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Effects on Cognitive Functioning of Acute, Subacute and Repeated Exposures to High Altitude.

ABSTRACT: Objective: Neurocognitive functions are affected by high altitude, however the altitude effects of acclimatization and repeated exposures are unclear. We investigated the effects of acute, subacute and repeated exposure to 5,050 m on cognition among altitude-naïve participants compared to control subjects tested at low altitude. Methods: Twenty-one altitude-naïve individuals (25.3 ± 3.8 years, 13 females) were exposed to 5,050 m for 1 week (Cycle 1) and re-exposed after a week of rest at sea-level (Cycle 2). Baseline (BL, 520 m), acute (Day 1, HA1) and acclimatization (Day 6, HA6, 5,050 m) measurements were taken in both cycles. Seventeen control subjects (24.9 ± 2.6 years, 12 females) were tested over a similar period in Calgary, Canada (1,103 m). The Reaction Time (RTI), Attention Switching Task (AST), Rapid Visual Processing (RVP) and One Touch Stockings of Cambridge (OTS) tasks were administered and outcomes were expressed in milliseconds/frequencies. Lake Louise Score (LLS) and blood oxygen saturation (SpO2) were recorded. Results: In both cycles, no significant changes were found with acute exposure on the AST total score, mean latency and SD. Significant changes were found upon acclimatization solely in the altitude group, with improved AST Mean Latency [HA1 (588 ± 92) vs. HA6 (526 ± 91), p < 0.001] and Latency SD [HA1 (189 ± 86) vs. HA6 (135 ± 65), p < 0.001] compared to acute exposure, in Cycle 1. No significant differences were present in the control group. When entering Acute SpO2 (HA1-BL), Acclimatization SpO2 (HA6-BL) and LLS score as covariates for both cycles, the effects of acclimatization on AST outcomes disappeared indicating that the changes were partially explained by SpO2 and LLS. The changes in AST Mean Latency [?BL (-61.2 ± 70.2) vs. ?HA6 (-28.0 ± 58), p = 0.005] and the changes in Latency SD [?BL (-28.4 ± 41.2) vs. ?HA6 (-0.2235 ± 34.8), p = 0.007] across the two cycles were smaller with acclimatization. However, the percent changes did not differ between cycles. These results indicate independent effects of altitude across repeated exposures. Conclusions: Selective and sustained attention are impaired at altitude and improves with acclimatization.The observed changes are associated, in part, with AMS score and SpO2. The gains in cognition with acclimatization during a first exposure are not carried over to repeated exposures.

SUBMITTER: Pun M

PROVIDER: S-EPMC6111975 | biostudies-literature | 2018

REPOSITORIES: biostudies-literature

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Effects on Cognitive Functioning of Acute, Subacute and Repeated Exposures to High Altitude.

Pun Matiram M Guadagni Veronica V Bettauer Kaitlyn M KM Drogos Lauren L LL Aitken Julie J Hartmann Sara E SE Furian Michael M Muralt Lara L Lichtblau Mona M Bader Patrick R PR Rawling Jean M JM Protzner Andrea B AB Ulrich Silvia S Bloch Konrad E KE Giesbrecht Barry B Poulin Marc J MJ

Frontiers in physiology 20180821

Objective: Neurocognitive functions are affected by high altitude, however the altitude effects of acclimatization and repeated exposures are unclear. We investigated the effects of acute, subacute and repeated exposure to 5,050 m on cognition among altitude-naïve participants compared to control subjects tested at low altitude. Methods: Twenty-one altitude-naïve individuals (25.3 ± 3.8 years, 13 females) were exposed to 5,050 m for 1 week (Cycle 1) and re-exposed after a we ...[more]

