A network physiology approach to oxygen saturation variability during normobaric hypoxia.

NEW FINDINGS: What is the central question of this study? What is the physiological interpretation of SpO2 fluctuations observed during normobaric hypoxia in healthy individuals? What is the main finding and its importance? There is a significant flow of information between SpO2 and other cardio-respiratory time series during graded hypoxia. Analysis of the pattern of SpO2 variations has potential for non-invasive assessment of the engagement of respiratory control system in health and disease. ABSTRACT: Peripheral capillary oxygen saturation ( SpO2 ) exhibits a complex pattern of fluctuations during hypoxia. The physiological interpretation of SpO2 variability is not well understood. In this study, we tested the hypothesis that SpO2 fluctuation carries information about integrated cardio-respiratory control in healthy individuals using a network physiology approach. We explored the use of transfer entropy in order to compute the flow of information between cardio-respiratory signals during hypoxia. Twelve healthy males (mean (SD) age 22 (4) years) were exposed to four simulated environments (fraction of inspired oxygen ( FIO2 ): 0.12, 0.145, 0.17, and 0.2093) for 45 min, in a single blind randomized controlled design. The flow of information between different physiological parameters ( SpO2 , respiratory frequency, tidal volume, minute ventilation, heart rate, end-tidal pressure of O2 and CO2 ) were analysed using transfer entropy. Normobaric hypoxia was associated with a significant increase in entropy of the SpO2 time series. The transfer entropy analysis showed that, particularly at FIO2 0.145 and 0.12, the flow of information between SpO2 and other physiological variables exhibits a bidirectional relationship. While reciprocal interactions were observed between different cardio-respiratory parameters during hypoxia, SpO2 remained the main hub of this network. SpO2 fluctuations during graded hypoxia exposure carry information about cardio-respiratory control. Therefore, SpO2 entropy analysis has the potential for non-invasive assessment of the functional connectivity of respiratory control system in various healthcare settings.

Head pre-cooling improves 5-km time-trial performance in male amateur runners in the heat.

This study aimed to evaluate the effect of head pre-cooling on the 5-km time-trial performance of amateur runners in the heat. In a counterbalanced design, 15 male amateur runners (22.6 ± 3.5 y; VO2 max in heat 42.3 ± 4.4 mLO2 /kg/min) completed two 5-km time trials performed in the heat (35°C, 50% relative humidity). In one trial (HCOOL), participants underwent 20 min of head cooling in a temperate environment (23°C, 70% relative humidity) prior to exercise. In another trial (CON), exercise was preceded by 20 min of rest under the same temperature conditions. Exercise time was shorter in HCOOL (25 min and 36 s ± 3 min) compared to CON (27 ± 3 min; p = 0.02). Rectal temperature was reduced during the pre-exercise intervention in HCOOL (p < 0.001), but not in CON (p = 0.55). Relative changes in rectal temperature and mean head temperature were lower throughout HCOOL when compared with CON condition (p = 0.005 and p = 0.022, respectively). Mean skin temperature, heart rate, and rating of perceived exertion did not differ between HCOOL and CON conditions throughout exercise (p = 0.20, p = 0.52 and 0.31, respectively). Thermal comfort was lower in HCOOL condition in pre-exercise (p = 0.014) with no differences observed throughout exercise (p = 0.61). 5-km running performance in a hot environment was improved after a 20-min head cooling intervention, suggesting that this method may be practical as pre-cooling strategy and easily administered to both professional and amateur runners alike.

Cognitive performance is associated with cerebral oxygenation and peripheral oxygen saturation, but not plasma catecholamines, during graded normobaric hypoxia.

