***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: Inspiring a hyperoxic ( H ) gas permits subjects to exercise at higher power outputs while training , but there is controversy as to whether this improves skeletal muscle oxidative capacity , maximal O(2 ) consumption ( Vo(2 max ) ) , and endurance performance to a greater extent than training in normoxia ( N ) . To determine whether the higher power output during H training leads to a greater increase in these parameters , nine recreationally active subjects were r and omly assigned in a single-blind fashion to train in H ( 60 % O(2 ) ) or N for 6 wk ( 3 sessions/wk of 10 x 4 min at 90 % Vo(2 max ) ) . Training heart rate ( HR ) was maintained during the study by increasing power output . After at least 6 wk of detraining , a second 6-wk training protocol was completed with the other breathing condition . Vo(2 max ) and cycle time to exhaustion at 90 % of pretraining Vo(2 max ) were tested in room air pre- and posttraining . Muscle biopsies were sample d pre- and posttraining for citrate synthase ( CS ) , beta-hydroxyacyl-coenzyme A dehydrogenase ( beta-HAD ) , and mitochondrial aspartate aminotransferase ( m-AsAT ) activity measurements . Training power outputs were 8 % higher ( 17 W ) in H vs. N. However , both conditions produced similar improvements in Vo(2 max ) ( 11 - 12 % ) ; time to exhaustion ( approximately 100 % ) ; and CS ( H , 30 % ; N , 32 % ) , beta-HAD ( H , 23 % ; N , 21 % ) , and m-AsAT ( H , 21 % ; N , 26 % ) activities . We conclude that the additional training stimulus provided by training in H was not sufficient to produce greater increases in the aerobic capacity of skeletal muscle and whole body Vo(2 max ) and exercise performance compared with training in UNLABELLED Both time-to-exhaustion ( TTE ) and time-trial ( TT ) exercise tests are commonly used to assess exercise performance , but no study has directly examined the reliability of comparable tests in the same subjects . PURPOSE To evaluate the reliability of comparable TTE and TT treadmill running tests of high and moderately high exercise intensity in endurance-trained male distance runners , and to vali date Hinckson and Hopkins TT prediction methods using log-log modeling from TTE results . METHODS After familiarization tests , eight endurance-trained male distance runners performed , in a r and omized , counterbalanced order , eight trials consisting of two 5-km TT and two 1500-m TT , and four TTE tests run at a speed equivalent to the average speed attained during both the 5-km and 1500-m TT distances . RESULTS Typical error of the estimate ( TEE ) expressed as a coefficient of variation for the 5-km TT , 5-km TTE , 1500-m TT , and 1500-m TTE were 2.0 , 15.1 , 3.3 , and 13.2 % , respectively . The st and ard error of the estimate for predicted TT running speed using log-log modeling from TTE results was 0.67 % , and the predicted versus criterion reliability of this method revealed TEE values of 1.6 % and 2.5 % for the prediction of 5-km and 1500-m TT , respectively . CONCLUSION The variability of 5-km and 1500-m TT tests was significantly less than for similar TTE treadmill protocol s. Despite the greater variability of the TTE tests , log-log modeling using the TTE test results reliably predicted actual TT 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 The aim of this study was to determine whether the decreased muscle and blood lactate during exercise with hyperoxia ( 60 % inspired O2 ) vs. room air is due to decreased muscle glycogenolysis , leading to decreased pyruvate and lactate production and efflux . We measured pyruvate oxidation via PDH , muscle pyruvate and lactate accumulation , and lactate and pyruvate efflux to estimate total pyruvate and lactate production during exercise . We hypothesized that 60 % O2 would decrease muscle glycogenolysis , result ing in decreased pyruvate and lactate contents , leading to decreased muscle pyruvate and lactate release with no change in PDH activity . Seven active male subjects cycled for 40 min at 70 % VO2 peak on two occasions when breathing 21 or 60 % O2 .  Arterial and femoral venous blood sample s and blood flow measurements were obtained throughout exercise , and muscle biopsies were taken at rest and after 10 , 20 , and 40 min of exercise . Hyperoxia had no effect on leg O2 delivery , O2 uptake , or RQ during exercise . Muscle glycogenolysis was reduced by 16 % with hyperoxia ( 267 + /- 19 vs. 317 + /- 21 mmol/kg dry wt ) , translating into a significant , 15 % reduction in total pyruvate production over the 40-min exercise period . Decreased pyruvate production during hyperoxia had no effect on PDH activity ( pyruvate oxidation ) but significantly decreased lactate accumulation ( 60 % : 22.6 + /- 6.4 vs. 21 % : 31.3 + /- 8.7 mmol/kg dry wt ) , lactate efflux , and total lactate production over 40 min of cycling . Decreased glycogenolysis in hyperoxia was related to an approximately 44 % lower epinephrine concentration and an attenuated accumulation of