PMID: 30246787

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Project description:Aim: High altitude (HA) hypoxia may affect cognitive performance and sleep quality. Further, vigilance is reduced following sleep deprivation. We investigated the effect on vigilance, actigraphic sleep indices, and their relationships with acute mountain sickness (AMS) during very HA exposure, acclimatization, and re-exposure. Methods: A total of 21 healthy altitude-naive individuals (25 ± 4 years; 13 females) completed 2 cycles of altitude exposure separated by 7 days at low altitude (LA, 520 m). Participants slept at 2900 m and spent the day at HA, (5050 m). We report acute altitude exposure on Day 1 (LA vs. HA1) and after 6 days of acclimatization (HA1 vs. HA6). Vigilance was quantified by reaction speed in the 10-min psychomotor vigilance test reaction speed (PVT-RS). AMS was evaluated using the Environmental Symptoms Questionnaire Cerebral Score (AMS-C score). Nocturnal rest/activity was recorded to estimate sleep duration using actigraphy. Results: In Cycle 1, PVT-RS was slower at HA1 compared to LA (4.1 ± 0.8 vs. 4.5 ± 0.6 s-1, respectively, p = 0.029), but not at HA6 (4.6 ± 0.7; p > 0.05). In Cycle 2, PVT-RS at HA1 (4.6 ± 0.7) and HA6 (4.8 ± 0.6) were not different from LA (4.8 ± 0.6, p > 0.05) and significantly greater than corresponding values in Cycle 1. In both cycles, AMS scores were higher at HA1 than at LA and HA6 (p < 0.05). Estimated sleep durations (TST) at LA, 1st and 5th nights were 431.3 ± 28.7, 418.1 ± 48.6, and 379.7 ± 51.4 min, respectively, in Cycle 1 and they were significantly reduced during acclimatization exposures (LA vs. 1st night, p > 0.05; LA vs. 5th night, p = 0.012; and 1st vs. 5th night, p = 0.054). LA, 1st and 5th nights TST in Cycle 2 were 477.5 ± 96.9, 430.9 ± 34, and 341.4 ± 32.2, respectively, and we observed similar deteriorations in TST as in Cycle 1 (LA vs. 1st night, p > 0.05; LA vs. 5th night, p = 0.001; and 1st vs. 5th night, p < 0.0001). At HA1, subjects who reported higher AMS-C scores exhibited slower PVT-RS (r = -0.56; p < 0.01). Subjects with higher AMS-C scores took longer time to react to the stimuli during acute exposure (r = 0.62, p < 0.01) during HA1 of Cycle 1. Conclusion: Acute exposure to HA reduces the PVT-RS. Altitude acclimatization over 6 days recovers the reaction speed and prevents impairments during subsequent altitude re-exposure after 1 week spent near sea level. However, acclimatization does not lead to improvement in total sleep time during acute and subacute exposures.

Project description:BackgroundFew studies have compared methods to correct for retest effects or practice effects in settings where an acute event could influence test performance, such as major surgery. Our goal in this study was to evaluate the use of different methods to correct for the effects of practice or retest on repeated test administration in the context of an observational study of older adults undergoing elective surgery.MethodsIn a cohort of older surgical patients (N = 560) and a non-surgical comparison group (N = 118), we compared changes on repeated cognitive testing using a summary measure of general cognitive performance (GCP) between patients who developed post-operative delirium and those who did not. Surgical patients were evaluated pre-operatively and at 1, 2, 6, 12, and 18 months following surgery. Inferences from linear mixed effects models using four approaches were compared: 1) no retest correction, 2) mean-difference correction, 3) predicted-difference correction, and 4) model-based correction.ResultsUsing Approaches 1 or 4, which use uncorrected data, both surgical groups appeared to improve or remain stable after surgery. In contrast, Approaches 2 and 3, which dissociate retest and surgery effects by using retest-adjusted GCP scores, revealed an acute decline in performance in both surgical groups followed by a recovery to baseline. Relative differences between delirium groups were generally consistent across all approaches: the delirium group showed greater short- and longer-term decline compared to the group without delirium, although differences were attenuated after 2 months. Standard errors and model fit were also highly consistent across approaches.ConclusionAll four approaches would lead to nearly identical inferences regarding relative mean differences between groups experiencing a key post-operative outcome (delirium) but produced qualitatively different impressions of absolute performance differences following surgery. Each of the four retest correction approaches analyzed in this study has strengths and weakness that should be evaluated in the context of future studies. Retest correction is critical for interpretation of absolute cognitive performance measured over time and, consequently, for advancing our understanding of the effects of exposures such as surgery, hospitalization, acute illness, and delirium.

Project description:Inadequate oxygen availability at high altitude leads to oxidative stress, resulting in hippocampal neurodegeneration and memory impairment. In our previous study, we found that the cognitive dysfunction occurred when male SD rat was rapidly exposed to 4200 m of high altitude for 3 days. And we also found that crocin showed a cognitive protective effect under hypoxia by regulating SIRT1/PGC-1α pathways in rat's hippocampus. In this article, focused on factors related to SIRT1/PGC-1α pathways, we proposed to further elucidate crocin's pharmacological mechanism. Adult male Sprague-Dawley rats were randomly divided into five groups: control group, hypoxia group (rats were rapidly transported to high altitude of 4200 m for 72 h), and crocins+hypoxia groups (pretreatment with crocin of 25, 50, and 100 mg/kg/d for 3 days). The learning and memory ability was tested by Morris water maze analysis. Hippocampal histopathological changes were observed by HE staining and Nissl staining. The expression of NRF1, TFAM, Bcl-2, Bax, and caspase-3 was detected by immunohistochemistry, RT-PCR, and western blotting test. The contents of malondialdehyde (MDA), superoxide dismutase (SOD), glutathione (GSH), and glutathione peroxidase (GSHPx) were detected by the TBA, WST, and colorimetry method. Neuronal apoptosis was observed by TUNEL staining. After crocin pretreatment, the traveled distance was significantly reduced and the percentage of time in the target quadrant was significantly increased tested by Morris water maze. And neuronal damage in the hippocampus was also significantly ameliorated based on HE staining and Nissl staining. Furthermore, in hippocampus tissue, mitochondrial biosynthesis-related factors of NRF1, TFAM expression was increased; oxidative stress factors of SOD, GSH, and GSHPx expression level were increased, and MDA and glutathione disulfide (GSSG) level were decreased; antiapoptotic protein Bcl-2 expression was increased, and proapoptotic proteins Bax and caspase-3 expression were decreased, with a manner of crocin dose dependent. Therefore, the cognitive protective mechanism of crocin in rat under acute hypoxia was related to promoting mitochondrial biosynthesis, ameliorating oxidative stress injury, and decreasing neuronal apoptosis.