NEW FINDINGS: What is the central question of this study? What are the mechanisms responsible for the decline in cognitive performance following exposure to acute normobaric hypoxia? What are the main findings and their importance? We found that (1) performance of a complex central executive task (n-back) was reduced at FIO2 0.12; (2) there was a strong correlation between performance of the n-back task and reductions in SpO2 and cerebral oxygenation; and (3) plasma adrenaline, noradrenaline, cortisol and copeptin were not correlated with cognitive performance. ABSTRACT: It is well established that hypoxia impairs cognitive function; however, the physiological mechanisms responsible for these effects have received relatively little attention. This study examined the effects of graded reductions in fraction of inspired oxygen ( FIO2 ) on oxygen saturation ( SpO2 ), cerebral oxygenation, cardiorespiratory variables, activity of the sympathoadrenal system (adrenaline, noradrenaline) and hypothalamic-pituitary-adrenal axis (cortisol, copeptin), and cognitive performance. Twelve healthy males [mean (SD), age: 22 (4) years, height: 178 (5) cm, mass: 75 (9) kg, FEV1 /FVC ratio: 85 (5)%] completed a four-task battery of cognitive tests to examine inhibition, selective attention (Eriksen flanker), executive function (n-back) and simple and choice reaction time (Deary-Liewald). Tests were completed before and following 60 min of exposure to FIO2 0.2093, 0.17, 0.145 and 0.12. Following 60 min of exposure, response accuracy in the n-back task was significantly reduced in FIO2 0.12 compared to baseline [82 (9) vs. 93 (5)%; P < 0.001] and compared to all other conditions at the same time point [ FIO2 0.2093: 92 (3)%; FIO2 0.17: 91 (6)%; FIO2 0.145: 85 (10)%; FIO2 12: 82 (9)%; all P < 0.05]. The performance of the other tasks was maintained. Δaccuracy and Δreaction time of the n-back task was correlated with both Δ SpO2 [r(9) = 0.66, P < 0.001 and r(9) = -0.36, P = 0.037, respectively] and Δcerebral oxygenation [r(7) = 0.55, P < 0.001 and r(7) = -0.38, P = 0.045, respectively]. Plasma adrenaline, noradrenaline, cortisol and copeptin were not significantly elevated in any condition or correlated with any of the tests of cognitive performance. These findings suggest that reductions in peripheral oxygen saturation and cerebral oxygenation, and not increased activity of the sympathoadrenal system and hypothalamic-pituitary-adrenal axis, as previously speculated, are responsible for a decrease in cognitive performance during normobaric hypoxia.

Creatine supplementation research fails to support the theoretical basis for an effect on cognition: Evidence from a systematic review.

Creatine supplementation has been put forward as a possible aid to cognition, particularly for vegans, vegetarians, the elderly, sleep deprived and hypoxic individuals. However, previous narrative reviews have only provided limited support for these claims. This is despite the fact that research has shown that creatine supplementation can induce increased brain concentrations of creatine, albeit to a limited extent. We carried out a systematic review to examine the current state of affairs. The review supported claims that creatine supplementation can increases brain creatine content but also demonstrated somewhat equivocal results for effects on cognition. It does, however, provide evidence to suggest that more research is required with stressed populations, as supplementation does appear to significantly affect brain content. Issues with research design, especially supplementation regimens, need to be addressed. Future research must include measurements of creatine brain content.

The effects of sleep deprivation, acute hypoxia, and exercise on cognitive performance: A multi-experiment combined stressors study.

INTRODUCTION: Both sleep deprivation and hypoxia have been shown to impair executive function. Conversely, moderate intensity exercise is known to improve executive function. In a multi-experiment study, we tested the hypotheses that moderate intensity exercise would ameliorate any decline in executive function after i) three consecutive nights of partial sleep deprivation (PSD) (Experiment 1) and ii) the isolated and combined effects of a single night of total sleep deprivation (TSD) and acute hypoxia (Experiment 2). METHODS: Using a rigorous randomised controlled crossover design, 12 healthy participants volunteered in each experiment (24 total, 5 females). In both experiments seven executive function tasks (2-choice reaction time, logical relations, manikin, mathematical processing, 1-back, 2-back, 3-back) were completed at rest and during 20 min semi-recumbent, moderate intensity cycling. Tasks were completed in the following conditions: before and after three consecutive nights of PSD and habitual sleep (Experiment 1) and in normoxia and acute hypoxia (FIO2 = 0.12) following one night of habitual sleep and one night of TSD (Experiment 2). RESULTS: Although the effects of three nights of PSD on executive functions were inconsistent, one night of TSD (regardless of hypoxic status) reduced executive functions. Significantly, regardless of sleep or hypoxic status, executive functions are improved during an acute bout of moderate intensity exercise. CONCLUSION: These novel data indicate that moderate intensity exercise improves executive function performance after both PSD and TSD, regardless of hypoxic status. The key determinants and/or mechanism(s) responsible for this improvement still need to be elucidated. Future work should seek to identify these mechanisms and translate these significant findings into occupational and skilled performance settings.

The effects of normobaric and hypobaric hypoxia on cognitive performance and physiological responses: A crossover study.

