***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: The effects of submaximal and maximal exercise on cerebral perfusion were assessed using a portable , recumbent cycle ergometer in nine unacclimatized subjects ascending to 5,260 m. At 150 m , mean ( SD ) cerebral oxygenation ( rSO2 % ) increased during submaximal exercise from 68.4 ( SD 2.1 ) to 70.9 ( SD 3.8 ) ( P < 0.0001 ) and at maximal oxygen uptake ( .VO2(max ) ) to 69.8 ( SD 3.1 ) ( P < 0.02 ) . In contrast , at each of the high altitudes studied , rSO2 was reduced during submaximal exercise from 66.2 ( SD 2.5 ) to 62.6 ( SD 2.1 ) at 3,610 m ( P < 0.0001 ) , 63.0 ( SD 2.1 ) to 58.9 ( SD 2.1 ) at 4,750 m ( P < 0.0001 ) , and 62.4 ( SD 3.6 ) to 61.2 ( SD 3.9 ) at 5,260 m ( P < 0.01 ) , and at .VO2(max ) to 61.2 ( SD 3.3 ) at 3,610 m ( P < 0.0001 ) , to 59.4 ( SD 2.6 ) at 4,750 m ( P < 0.0001 ) , and to 58.0 ( SD 3.0 ) at 5,260 m ( P < 0.0001 ) . Cerebrovascular resistance tended to fall during submaximal exercise ( P = not significant ) and rise at .VO2(max ) , following the changes in arterial oxygen saturation and end-tidal CO(2 ) . Cerebral oxygen delivery was maintained during submaximal exercise at 150 m with a nonsignificant fall at .VO2(max ) , but at high altitude peaked at 30 % of .VO2(max ) and then fell progressively at higher levels of exercise . The fall in rSO2 and oxygen delivery during exercise may limit exercise at altitude and is likely to contribute to the problems of acute mountain sickness and high-altitude cerebral edema We sought to describe cerebrovascular responses to incremental exercise and test the hypothesis that changes in cerebral oxygenation influence maximal performance . Eleven men cycled in three conditions : 1 ) sea level ( SL ) ;  2 )  acute hypoxia  [ AH ; hypobaric chamber , inspired Po(2 ) ( Pi(O(2 ) ) ) 86 Torr ] ; and 3 )  chronic hypoxia  [ CH ; 4,300 m , Pi(O(2 ) ) 86 Torr ] . At maximal work rate ( W(max ) ) , fraction of inspired oxygen ( Fi(O(2 ) ) ) was surreptitiously increased to 0.60 , while subjects were encouraged to continue pedaling . Changes in cerebral ( frontal lobe ) ( C(OX ) ) and muscle ( vastus lateralis ) oxygenation ( M(OX ) ) ( near infrared spectroscopy ) , middle cerebral artery blood flow velocity ( MCA V(mean ) ; transcranial Doppler ) , and end-tidal Pco(2 ) ( Pet(CO(2 ) ) ) were analyzed across % W(max ) ( significance at P < 0.05 ) . At SL , Pet(CO(2 ) ) , MCA V(mean ) , and C(OX ) fell as work rate rose from 75 to 100 % W(max ) . During AH , Pet(CO(2 ) ) and MCA V(mean ) declined from 50 to 100 % W(max ) , while C(OX ) fell from rest . With CH , Pet(CO(2 ) ) and C(OX ) dropped throughout exercise , while MCA V(mean ) fell only from 75 to 100 % W(max ) . M(OX ) fell from rest to 75 % W(max ) at SL and AH and throughout exercise in CH . The magnitude of fall in C(OX ) , but not M(OX ) , was different between conditions ( CH > AH > SL ) . Fi(O(2 ) ) 0.60 at W(max ) did not prolong exercise at SL , yet allowed subjects to continue for 96 + /- 61 s in AH and 162 + /- 90 s in CH . During Fi(O(2 ) ) 0.60 , C(OX ) rose and M(OX ) remained constant as work rate increased . Thus cerebral hypoxia appeared to impose a limit to maximal exercise during hypobaric hypoxia ( Pi(O(2 ) ) 86 Torr ) , since its reversal was associated with improved performance The combined effects of hyperventilation and arterial desaturation on cerebral oxygenation ( [ Formula : see text ] ) were determined using near-infrared spectroscopy . Eleven competitive oarsmen were evaluated during a 6-min maximal ergometer row . The study was r and omized in a double-blind fashion with an inspired O2 fraction of 0.21 or 0.30 in a crossover design . During exercise with an inspired O2 fraction of 0.21 , the arterial CO2 pressure ( 35 ± 1 mmHg ; mean ± SE ) and O2 pressure ( 77 ± 2 mmHg ) as well as the hemoglobin saturation ( 91.9 ± 0.7 % ) were reduced ( P < 0.05).[Formula : see text ] was reduced from 80 ± 2 to 63 ± 2 % ( P < 0.05 ) , and the near-infrared spectroscopy-determined concentration changes in deoxy- ( ΔHb ) and oxyhemoglobin ( ΔHbO2 ) of the vastus lateralis muscle increased 22 ± 3 μM and decreased 14 ± 3 μM , respectively ( P < 0.05 ) . Increasing the inspired O2fraction to 0.30 did not affect ventilation ( 174 ± 4 l/min ) , but arterial CO2 pressure ( 37 ± 2 mmHg ) , O2 pressure ( 165 ± 5 mmHg ) , and hemoglobin O2saturation ( 99 ± 0.1 % ) increased ( P < 0.05).