Project description:BACKGROUND:Mobile assessment of the effects of acute marijuana on cognitive functioning in the natural environment would provide an ecologically valid measure of the impacts of marijuana use on daily functioning. OBJECTIVE:This study aimed to examine the association of reported acute subjective marijuana high (rated 0-10) with performance on 3 mobile cognitive tasks measuring visuospatial working memory (Flowers task), attentional bias to marijuana-related cues (marijuana Stroop), and information processing and psychomotor speed (digit symbol substitution task [DSST]). The effect of distraction as a moderator of the association between the rating of subjective marijuana high and task performance (ie, reaction time and number of correct responses) was explored. METHODS:Young adults (aged 18-25 years; 37/60, 62% female) who reported marijuana use at least twice per week were recruited through advertisements and a participant registry in Pittsburgh, Pennsylvania. Phone surveys and mobile cognitive tasks were delivered 3 times per day and were self-initiated when starting marijuana use. Completion of phone surveys triggered the delivery of cognitive tasks. Participants completed up to 30 days of daily data collection. Multilevel models examined associations between ratings of subjective marijuana high (rated 0-10) and performance on each cognitive task (reaction time and number of correct responses) and tested the number of distractions (rated 0-4) during the mobile task session as a moderator of the association between ratings of subjective marijuana high and task performance. RESULTS:Participants provided 2703 data points, representing 451 reports (451/2703, 16.7%) of marijuana use. Consistent with slight impairing effects of acute marijuana use, an increase in the average rating of subjective marijuana high was associated with slower average reaction time on all 3 tasks-Flowers (B=2.29; SE 0.86; P=.008), marijuana Stroop (B=2.74; SE 1.09; P=.01), and DSST (B=3.08; SE 1.41; P=.03)-and with fewer correct responses for Flowers (B=-0.03; SE 0.01; P=.01) and DSST (B=-0.18; SE 0.07; P=.01), but not marijuana Stroop (P=.45). Results for distraction as a moderator were statistically significant only for certain cognitive tasks and outcomes. Specifically, as hypothesized, a person's average number of reported distractions moderated the association of the average rating of subjective marijuana high (over and above a session's rating) with the reaction time for marijuana Stroop (B=-52.93; SE 19.38; P=.006) and DSST (B=-109.72; SE 42.50; P=.01) and the number of correct responses for marijuana Stroop (B=-0.22; SE 0.10; P=.02) and DSST (B=4.62; SE 1.81; P=.01). CONCLUSIONS:Young adults' performance on mobile cognitive tasks in the natural environment was associated with ratings of acute subjective marijuana high, consistent with slight decreases in cognitive functioning. Monitoring cognitive functioning in real time in the natural environment holds promise for providing immediate feedback to guide personal decision making.

