***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: Rationale Sleep deprivation has a negative effect on cognitive and psychomotor performance and mood state , partially due to decreases in creatine levels in the brain . Therefore , creatine supplementation should lessen the negative effects of sleep deprivation . Objectives The objective of this study was to examine the effect of creatine supplementation and sleep deprivation , with mild exercise , on cognitive and psychomotor performance , mood state , and plasma concentrations of catecholamines and cortisol . MethodS ubjects were divided into a  creatine group ( n=10 ) and a placebo group ( n=9 ) . They took 5 g of creatine monohydrate or a placebo , dependent on their group , four times a time a day for 7 days , immediately prior to the experiment . The study was double blind . Subjects undertook tests of r and om movement generation ( RMG ) , verbal and spatial recall , choice reaction time , static balance and mood state pre-test ( 0 h ) , after 6 , 12 and 24 h of sleep deprivation , with intermittent exercise . They were tested for plasma concentrations of catecholamines and cortisol at 0 and 24 h. Results At 24 h , the creatine group demonstrated significantly less change in performance from 0 h ( Δ ) in RMG , choice reaction time , balance and mood state . There were no significant differences between groups in plasma concentrations of catecholamines and cortisol . Norepinephrine and dopamine concentrations were significantly higher at 24 h than 0 h , but cortisol were lower . Conclusions Following 24-h sleep deprivation , creatine supplementation had a positive effect on mood state and tasks that place a heavy stress on the prefrontal cortex 1 . Prolonged ( > 10 h ) exposure to hypoxia and high altitude ( > 5000 m ) invariably have detrimental effects on cognitive performance . Paradoxically , mild improvements in cognitive function in patients with chronic obstructive pulmonary disease after cessation of oxygen therapy have been reported . 2 . We studied in each of 10 healthy subjects the effect of an acute altitude challenge [ rapid helicopter transport to the Jungfraujoch ( 3450 m ) , experiment 1 ] and of an acute exposure to mild hypoxia ( fractional inspiratory oxygen concentration 14.5 % experiment 2 ) on a simple test of cognitive performance ( the time needed to read briefly displayed letters ) . 3 . Under both hypoxic conditions the time needed to read briefly presented letters decreased , from 12.1 + /- SD 3.8 ms to 8.3 + /- 1.5 ms ( P < 0.01 ) in experiment 1 , and from 11.9 + /- 1.9 ms to 8.1 + /- 1.1 ms ( P < 0.01 ) in experiment 2 . 4 . A rapid and mild hypoxic challenge seems to improve a simple measure of cognitive performance above normal values . The common notion that exposure to hypoxia and altitude invariably impairs cognitive performance may have to be re-evaluated This individual differences study examined the separability of three often postulated executive functions-mental set shifting ( " Shifting " ) , information updating and monitoring ( " Updating " ) , and inhibition of prepotent responses ("Inhibition")- and their roles in complex " frontal lobe " or " executive " tasks . One hundred thirty-seven college students performed a set of relatively simple experimental tasks that are considered to predominantly tap each target executive function as well as a set of frequently used executive tasks : the Wisconsin Card Sorting Test ( WCST ) , Tower of Hanoi ( TOH ) , r and om number generation ( RNG ) , operation span , and dual tasking .  Confirmatory factor analysis indicated that the three target executive functions are moderately correlated with one another , but are clearly separable . Moreover , structural equation modeling suggested that the three functions contribute differentially to performance on complex executive tasks . Specifically , WCST performance was related most strongly to Shifting , TOH to Inhibition , RNG to Inhibition and Updating , and operation span to Updating . Dual task performance was not related to any of the three target functions . These results suggest that it is important to recognize both the unity and diversity of executive functions and that latent variable analysis is a useful approach to study ing the organization and roles of executive functions The effect of hypoxaemia ( mean SpO2 78 % ) on cognitive function was measured in two groups of twelve normal subjects . A series of psychometric tests was administered to each subject in the same sequence and consisted of the Reitan trail-making test , a digit symbol substitution test , a visuospatial orientation test and the simple unprepared reaction-time test .  