[Formula : see text ] remained close to the resting level during exercise ( 79 ± 2 vs. 81 ± 2 % ) , and although the muscle ΔHb ( 18 ± 2 μM ) and ΔHbO2 ( -12 ± 3 μM ) were similar to those established without O2 supplementation , work capacity increased from 389 ± 11 to 413 ± 10 W ( P < 0.05 ) . These results indicate that an elevated inspiratory O2fraction increases exercise performance related to maintained cerebral oxygenation rather than to an effect on the working muscles Background —A classic , unresolved physiological question is whether central cardiorespiratory and /or local skeletal muscle circulatory factors limit maximal aerobic capacity ( & OV0312;o2max ) in humans . Severe heat stress drastically reduces & OV0312;o2max , but the mechanisms have never been studied . Methods and Results —To determine the main contributing factor that limits & OV0312;o2max with and without heat stress , we measured hemodynamics in 8 healthy males performing intense upright cycling exercise until exhaustion starting with either high or normal skin and core temperatures ( + 10 ° C and + 1 ° C ) . Heat stress reduced & OV0312;o2max , 2-legged & OV0312;o2 , and time to fatigue by 0.4±0.1 L/min ( 8 % ) , 0.5±0.2 L/min ( 11 % ) , and 2.2±0.4 minutes ( 28 % ) , respectively ( all P < 0.05 ) , despite heart rate and core temperature reaching similar peak values . However , before exhaustion in both heat stress and normal conditions , cardiac output , leg blood flow , mean arterial pressure , and systemic and leg O2 delivery declined significantly ( all 5 % to 11 % , P < 0.05 ) , yet arterial O2 content and leg vascular conductance remained unchanged . Despite increasing leg O2 extraction , leg & OV0312;o2 declined 5 % to 6 % before exhaustion in both heat stress and normal conditions , accompanied by enhanced muscle lactate accumulation and ATP and creatine phosphate hydrolysis . Conclusions —These results demonstrate that in trained humans , severe heat stress reduces & OV0312;o2max by accelerating the declines in cardiac output and mean arterial pressure that lead to decrements in exercising muscle blood flow , O2 delivery , and O2 uptake . Furthermore , the impaired systemic and skeletal muscle aerobic capacity that precedes fatigue with or without heat stress is largely related to the failure of the heart to maintain cardiac output and O2 delivery to locomotive muscle The present study tested the hypothesis that perceived exertion during prolonged exercise in hot environments is associated with changes in cerebral electrical activity rather than changes in the electromyogram ( EMG ) of the exercising muscles . Therefore ,  electroencephalogram ( EEG )  in three positions ( frontal , central , and occipital cortex ) ,  EMG , rating of perceived exertion ( RPE ) , and core temperature were measured in 14 subjects during  submaximal exercise in normal ( 18 degrees C , control ) and hot ( 40 degrees C , hyperthermia ) environments .  RPE increased from 11 + /- 1 units at 5 min to 20 + /- 0 units at exhaustion ( 50 + /- 3 min ) in the trial with progressive hyperthermia , whereas exercise in the control trial was maintained with a stable core temperature for 1 h without exhausting the subjects . Altered EEG activity was observed in all electrode positions , and stepwise forward-regression analysis identified core temperature and a frequency index of the EEG over the frontal cortex as the best predictors of RPE . In contrast , there were no significant correlations between RPE and any of the measured EMG parameters ( median spectral frequency , root mean square , or amplitude ) , and the EMG parameters were not different in hyperthermia compared with control . Thus hyperthermia does not seem to affect the activation pattern of the muscles . Rather , the linear correlation among core temperature , EEG frequency index , and RPE indicates that alterations in cerebral activity may be associated with the hyperthermia-induced development of fatigue during prolonged exercise in hot environments