***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: Abstract Energy substrate oxidation was measured using indirect respiratory calorimetry combined with tracer technique in five healthy young male subjects , during a 80-min exercise period on ergocycle with ingestion of 140 g of 13C-labelled glucose , in normoxia and acute hypobaric hypoxia ( 445 mmHg or 4,300 m ) , at the same relative $ $ { \left ( { 77\% \dot{V}_{{{\text{O}}_{2 } \max } } } \right ) } $ $ and absolute workload ( 161±8 W , corresponding to 77 and 54 % $ $ \dot{V}_{{{\text{O}}_{{\text{2 } } } { \text{max } } } } $ $ in hypoxia and normoxia ) . The oxidation rate of exogenous glucose was not significantly different in the three experimental situations : 21.4±2.9 , 20.2±1.2 and 17.2±0.6 g over the last 40 min of exercise at ~77 and ~54 % $ $ \dot{V}_{{{\text{O}}_{{\text{2 } } } { \text{max } } } } $ $ in normoxia and in hypoxia , respectively , providing 12.5±1.5 , 16.8±1.1 and 14.9±1.1 % of the energy yield , although ingestion of glucose during exercise result ed in a higher plasma glucose concentration in hypoxia than normoxia . The contribution of carbohydrate ( CHO ) oxidation to the energy yield was significantly higher in hypoxia ( 92.0±2.1 % ) than in normoxia for both a given absolute ( 75.3±5.2 % ) and relative workload ( 78.1±1.8 % ) . This greater reliance on CHO oxidation in hypoxia was entirely due to the significantly larger contribution of endogenous glucose oxidation to the energy yield : 75.9±1.7 % versus 66.6±3.3 and 55.2±3.7 % in normoxia at the same relative and absolute workload Seven healthy young male adults were subjected to a total of 56 tests to ascertain the effects of L-carnitine ( L-C ) and a placebo ( P ) on ventilation , O2 intake ( VO2 ) , CO2 output , heart rate , blood pressure and serum lactic acid , non-esterified fatty acid , glycerol and glucose during strenuous and aerobic/anaerobic threshold-level treadmill exercise . The tests were made in conditions of normoxia ( O2 = 20.9 % ) and hypoxia ( O2 = 13.0 % , equivalent to 3,500 m above sea level ) . The only clear difference was in the respiratory quotient ( RQ = 0.883 , SD 0.025 vs 0.904 , SD 0.035 ) after L-C and P administration respectively ( P less than 0.01 ) , under normal oxygenation and 0.861 , SD 0.052 following L-C vs 0.926 , SD 0.040 after P ( P less than 0.01 ) in acute hypoxia at VO2 levels around the anaerobic threshold . The lower RQ values of the L-C-treated subjects during hypoxia indicate a lower rate of carbohydrate transformation Acute exposure to  high altitude ( > 3500 m ) is associated with marked changes in appetite regulation and substrate oxidation but the effects of lower altitudes are unclear . This study examined appetite , gut hormone , energy intake and substrate oxidation responses to breakfast ingestion and exercise at simulated moderate and severe altitudes compared with sea-level . Twelve healthy males ( mean ± SD ; age 30 ± 9years , body mass index 24.4 ± 2.7 kg·m-2 ) completed in a r and omised crossover order three , 305 min experimental trials at a simulated altitude of 0 m , 2150 m ( ∼15.8 % O2 ) and 4300 m ( ∼11.7 % O2 ) in a normobaric chamber . Participants entered the chamber at 8 am following a 12 h fast . A st and ardised breakfast was consumed inside the chamber at 1 h. One hour after breakfast , participants performed a 60 min treadmill walk at 50 % of relative V˙O2max . An ad-libitum buffet meal was consumed 1.5 h after exercise . Blood sample s were collected prior to altitude exposure and at 60 , 135 , 195 , 240 and 285 min . No trial based differences were observed in any appetite related measure before exercise . Post-exercise area under the curve values for acylated ghrelin , pancreatic polypeptide and composite appetite score were lower ( all P < 0.05 ) at 4300 m compared with sea-level and 2150 m. There were no differences in glucagon-like peptide-1 between conditions ( P = 0.895 ) . Mean energy intake was lower at 4300 m ( 3728 ± 3179 kJ ) compared with sea-level ( 7358 ± 1789 kJ ; P = 0.007 ) and 2150 m ( 7390 ± 1226 kJ ; P = 0.004 ) . Proportional reliance on carbohydrate as a fuel was higher ( P = 0.01 ) before breakfast but lower during ( P = 0.02 ) and after exercise ( P = 0.01 ) at 4300 m compared with sea-level . This study suggests that altitude-induced anorexia and a subsequent reduction in energy intake occurs after exercise during exposure to severe but not moderate simulated altitude . Acylated ghrelin concentrations may contribute to this effect Recent studies have shown that exercise training at moderate altitude or in moderate hypoxia improved glycemic parameters . From these data , it has been supposed that endurance exercise in moderate hypoxia affects substrate utilization and that exposure to moderate hypoxia in combination with exercise may be utilized as part of metabolic or diabetes prevention program . However , the influence of exercise at moderate hypoxia on circulating metabolites and hormones in terms of substrate utilization is unclear . The purpose of this study was to eluci date the influence of exercise in moderate hypoxia on substrate utilization . We determined cardiorespiratory , metabolic , and hormonal parameters during exercise and postexercise recovery at a simulated moderate altitude of 2000 m , and then we compared these variables with values obtained at sea level . Seven men participated in this study ; subjects reported to the laboratory on 4 occasions .  