Psychomotor performance was assessed in a double-blind manner while the subjects were breathing first air and then either air or a hypoxic mixture . While there was improvement in time for the trail-making test during a repeat study breathing air , there was significant deterioration of time to completion of the test in conditions of hypoxia . A significant learning effect in the orientation test was seen in the control group but this did not occur in hypoxic subjects . Hypoxaemia was shown to cause a significant impairment of simple unprepared reaction time compared with controls . All the changes in cognitive function were small and there were no subjective differences in the air or hypoxic groups . The usefulness of the Reitan trail-making and the simple unprepared reaction-time test in the assessment of psychomotor performance deficit under conditions of hypoxaemia has been demonstrated by this study in normal subjects . It was concluded that a mean oxygen saturation of 78 % caused only minor changes in cognitive function in normal subjects This study investigated the effects of heat exposure , exercise-induced dehydration and fluid ingestion on cognitive performance .  Seven healthy men , unacclimatized to heat , were kept euhydrated or were dehydrated by controlled passive exposure to heat ( H , two sessions ) or by treadmill exercise ( E , two sessions ) up to a weight loss of 2.8 % . On completion of a 1-h recovery period , the subjects drank a solution containing 50 g l(-1 ) glucose and 1.34 g l(-1 ) NaCl in a volume of water corresponding to 100 % of his body weight loss induced by dehydration . ( H1 and E1 ) or levels of fluid deficit were maintained ( H0 , E0 ) . In the E0 , H0 and control conditions , the subject drank a solution containing the same quantity of glucose diluted in 100 ml of water .  Psychological tests were administered 30 min after the dehydration phase and 2 h after fluid ingestion . Both dehydration conditions impaired cognitive abilities ( i.e. perceptive discrimination , short-term memory ) , as well as subjective estimates of fatigue , without any relevant differences between the methods . By 3.5 h after fluid deficit , dehydration ( H0 and E0 ) no longer had any adverse effect , although the subjects felt increasingly tired . Thus , there was no beneficial effect of fluid ingestion ( H1 and E1 ) on the cognitive variables . However , long-term memory retrieval was impaired in both control and dehydration situations , whereas there was no decrement in performance in the fluid ingestion condition ( H1 , E1 ) Hypoxia changes the regional distribution of cerebral blood flow and stimulates the ventilatory chemoreflex , thereby reducing CO2 tension . We examined the effects of both hypoxia and isocapnic hypoxia on acute changes in internal carotid ( ICA ) and vertebral artery ( VA ) blood flow . Ten healthy male subjects underwent the following two r and omly assigned respiratory interventions after a resting baseline period with room air : ( i ) hypoxia ; and ( ii ) isocapnic hypoxia with a controlled gas mixture ( 12 % O2 ; inspiratory mmHg ) . In the isocapnic hypoxia intervention , subjects were instructed to maintain the rate and depth of breathing to maintain the level of end-tidal partial pressure of CO2 ( ) during the resting baseline period . The ICA and VA blood flow ( velocity × cross-sectional area ) were measured using Doppler ultrasonography . The was decreased ( -6.3 ± 0.9 % , P < 0.001 ) during hypoxia by hyperventilation ( minute ventilation + 12.9 ± 2.2 % , P < 0.001 ) , while was unchanged during isocapnic hypoxia . The ICA blood flow was unchanged ( P = 0.429 ) , while VA blood flow increased ( + 10.3 ± 3.1 % , P = 0.010 ) during hypoxia . In contrast , isocapnic hypoxia increased both ICA ( + 14.5 ± 1.4 % , P < 0.001 ) and VA blood flows ( + 10.9 ± 2.4 % , P < 0.001 ) . Thus , hypoxic vasodilatation outweighed hypocapnic vasoconstriction in the VA , but not in the ICA . These findings suggest that acute hypoxia elicits an increase in posterior cerebral blood flow , possibly to maintain essential homeostatic functions of the brainstem In normoxic conditions , a reduction in arterial carbon dioxide tension causes cerebral vasoconstriction , thereby reducing cerebral blood flow and modifying dynamic cerebral autoregulation ( dCA ) . It is unclear to what extent these effects are altered by acute hypoxia and the associated hypoxic ventilatory response ( respiratory chemoreflex ) . This study tested the hypothesis that acute hypoxia attenuates arterial CO2 tension-mediated regulation of cerebral blood flow to help maintain cerebral O2 homeostasis .  