – die Verfügbarkeit von A1-Adenosinrezeptoren (A1AR) im menschlichen Gehirn entsprechend reduziert wird. Akute normobare Hypoxie führte im Gehirn zu einer Reduktion der A1AR-Verfügbarkeit, während sich die Perfusion und die Herzfrequenz erhöhten und sich die Reaktionsgeschwindigkeit verringerte. Unseres Wissens sind wir die erste Studie, die beim Menschen eine Verringerung der A1AR-Verfügbarkeit unter Hypoxie nachgewiesen hat. Die so reduzierte neuronale Aktivität bei gleichzeitig erhöhter Durchblutung wirken gemeinsam dem verringerten Sauerstoffangebot entgegen und könnte für zukünftige Gegenmaßnahmen eingesetzt werden.

AbstractAstronauts in space often experience sleep loss. In the AGBRESA (Artificial Gravity Bed Rest) study, we examined 24 participants (mean age ± SD, 33 ± 9 years) during two months of 6o head-down tilt (HDT) bed rest, which is a well-established spaceflight analogue. Polysomnography was recorded during baseline (BDC-9), HDT (nights 1, 8, 30 and 58) and recovery (R, nights 1 and 12). Mixed ANOVAs with post-hoc step-down Bonferroni adjustment indicated that compared to BDC-9, arousals were increased, while sleep duration, N3, and sleep efficiency were all decreased during HDT. Significant quadratic associations between sleep duration and quality with time into HDT did not indicate adaptive improvements during the course of HDT. While sleep duration recovered quickly after the end of bed rest, participants still displayed protracted sleep fragmentation. We conclude that physiological changes caused by exposure to microgravity may contribute to persistent sleep deficits experienced during real space missions.

Between 1/15 000 and 1/50 000 passengers experience acute medical problems during a flight, with cardiac arrests requiring cardiopulmonary resuscitation (CPR) accounting for 0.3 % of medical emergencies. Hypoxia in the aircraft cabin could affect the oxygen supply and physical performance of the rescuer, so a randomized, controlled, double-blind study was conducted to test the hypothesis that hypoxia reduces the effectiveness of CPR. 24 healthcare professionals were randomized into 2 different study arms, each testing 2 conditions. Mixed ANOVAs with post-hoc false discovery rates with pairwise comparisons showed that prolonged exposure to hypoxia, equivalent to the conditions of a long-duration flight, may impair the quality of chest compressions. Supplemental oxygen for medical personnel is an effective countermeasure.

We conducted an observational field study at Frankfurt Airport before (2011) and after (2012) implementation of a night-flight ban (23:00-5:00) to determine whether reduced nighttime flight traffic protects airport residents from sleep fragmentation. We recorded sleep-EEG and noise exposure in residents' bedrooms in early sleepers (bedtime: 22:00-22:30, rise time: 6:00-6:30; 2011: N = 49; 2012: N = 42) and late sleepers (bedtime: 23:00-23:30, rise time 7:00-7:30; 2012 only: N = 41). Early sleepers were exposed to 26.8 +/- 15.7 (mean per time in bed +/- STD) overflights in 2011, and 14.9 +/- 9.3 in 2012. Late sleepers were exposed to 24.6 +/- 14.7 overflights in 2012. Number of awakenings was 27.5% lower in early sleepers in 2012 than in 2011 (p < 0.001). Noise-associated awakenings predicted from the exposure-response model were higher in late compared to early sleepers in 2012. A night-flight ban is most effective when it largely overlaps with the sleep episode.