We have compared the effect of increasing optode separation ( range 0.7 - 5.5 cm ) on the sensitivity of near infrared spectroscopy ( NIRS ) to discrete reductions in scalp and cerebral oxygenation in 10 healthy men ( mean age 32 , range 26 - 39 yr ) using multichannel NIRS . During cerebral oligaemia ( a mean reduction in middle cerebral artery flow velocity of 47 % ) induced by a mean reduction in end-tidal PCO2 of 2.4 kPa , the decrease in oxyhaemoglobin detected by NIRS became significantly greater with increasing optode separation ( P < 0.0001 ) . In response to scalp hyperaemia induced by inflation and release of a pneumatic scalp tourniquet , increases in oxyhaemoglobin became significantly smaller with increasing optode separation ( P < 0.0002 ) . These results are consistent with theoretical models of the behaviour of NIR light in the adult head and support the concept of using multi-detector NIRS to separate intra- and extracranial NIR signal changes . However , the emitter-detector separation used by currently available cerebral oximeters is not large enough to provide optimal spatial resolution The basic parameters for physiological measurements provided by near-infrared spectroscopy are the local absorption and scattering coefficients . For the adult human head , they have been difficult to measure noninvasively because of the layered structure of the head . The results of measurements of absorption and reduced scattering coefficients through the forehead on 30 adult volunteers using a multidistance frequency domain method are reported . The optode separation distance ranged from 10 to 80 mm and measurements were recorded at 758 and 830 nm . The measured absorption and reduced scattering coefficients of the forehead were used to evaluate the hemoglobin content in the scalp and brain as well as cerebral oxygen saturation . We found that cerebral oxygenation was relatively narrowly distributed within the subject group ( the st and ard deviation was about 3 % for scalp and 6 % for brain , respectively ) , whereas hemoglobin concentrations had a relatively broader distribution . We found that as the optode distance increased , the absorption coefficients increased and the scattering coefficients decreased , retrieving the optical values of scalp and brain for shorter and longer optode distances , respectively . We present the transition curves of the absorption and reduced scattering coefficients as functions of the optode distance . In order to verify the values for each layer , a comparison between the experimental data and a prediction based on the two-layer model of the adult head was carried out . The thicknesses of scalp and skull for the two-layer model were obtained by magnetic resonance imaging of a subject 's head . The optical parameters obtained from the two-layer model agreed very well with those measured by the multidistance method During maximal exercise in humans , fatigue is preceded by reductions in systemic and skeletal muscle blood flow , O(2 ) delivery and uptake . Here , we examined whether the uptake of O(2 ) and substrates by the human brain is compromised and whether the fall in stroke volume of the heart underlying the decline in systemic O(2 ) delivery is related to declining venous return . We measured brain and central haemodynamics and oxygenation in healthy males ( n 
    Output:
    
After peaking at hard intensities , cerebral oxygen levels dropped during very hard intensities .
People who were aerobically trained attained higher levels of cortical oxygen , dHb , and tHb than untrained people during very hard intensities .
Among untrained people , a marked drop in oxygen levels and a small increase in dHb at very hard intensities accompanied declines in tHb , implying reduced blood flow .
In conclusion , prefrontal oxygenation measured with NIRS in healthy people showed a quadratic response to incremental exercise , rising between moderate and hard intensities , then falling at very hard intensities .
Training status influenced the responses .
While method ological improvements in measures of brain oxygen are forthcoming , these results extend the evidence relevant to existing models of central limitations to maximal exercise