Eight subjects performed three r and omly assigned respiratory interventions following a resting baseline period , as follows : ( 1 )  normoxia ( 21 % O2 ) ; ( 2 )  hypoxia  ( 12 %  O2 ) ; and ( 3 )  hypoxia with wilful restraint of the respiratory chemoreflex . During each intervention , 0 , 2.0 , 3.5 or 5.0 % CO2 was sequentially added ( 8 min stages ) to inspired gas mixtures to assess changes in steady-state cerebrovascular CO2 reactivity and dCA . During normoxia , the addition of CO2 increased internal carotid artery blood flow and middle cerebral artery mean blood velocity ( MCA Vmean ) , while reducing dCA ( change in phase = -0.73 ± 0.22 rad , P = 0.005 ) . During acute hypoxia , internal carotid artery blood flow and MCA Vmean remained unchanged , but cerebrovascular CO2 reactivity ( internal carotid artery , P = 0.003 ; MCA Vmean , P = 0.031 ) and CO2-mediated effects on dCA ( P = 0.008 ) were attenuated . The effects of hypoxia were not further altered when the respiratory chemoreflex was restrained . These findings support the hypothesis that arterial CO2 tension-mediated effects on the cerebral vasculature are reduced during acute hypoxia . These effects could limit the degree of hypocapnic vasoconstriction and may help to regulate cerebral blood flow and cerebral O2 homeostasis during acute periods of hypoxia Whole body O2 uptake ( VO2 ) during maximal and submaximal exercise has been shown to be preserved in the setting of beta-adrenergic blockade at high altitude , despite marked reductions in heart rate during exercise . An increase in stroke volume at high altitude has been suggested as the mechanism that preserves systemic O2 delivery ( blood flow x arterial O2 content ) and thereby maintains VO2 at sea-level values . To test this hypothesis , we studied the effects of nonselective beta-adrenergic blockade on submaximal exercise performance in 11 normal men ( 26 + /- 1 yr ) at sea level and on arrival and after 21 days at 4,300 m. Six subjects received propranolol ( 240 mg/day ) , and five subjects received placebo . At sea level , during submaximal exercise , cardiac output and O2 delivery were significantly lower in propranolol- than in placebo-treated subjects . Increases in stroke volume and O2 extraction were responsible for the maintenance of VO2 . At 4,300 m , beta-adrenergic blockade had no significant effect on VO2 , ventilation , alveolar PO2 , and arterial blood gases during submaximal exercise . Despite increases in stroke volume , cardiac output and thereby O2 delivery were still reduced in propranolol-treated subjects compared with subjects treated with placebo . Further reductions in already low levels of mixed venous O2 saturation were responsible for the maintenance of VO2 on arrival and after 21 days at 4,300 m in propranolol-treated subjects . Despite similar workloads and VO2 , propranolol-treated subjects exercised at greater perceived intensity than subjects given placebo at 4,300 m. The values for mixed venous O2 saturation during submaximal exercise in propranolol-treated subjects at 4,300 m approached those reported at simulated altitudes > 8,000 m. Thus beta-adrenergic blockade at 4,300 m results in significant reduction in O2 delivery during submaximal exercise due to incomplete compensation by stroke volume for the reduction in exercise heart rate . Total body VO2 is maintained at a constant level by an interaction between mixed venous O2 saturation , the arterial O2-carrying capacity , and hemodynamics during exercise with acute and chronic hypoxia PURPOSE Slight differences in physiological responses and nitric oxide ( NO ) have been reported at rest between hypobaric hypoxia  ( HH ) and normobaric hypoxia  ( NH ) during short exposure . Our study reports NO and oxidative stress at rest and physiological responses during moderate exercise in 
    Output:
    
HighlightsHypoxia has a negative effect on cognition .
Effect on central executive and non‐executive tasks did not differ significantly .
Low ( < 60 mmHg ) arterial partial pressure of oxygen predicts poor cognition .
Hypobaric versus normobaric hypoxic conditions was not a significant moderator .
There were no significant differences between central executive and non‐executive , perception/attention and short‐term memory , tasks .