HomeCirculationVol. 149, No. 18Peripheral Oxygenation and Pulmonary Hemodynamics in Individuals With Fontan Circulation During 24-Hour High-Altitude Exposure Simulation No AccessLetterRequest AccessFull TextAboutView Full TextView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toNo AccessLetterRequest AccessFull TextPeripheral Oxygenation and Pulmonary Hemodynamics in Individuals With Fontan Circulation During 24-Hour High-Altitude Exposure Simulation Nicole Müller, Julian Alexander Härtel, Jan Schmitz, Ute Baur, Melanie von der Wiesche, Iris Rieger, Darius Gerlach, Jon von Stritzky, Anja Bach, Christopher Hart, Janina Bros, Benedikt Seeger, Emily Zollmann, Marijke Grau, Boris Dragutinovic, Laura-Maria de Boni, Jan-Niklas Hönemann, Wilhelm Bloch, Daniel Aeschbach, Eva-Maria Elmenhorst, Ulrike Herberg, Alena Hess, Moritz Schumann, Tobias Kratz, Jens Jordan, Johannes Breuer and Jens Tank Nicole MüllerNicole Müller https://orcid.org/0000-0001-9211-9209 Department of Pediatric Cardiology (N.M., J.A.H., U.B., C.H., A.H., T.K., J.B.), University of Bonn Medical Center, Germany. , Julian Alexander HärtelJulian Alexander Härtel https://orcid.org/0000-0003-0852-2850 Department of Pediatric Cardiology (N.M., J.A.H., U.B., C.H., A.H., T.K., J.B.), University of Bonn Medical Center, Germany. , Jan SchmitzJan Schmitz Institute of Aerospace Medicine, German Aerospace Center, Cologne, Germany (J.S., M.v.d.W., I.R. D.G., J.v.S., A.B., L-M.d.B., J-N.H., D.A., E-M.E., J.J., J.T.). Department of Anesthesiology and Intensive Care Medicine, University Hospital of Cologne, Germany (J.S.). , Ute BaurUte Baur Department of Pediatric Cardiology (N.M., J.A.H., U.B., C.H., A.H., T.K., J.B.), University of Bonn Medical Center, Germany. , Melanie von der WiescheMelanie von der Wiesche https://orcid.org/0000-0002-6487-2460 Institute of Aerospace Medicine, German Aerospace Center, Cologne, Germany (J.S., M.v.d.W., I.R. D.G., J.v.S., A.B., L-M.d.B., J-N.H., D.A., E-M.E., J.J., J.T.). , Iris RiegerIris Rieger Institute of Aerospace Medicine, German Aerospace Center, Cologne, Germany (J.S., M.v.d.W., I.R. D.G., J.v.S., A.B., L-M.d.B., J-N.H., D.A., E-M.E., J.J., J.T.). , Darius GerlachDarius Gerlach https://orcid.org/0000-0001-7044-6065 Institute of Aerospace Medicine, German Aerospace Center, Cologne, Germany (J.S., M.v.d.W., I.R. D.G., J.v.S., A.B., L-M.d.B., J-N.H., D.A., E-M.E., J.J., J.T.). , Jon von StritzkyJon von Stritzky https://orcid.org/0009-0007-7141-3952 Institute of Aerospace Medicine, German Aerospace Center, Cologne, Germany (J.S., M.v.d.W., I.R. D.G., J.v.S., A.B., L-M.d.B., J-N.H., D.A., E-M.E., J.J., J.T.). , Anja BachAnja Bach Institute of Aerospace Medicine, German Aerospace Center, Cologne, Germany (J.S., M.v.d.W., I.R. D.G., J.v.S., A.B., L-M.d.B., J-N.H., D.A., E-M.E., J.J., J.T.). , Christopher HartChristopher Hart https://orcid.org/0000-0001-5880-3576 Department of Pediatric Cardiology (N.M., J.A.H., U.B., C.H., A.H., T.K., J.B.), University of Bonn Medical Center, Germany. , Janina BrosJanina Bros https://orcid.org/0009-0008-1014-0425 Department of Pediatric Cardiology (N.M., J.A.H., U.B., C.H., A.H., T.K., J.B.), University of Bonn Medical Center, Germany. , Benedikt SeegerBenedikt Seeger Department of Molecular and Cellular Sports Medicine, German Sport University Cologne, Germany (J.B., B.S., E.Z., M.G., B.D., W.B., M.S.). , Emily ZollmannEmily Zollmann https://orcid.org/0000-0001-7137-3013 Department of Molecular and Cellular Sports Medicine, German Sport University Cologne, Germany (J.B., B.S., E.Z., M.G., B.D., W.B., M.S.). , Marijke GrauMarijke Grau https://orcid.org/0000-0003-1980-9195 Department of Molecular and Cellular Sports Medicine, German Sport University Cologne, Germany (J.B., B.S., E.Z., M.G., B.D., W.B., M.S.). , Boris DragutinovicBoris Dragutinovic Department of Molecular and Cellular Sports Medicine, German Sport University Cologne, Germany (J.B., B.S., E.Z., M.G., B.D., W.B., M.S.). , Laura-Maria de BoniLaura-Maria de Boni https://orcid.org/0000-0001-7785-482X Institute of Aerospace Medicine, German Aerospace Center, Cologne, Germany (J.S., M.v.d.W., I.R. D.G., J.v.S., A.B., L-M.d.B., J-N.H., D.A., E-M.E., J.J., J.T.). , Jan-Niklas HönemannJan-Niklas Hönemann Institute of Aerospace Medicine, German Aerospace Center, Cologne, Germany (J.S., M.v.d.W., I.R. D.G., J.v.S., A.B., L-M.d.B., J-N.H., D.A., E-M.E., J.J., J.T.). University of Cologne, Faculty of Medicine and University Hospital Cologne, Clinic III for Internal Medicine, Cologne, Germany (J.