This partially randomised controlled, crossover study sought to investigate the effects of normobaric hypoxia (NH) and hypobaric hypoxia (HH) on cognitive performance, the physiological response at rest and after a 3-min step-test. Twenty healthy participants (10 females and 10 males, 27.6±6.2yrs, 73.6±13.7kg, 175.3±8.9cm) completed a cognitive performance test, followed by the modified Harvard-step protocol, in four environments: normobaric normoxia (NN; PiO2: 146.0±1.5mmHg), NH (PiO2: 100.9±1.3mmHg), HH at the first day of ascent (HH1: PiO2 = 105.6±0.4mmHg) and HH after an overnight stay (HH2: PiO2 = 106.0±0.5mmHg). At rest and/or exercise, SpO2, NIRS, and cardiovascular and perceptual data were collected. The cerebral tissue oxygenation index and the cognitive performance (throughput, accuracy, and reaction time) were not different between the hypoxic conditions (all p>0.05). In NH, SpO2 was higher compared to HH1 (ΔSpO2 NH vs HH1: 1.7±0.5%, p = 0.003) whilst heart rate (ΔHR NH vs HH2: 5.8±2.6 bpm, p = 0.03) and sympathetic activation (ΔSNSi NH vs HH2: 0.8±0.4, p = 0.03) were lower in NH compared to HH2. Heart rate (ΔHR HH1 vs HH2: 6.9±2.6 bpm, p = 0.01) and sympathetic action (ΔSNSi HH1 vs HH2: 0.9±0.4, p = 0.02) were both lower in HH1 compared to HH2. In conclusion, cognitive performance and cerebral oxygenation didn't differ between the hypoxic conditions. SpO2 was only higher in NH compared to HH1. In HH2, heart rate and sympathetic activation were higher compared to both NH and HH1. These conclusions account for a PiO2 between 100-106 mmHg.

Inkjet Printing Infiltration of the Doped Ceria Interlayer in Commercial Anode-Supported SOFCs.

Single-step inkjet printing infiltration with doped ceria Ce0.9Ye0.1O1.95 (YDC) and cobalt oxide (CoxOy) precursor inks was performed in order to modify the properties of the doped ceria interlayer in commercial (50 × 50 × 0.5 mm3 size) anode-supported SOFCs. The penetration of the inks throughout the La0.8Sr0.2Co0.5Fe0.5O3-δ porous cathode to the Gd0.1Ce0.9O2 (GDC) interlayer was achieved by optimisation of the inks' rheology jetting parameters. The low-temperature calcination (750 °C) resulted in densification of the Gd-doped ceria porous interlayer as well as decoration of the cathode scaffold with nanoparticles (~20-50 nm in size). The I-V testing in pure hydrogen showed a maximum power density gain of ~20% at 700 °C and ~97% at 800 °C for the infiltrated cells. The latter effect was largely assigned to the improvement in the interfacial Ohmic resistance due to the densification of the interlayer. The EIS study of the polarisation losses of the reference and infiltrated cells revealed a reduction in the activation polarisations losses at 700 °C due to the nano-decoration of the La0.8Sr0.2Co0.5Fe0.5O3-δ scaffold surface. Such was not the case at 800 °C, where the drop in Ohmic losses was dominant. This work demonstrated that single-step inkjet printing infiltration, a non-disruptive, low-cost technique, can produce significant and scalable performance enhancements in commercial anode-supported SOFCs.

Effects of Normobaric Hypoxia on Oxygen Saturation Variability.

Background: The study is the first to evaluate the effects of graded normobaric hypoxia on SpO2 variability in healthy individuals. Materials and Methods: Twelve healthy males (mean [standard deviation] age 22 [4] years) were exposed to four simulated environments (fraction of inspired oxygen [FIO2]: 0.12, 0.145, 0.17, and 0.21) for 45 minutes, in a balanced crossover design. Results: Sample entropy, a tool that quantifies the irregularity of pulse oximetry fluctuations, was used as a measure of SpO2 variability. SpO2 entropy increased as the FIO2 decreased, and there was a strong significant negative correlation between mean SpO2 and its entropy during hypoxic exposure (r = -0.841 to -0.896, p < 0.001). In addition, SpO2 sample entropy, but not mean SpO2, was correlated (r = 0.630-0.760, p < 0.05) with dyspnea in FIO2 0.17, 0.145, and 0.12 and importantly, SpO2 sample entropy at FIO2 0.17 was correlated with dyspnea at FIO2 0.145 (r = 0.811, p < 0.01). Conclusions: These findings suggest that SpO2 variability analysis may have the potential to be used in a clinical setting as a noninvasive measure to identify the negative sequelae of hypoxemia.