Project description:The molecular signalling pathways that regulate inflammation and the response to hypoxia share significant crosstalk and appear to play major roles in high-altitude acclimatization and adaptation. Several studies demonstrate increases in circulating candidate inflammatory markers during acute high-altitude exposure, but significant gaps remain in our understanding of how inflammation and immune function change at high altitude and whether these responses contribute to high-altitude pathologies, such as acute mountain sickness. To address this, we took an unbiased transcriptomic approach, including RNA sequencing and direct digital mRNA detection with NanoString, to identify changes in the inflammatory profile of peripheral blood throughout 3 days of high-altitude acclimatization in healthy sea-level residents (n = 15; five women). Several inflammation-related genes were upregulated on the first day of high-altitude exposure, including a large increase in HMGB1 (high mobility group box 1), a damage-associated molecular pattern (DAMP) molecule that amplifies immune responses during tissue injury. Differentially expressed genes on the first and third days of acclimatization were enriched for several inflammatory pathways, including nuclear factor-κB and Toll-like receptor (TLR) signalling. Indeed, both TLR4 and LY96, which encodes the lipopolysaccharide binding protein (MD-2), were upregulated at high altitude. Finally, FASLG and SMAD7 were associated with acute mountain sickness scores and peripheral oxygen saturation levels on the first day at high altitude, suggesting a potential role of immune regulation in response to high-altitude hypoxia. These results indicate that acute high-altitude exposure upregulates inflammatory signalling pathways and might sensitize the TLR4 signalling pathway to subsequent inflammatory stimuli. KEY POINTS: Inflammation plays a crucial role in the physiological response to hypoxia. High-altitude hypoxia exposure causes alterations in the inflammatory profile that might play an adaptive or maladaptive role in acclimatization. In this study, we characterized changes in the inflammatory profile following acute high-altitude exposure. We report upregulation of novel inflammation-related genes in the first 3 days of high-altitude exposure, which might play a role in immune system sensitization. These results provide insight into how hypoxia-induced inflammation might contribute to high-altitude pathologies and exacerbate inflammatory responses in critical illnesses associated with hypoxaemia.

Project description:Horse training exposes horses to an array of cognitive and ethological challenges. Horses are routinely required to perform behaviours that are not aligned to aspects of their ethology, which may delay learning. While horses readily form habits during training, not all of these responses are considered desirable, resulting in the horse being subject to retraining. This is a form of cognitive flexibility and is critical to the extinction of habits and the learning of new responses. It is underpinned by complex neural processes which can be impaired by chronic or repeated stress. Domestic horses may be repeatedly exposed to multiples stressors. The potential contribution of stress impairments of cognitive flexibility to apparent training failures is not well understood, however research from neuroscience can be used to understand horses' responses to training. We trained horses to acquire habit-like responses in one of two industry-style aversive instrumental learning scenarios (moving away from the stimulus-instinctual or moving towards the stimulus-non-instinctual) and evaluated the effect of repeated stress exposures on their cognitive flexibility in a reversal task. We measured heart rate as a proxy for noradrenaline release, salivary cortisol and serum Brain Derived Neurotrophic Factor (BDNF) to infer possible neural correlates of the learning outcomes. The instinctual task which aligned with innate equine escape responses to aversive stimuli was acquired significantly faster than the non-instinctual task during both learning phases, however contrary to expectations, the repeated stress exposure did not impair the reversal learning. We report a preliminary finding that serum BDNF and salivary cortisol concentrations in horses are positively correlated. The ethological salience of training tasks and cognitive flexibility learning can significantly affect learning in horses and trainers should adapt their practices where such tasks challenge innate equine behaviour.

Project description:In recent years, several jurisdictions have revised their regulation policy toward both medical and recreational use of cannabis. These changes have elicited concerns regarding how legalization impacts academic achievement and work performance. This review evaluates the acute and long-term (residual) association between cannabis use and cognitive functioning that underlies poor academic and work performance. Relative to other reviews, this article focuses on cross-over randomized controlled trials and prospective designs given that they allow to test the impairing effects of cannabis exposure at the within-subject level. Acute cannabis cognitive effects are discussed separately for known confounding factors such as levels of delta-9-tetrahydrocannabinol (Δ9-THC), Δ9-THC:cannabidiol ratio, previous cannabis use and, comorbidity with psychosis-spectrum disorders. The cognitive residual effects of cannabis are detailed in relation to duration of abstinence, frequency of use, comorbidity with psychosis-spectrum disorders, types of cognitive domains assessed, and age of cannabis use initiation. Moreover, considering the fact that adequate longitudinal studies can make inferences about causality between cannabis use and impaired cognitive functioning when disentangling between-subject from within-subject variation, proofs for the three main non-mutually exclusive hypotheses about this relationship will be presented: i) the cognitive vulnerability hypothesis as part of the more general common antecedent hypothesis, ii) the concurrent cannabis impairing hypothesis, and iii) the neurotoxic hypothesis of cannabis. Current research provides evidence for mild to moderate acute cannabis effects on episodic and working memory, processing speed, and executive functions. Mild residual impairing effects were also observed in these exact same cognitive domains, suggesting that adverse effects following cannabis intoxication persist at least days or weeks following cannabis abstinence. Relative to adult-onset, adolescent-onset cannabis use seems to explain the dose-response relationship and is associated with longer lasting residual effects even in mild users (<weekly). The association between cannabis and cognition is likely explained by common antecedents, such that genetic and shared environment factors predispose individuals to both cannabis use and cognitive deficits, and to a lesser degree, neurotoxic effects.

Dataset Information

Effects on Cognitive Functioning of Acute, Subacute and Repeated Exposures to High Altitude.

Publications

Effects on Cognitive Functioning of Acute, Subacute and Repeated Exposures to High Altitude.

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