-N.H.). Department of Internal Medicine III, Division of Cardiology, Pneumology, Angiology, and Intensive Care, University of Cologne, Germany (J-N.H., J.J.). , Wilhelm BlochWilhelm Bloch Department of Molecular and Cellular Sports Medicine, German Sport University Cologne, Germany (J.B., B.S., E.Z., M.G., B.D., W.B., M.S.). , Daniel AeschbachDaniel Aeschbach https://orcid.org/0000-0002-6054-5753 Institute of Experimental Epileptology and Cognition Research (D.A.), University of Bonn Medical Center, Germany. Institute of Aerospace Medicine, German Aerospace Center, Cologne, Germany (J.S., M.v.d.W., I.R. D.G., J.v.S., A.B., L-M.d.B., J-N.H., D.A., E-M.E., J.J., J.T.). , Eva-Maria ElmenhorstEva-Maria Elmenhorst https://orcid.org/0000-0003-0336-6705 Institute of Aerospace Medicine, German Aerospace Center, Cologne, Germany (J.S., M.v.d.W., I.R. D.G., J.v.S., A.B., L-M.d.B., J-N.H., D.A., E-M.E., J.J., J.T.). Institute for Occupational, Social and Environmental Medicine (E-M.E.), Medical Faculty, Rheinisch-Westfälische Technische Hochschule Aachen University, Germany. , Ulrike HerbergUlrike Herberg https://orcid.org/0000-0002-9386-0258 Department of Pediatric Cardiology (U.H.), Medical Faculty, Rheinisch-Westfälische Technische Hochschule Aachen University, Germany. , Alena HessAlena Hess Department of Pediatric Cardiology (N.M., J.A.H., U.B., C.H., A.H., T.K., J.B.), University of Bonn Medical Center, Germany. , Moritz SchumannMoritz Schumann Department of Molecular and Cellular Sports Medicine, German Sport University Cologne, Germany (J.B., B.S., E.Z., M.G., B.D., W.B., M.S.). Department of Sports Medicine and Exercise Therapy, Institute of Human Movement Science and Health, Chemnitz University of Technology, Germany (M.S.). , Tobias KratzTobias Kratz https://orcid.org/0000-0003-3369-4494 Department of Pediatric Cardiology (N.M., J.A.H., U.B., C.H., A.H., T.K., J.B.), University of Bonn Medical Center, Germany. , Jens JordanJens Jordan https://orcid.org/0000-0003-4518-0706 Institute of Aerospace Medicine, German Aerospace Center, Cologne, Germany (J.S., M.v.d.W., I.R. D.G., J.v.S., A.B., L-M.d.B., J-N.H., D.A., E-M.E., J.J., J.T.). Medical Faculty, University of Cologne, Albertus-Magnus-Platz, Cologne, Germany (J.J.). Department of Internal Medicine III, Division of Cardiology, Pneumology, Angiology, and Intensive Care, University of Cologne, Germany (J-N.H., J.J.). , Johannes BreuerJohannes Breuer https://orcid.org/0000-0001-7572-0692 Department of Molecular and Cellular Sports Medicine, German Sport University Cologne, Germany (J.B., B.S., E.Z., M.G., B.D., W.B., M.S.). and Jens TankJens Tank Correspondence to: Jens Tank, MD, Linder Hoehe, 51147 Cologne, Germany. Email E-mail Address: [email protected] https://orcid.org/0000-0002-5672-1187 Institute of Aerospace Medicine, German Aerospace Center, Cologne, Germany (J.S., M.v.d.W., I.R. D.G., J.v.S., A.B., L-M.d.B., J-N.H., D.A., E-M.E., J.J., J.T.). Originally published29 Apr 2024https://doi.org/10.1161/CIRCULATIONAHA.123.067601Circulation. 2024;149:1466–1468FootnotesRegistration: URL: https://drks.de/search/en/trial/DRKS00025989; Unique identifier: DRKS000025989.For Sources of Funding and Disclosures, see page 1468.Circulation is available at www.ahajournals.org/journal/circCorrespondence to: Jens Tank, MD, Linder Hoehe, 51147 Cologne, Germany. Email jens.tank@dlr.deREFERENCES1. Hoffmann F, Limper U, Zaha VG, Reuter H, Zange L, Schulz-Menger J, Hein M, Baldus S, Levine BD, Jordan J, et al. Evolution of pulmonary hypertension during severe sustained hypoxia.Circulation. 