potent phosphorylase activators ADPf and AMPf during exercise . Greater phosphorylation potential during hyperoxia was related to a significantly diminished rate of PCr utilization . The tighter metabolic match between pyruvate production and oxidation result ed in a decrease in total lactate production and efflux over 40 min of exercise during hyperoxia Abstract Six male rowers rowed maximally for 2500 m in ergometer tests during normoxia  ( fractional concentration of oxygen in inspired air , FIO2 0.209 ) , in hyperoxia  ( FIO2 0.622 ) and in hypoxia  ( FIO2 0.158 ) in a r and omized single-blind fashion . Oxygen consumption ( V˙O2 ) , force production of strokes as well as integrated electromyographs ( iEMG ) and mean power frequency ( MPF ) from seven muscles were measured in 500-m intervals . The iEMG signals from individual muscles were summed to represent overall electrical activity of these muscles ( sum-iEMG ) . Maximal force of a stroke ( Fmax ) decreased from the 100 % pre-exercise maximal value to 67 ( SD 12)% , 63 ( SD 15)% and 76 ( SD 13)% ( P<0.05 to normoxia , ANOVA ) and impulse to 78 ( SD 4)% , 75 ( SD 14)% and 84 ( SD 7)% ( P<0.05 ) in normoxia , hypoxia and hyperoxia , respectively . A strong correlation between Fmax and V˙O2 was found in normoxia but not in hypoxia and hyperoxia . The mean sum-iEMG tended to be lower ( P<0.05 ) in hypoxia than in normoxia but hyperoxia had no significant effect on it . In general , FIO2 did not affect MPF of individual muscles . In conclusion , it was found that force output during ergometer rowing  was impaired during hypoxia and improved during hyperoxia when compared with normoxia . Moreover , the changes in force output were only partly accompanied by changes in muscle electrical activity as sum-iEMG was affected by hypoxic but not by hyperoxic gas . The lack of a significant correlation between Fmax and V˙O2 during hypoxia and hyperoxia may suggest a partial uncoupling of these processes and the existence of other limiting factors in addition to V˙O2 This investigation explored the influence of supplemental oxygen administered during the recovery periods of an interval-based running session on the post-exercise markers of reactive oxygen species ( ROS ) and inflammation . Ten well-trained male endurance athletes completed two sessions of 10 × 3 min running intervals at 85 % of the maximal oxygen consumption velocity ( vVO2peak ) on a motorised treadmill . A 90-s recovery period was given between each interval , during which time the participants were administered either a hyperoxic ( HYP ) ( Fraction of Inspired Oxygen ( FIO2 ) 99.5 % ) or normoxic ( NORM ) ( FIO2 21 % ) gas , in a r and omized , single-blind fashion . Pulse oximetry ( SpO2 ) , heart rate ( HR ) , blood lactate ( BLa ) , perceived exertion ( RPE ) , and perceived recovery ( TQRper )  were recorded during each trial . Venous blood sample s were taken pre-exercise , post-exercise and 1 h post-exercise to measure Interleukin-6 ( IL-6 ) and Isoprostanes ( F2-IsoP ) . The SpO2 was significantly lower than baseline following all interval repetitions in both experimental trials ( p < 0.05 ) . The SpO2 recovery time was significantly quicker in the HYP when compared to the NORM ( p < 0.05 ) , with a trend for improved perceptual recovery . The IL-6 and F2-IsoP were significantly elevated immediately post-exercise , but had significantly decreased by 1 h post-exercise in both trials ( p < 0.05 ) . There were no differences in IL-6 or F2-IsoP levels between trials . Supplemental oxygen provided during the recovery periods of interval based exercise improves the recovery time of SPO2 but has no effect on post-exercise ROS or inflammatory responses It has been shown that peak oxygen uptake ( % MathType!MTEF!2!1!+- % feaafaart1ev1aqatCvAUfeBSn0BKvguHDwzZbqefeKCPfgBGuLBPn % 2BKvginnfarmWu51MyVXgatuuDJXwAK1uy0HwmaeHbfv3ySLgzG0uy % 0Hgip5wzaebbnrfifHhDYfgasaacH8srps0lbbf9q8WrFfeuY-Hhbb % f9v8qqaqFr0xc9pk0xbba9q8WqFfea0-yr0RYxir-Jbba9q8aq0-yq % -He9q8qqQ8frFve9Fve9Ff0dmeaabaqaceGacaGaaeqabaWaaeWaea % aakeaaceWGwbGbaiaaaaa!3A5B ! $ $ { \dot{V}}$$ O2peak ) during leg exercise is enhanced by an increased inspiratory oxygen fraction ( FiO2 ) , indicating that oxygen supply is the limiting factor . Whether oxygen supply is a limiting factor in arm exercise performance is unknown . The purpose of this study , therefore , was to examine the effect of different levels of FiO2 on % MathType!MTEF!2!1!+- % feaafaart1ev1aqatCvAUfeBSn0BKvguHDwzZbqefeKCPfgBGuLBPn % 2BKvginnfarmW 
    Output:
    
Conclusion Acute exercise performance is increased with hyperoxia .
An FiO2 ≥ 0.30 appears to be beneficial for performance , with a higher FiO2 being correlated to greater performance improvement in TTs , TTE , and dynamic muscle function tests .
Exercise training and recovery supplemented with hyperoxic gas appears to have a beneficial effect on subsequent exercise performance , but small sample size and wide disparity in experimental protocol s preclude definitive conclusions