2020; 141:1504–1506. doi: 10.1161/CIRCULATIONAHA.119.045192LinkGoogle Scholar2. Muller N, Herberg U, Jung T, Breuer J, Hartel JA. Adequate exercise response at artificial altitude in Fontan patients.Front Pediatr. 2022; 10:947433. doi: 10.3389/fped.2022.947433CrossrefMedlineGoogle Scholar3. Staempfli R, Schmid JP, Schenker S, Eser P, Trachsel LD, Deluigi C, Wustmann K, Thomet C, Greutmann M, Tobler D, et al. Cardiopulmonary adaptation to short-term high altitude exposure in adult Fontan patients.Heart. 2016; 102:1296–1301. doi: 10.1136/heartjnl-2016-309682CrossrefMedlineGoogle Scholar4. Joseph AA, Merboldt KD, Voit D, Zhang S, Uecker M, Lotz J, Frahm J. Real-time phase-contrast MRI of cardiovascular blood flow using undersampled radial fast low-angle shot and nonlinear inverse reconstruction.NMR Biomed. 2012; 25:917–924. doi: 10.1002/nbm.1812CrossrefMedlineGoogle Scholar5. Elmenhorst EM, Rooney D, Benderoth S, Wittkowski M, Wenzel J, Aeschbach D. Sleep-induced hypoxia under flight conditions: implications and countermeasures for long-haul flight crews and passengers.Nat Sci Sleep. 2022; 14:193–205. doi: 10.2147/NSS.S339196CrossrefMedlineGoogle Scholar eLetters(0)eLetters should relate to an article recently published in the journal and are not a forum for providing unpublished data. Comments are reviewed for appropriate use of tone and language. Comments are not peer-reviewed. Acceptable comments are posted to the journal website only. Comments are not published in an issue and are not indexed in PubMed. Comments should be no longer than 500 words and will only be posted online. References are limited to 10. Authors of the article cited in the comment will be invited to reply, as appropriate.Comments and feedback on AHA/ASA Scientific Statements and Guidelines should be directed to the AHA/ASA Manuscript Oversight Committee via its Correspondence page.Sign In to Submit a Response to This Article Previous Back to top Next FiguresReferencesRelatedDetails April 30, 2024Vol 149, Issue 18 Advertisement Article InformationMetrics © 2024 American Heart Association, Inc.https://doi.org/10.1161/CIRCULATIONAHA.123.067601PMID: 38683898 Originally publishedApril 29, 2024 KeywordsFontan procedurehypoxiapulmonary artery pressurepulmonary blood flowPDF download Advertisement SubjectsCongenital Heart DiseaseHeart FailureHemodynamicsMagnetic Resonance Imaging (MRI)Physiology

Sleep deprivation and circadian rhythm disruptions are highly prevalent in shift workers, and also among astronauts. Resulting sleepiness can reduce cognitive performance, lead to catastrophic occupational events, and jeopardize space missions. We investigated whether 24 hours of total sleep deprivation would affect performance not only in the Psychomotor Vigilance Task (PVT), but also in a complex operational task, i.e. simulated manual spacecraft docking. Sixty-two healthy participants completed the manual docking simulation 6df and the PVT once after a night of total sleep deprivation and once after eight hours of scheduled sleep in a counterbalanced order. We assessed the impact of sleep deprivation on docking as well as PVT performance and investigated if sustained attention is an essential component of operational performance after sleep loss. The results showed that docking accuracy decreased significantly after sleep deprivation in comparison to the control condition, but only at difficult task levels. PVT performance deteriorated under sleep deprivation. Participants with larger impairments in PVT response speed after sleep deprivation also showed larger impairments in docking accuracy. In conclusion, sleep deprivation led to impaired 6df performance, which was partly explained by impairments in sustained attention. Elevated motivation levels due to the novelty and attractiveness of the task may have helped participants to compensate for the effects of sleepiness at easier task levels. Continued testing of manual docking skills could be a useful tool both to detect sleep loss-related impairments and assess astronauts’ readiness for duty during long-duration missions.

Abstract Evidence has shown that both sleep loss and daily caffeine intake can induce changes in grey matter (GM). Caffeine is frequently used to combat sleepiness and impaired performance caused by insufficient sleep. It is unclear (1) whether daily use of caffeine could prevent or exacerbate the GM alterations induced by 5-day sleep restriction (i.e. chronic sleep restriction, CSR), and (2) whether the potential impact on GM plasticity depends on individual differences in the availability of adenosine receptors, which are involved in mediating effects of caffeine on sleep and waking function. Thirty-six healthy adults participated in this double-blind, randomized, controlled study (age = 28.9 ± 5.2 y/; F:M = 15:21; habitual level of caffeine intake < 450 mg; 29 homozygous C/C allele carriers of rs5751876 of ADORA2A, an A2A adenosine receptor gene variant). Each participant underwent a 9-day laboratory visit consisting of one adaptation day, 2 baseline days (BL), 5-day sleep restriction (5 h time-in-bed), and a recovery day (REC) after an 8-h sleep opportunity. Nineteen participants received 300 mg caffeine in coffee through the 5 days of CSR (CAFF group), while 17 matched participants received decaffeinated coffee (DECAF group). We examined GM changes on the 2nd BL Day, 5th CSR Day, and REC Day using magnetic resonance imaging and voxel-based morphometry. Moreover, we used positron emission tomography with [18F]-CPFPX to quantify the baseline availability of A1 adenosine receptors (A1R) and its relation to the GM plasticity. The results from the voxel-wise multimodal whole-brain analysis on the Jacobian-modulated T1-weighted images controlled for variances of cerebral blood flow indicated a significant interaction effect between caffeine and CSR in four brain regions: (a) right temporal-occipital region, (b) right dorsomedial prefrontal cortex (DmPFC), (c) left dorsolateral prefrontal cortex (DLPFC), and (d) right thalamus. The post-hoc analyses on the signal intensity of these GM clusters indicated that, compared to BL, GM on the CSR day was increased in the DECAF group in all clusters but decreased in the thalamus, DmPFC, and DLPFC in the CAFF group. Furthermore, lower baseline subcortical A1R availability predicted a larger GM reduction in the CAFF group after CSR of all brain regions except for the thalamus. In conclusion, our data suggest an adaptive GM upregulation after 5-day CSR, while concomitant use of caffeine instead leads to a GM reduction. The lack of consistent association with individual A1R availability may suggest that CSR and caffeine affect thalamic GM plasticity predominantly by a different mechanism. Future studies on the role of adenosine A2A receptors in CSR-induced GM plasticity are warranted.

AbstractAir traveler numbers are predicted to reach 4.0 billion in 2024. Between 1/15,000–50,000 passengers will experience acute medical problems inflight with cardiac arrests requiring cardiopulmonary resuscitation (CPR) accounting for 0.3% of medical emergencies. Hypoxia in airplane cabins could impair oxygenation and physical performance of caregivers. We conducted a randomized controlled, double-blind study to test the hypothesis that hypoxia decreases the effectiveness in performing CPR. We randomized 24 healthcare professionals to two different study arms, each consisting of two conditions: arm (1) ‘hypoxia (FiO2 15%, equivalent to 2400 m altitude)’ versus ‘normoxia’; arm (2) ‘hypoxia + supplemental oxygen’ versus ‘normoxia + supplemental oxygen’. The order of conditions was counterbalanced and a minimum wash-out period of 24 h was granted between conditions. In each condition participants performed a 5-min cardiac compression only CPR (CCO-CPR) using a full-body manikin after one, three and six hours in an altitude chamber. Mixed ANOVAs with post-hoc false-discovery-rate adjusted pairwise comparisons indicated that although compression frequency was maintained, the number of compressions with correct depth was decreased at all times during hypoxia compared to normoxia (all p < 0.002). After 6 h hypoxia exposure, mean compression depth was below the recommended compression depth defined by ERC/AHA guidelines and reduced compared to normoxia (42.4 ± 12.6 mm vs. 54.6 ± 4.3 mm, p < 0.0001). Supplemental oxygen during CCO-CPR in hypoxia prevented the decrease of compression-depth (55.3 ± 3 mm). Extended hypoxia exposure akin to conditions in airplane cabins can reduce quality of chest compressions during CPR. Supplemental oxygen for healthcare providers is an effective countermeasure.

Due to the recommendation of the European Commission, the railway companies have been replacing the conventional brake system of freight wagons. Since the retrofitting may lead to a change in noise characteristics, we aimed at examining its effectiveness to increase the pleasantness of the sounds. Realistic railway pass-by sounds were synthesized. We conducted a laboratory study with 44 participants who were asked which of pairwise presented sounds they perceived as more pleasant. Preference rankings were derived based on a metric scale. Participants preferred retrofitted freight trains to those with a conventional brake system. The more wagons of a train were retrofitted, the more pleasant the sound was rated. Pleasantness decreased with increasing sound pressure level. Since long-term exposure to unpleasant railway sounds may increase the number of highly annoyed residents, our findings provide important information to policy makers supporting the ban of freight train wagons with conventional brake systems.