Two maximal exercise tests were performed to estimate peak oxygen uptake at the simulated 2000-m altitude and sea level on different days . Afterward , submaximal exercise tests were carried out at a simulated altitude of 2000 m or sea level , separated by 1 week . Subjects performed submaximal exercise at the same relative exercise intensity ( 50 % peak oxygen uptake ) at a simulated altitude of 2000 m and at sea level for 30 minutes . The tests were performed in r and om order , and subjects were blinded to the respective altitudes . Venous blood sample s and expired gases were obtained before , during exercise ( 15 and 30 minutes ) , and during postexercise recovery periods ( 15 , 30 , 45 , and 60 minutes ) . The respiratory exchange ratio during exercise and recovery at moderate altitude was greater than at sea level . The epinephrine and norepinephrine concentrations during exercise and recovery were higher ( P < .05 ) at moderate altitude than at sea level . Free fatty acids and glycerol concentrations during recovery were lower ( P < .05 ) at moderate altitude than at sea level . These results suggest that carbohydrate utilization is increased during exercise and postexercise recovery period in moderate hypoxia as compared with normoxia . It is also suggested that moderate hypoxia influences the changes in circulating metabolites and hormones in terms of substrate metabolism during exercise and the recovery Acute hypoxia increases heart rate ( HR ) and cardiac output ( Qt ) at a given oxygen consumption ( VO2 ) during submaximal exercise . It is widely believed that the underlying mechanism involves increased sympathetic activation and circulating catecholamines acting on cardiac beta receptors . Recent evidence indicating a continued role for parasympathetic modulation of HR during moderate exercise suggests that increased parasympathetic withdrawal plays a part in the increase in HR and Qt during hypoxic exercise . To test this , we separately blocked the beta-sympathetic and parasympathetic arms of the autonomic nervous system ( ANS ) in six healthy subjects ( five male , one female ; mean + /- S.E.M. age = 31.7+/-1.6 years , normoxic maximal VO2 (VO2,max)=3.1+/-0.3 l min(-1 ) ) during  exercise in conditions of normoxia and acute hypoxia ( inspired oxygen fraction=0.125 ) to VO2,max . Data were collected on different days under the following conditions : (1)control , ( 2 ) after 8.0 mg propranolol i.v . and ( 3 ) after 0.8 mg glycopyrrolate i.v . Qt was measured using open-circuit acetylene uptake . Hypoxia increased venous [ adrenaline ] and [ noradrenaline ] but not [ dopamine ] at a given VO2 ( P<0.05 , P<0.01 and P=0.2 , respectively ) . HR/VO2 and Qt/VO2 increased during hypoxia in all three conditions ( P<0.05 ) . Unexpectedly , the effects of hypoxia on HR and Qt were not significantly different from control with either beta-sympathetic or parasympathetic inhibition . These data suggest that although acute exposure to hypoxia increases circulating [ catecholamines ] , the effects of hypoxia on HR and Qt do not necessarily require intact cardiac muscarinic and beta receptors . It may be that cardiac alpha receptors play a primary role in elevating HR and Qt during hypoxic exercise , or perhaps offer an alternative mechanism when other ANS pathways are blocked Carbohydrate supplementation ( CHOS ) typically improves prolonged time-trial ( TT ) performance at sea level ( SL ) . This study determined whether CHOS also improves TT performance at high altitude ( ALT ; 4,300 M ) despite increased hypoxemia and while in negative energy balance ( approximately 1,250 kcal/day ) . Two groups of fasting , fitness-matched men performed a 720-kJ cycle TT at SL and while living at ALT on days 3 ( ALT3 ) and 10 ( ALT10 ) . Eight men drank a 10 % carbohydrate solution ( 0.175 g/kg body wt ) and eight drank a placebo ( PLA ; double blind ) at the start of and every 15 min of the TT . Blood glucose during each TT was higher ( P < 0.05 ) for CHOS than for PLA . At SL , TT duration ( approximately 59 min ) and watts ( approximately 218 or approximately 61 % of peak watts ; % SL Wpeak ) were similar for both groups . At ALT , the TT was longer for both groups ( P < 0.01 ) but was shorter for CHOS than for PLA on ALT3 ( means + /- SE : 80 + /- 7 vs. 105 + /- 9 min ; P < 0.01 ) and ALT10 ( 77 + /- 7 vs. 90 + /- 5 min ; P < 0.01 ) . At ALT , % SL Wpeak was reduced ( P < 0.01 ) with the reduction on ALT3 being larger for PLA ( to 33 + /- 3 % ) than for CHOS ( to 43 + /- 2 % ; P < 0.05 ) . On ALT3 , O2 saturation fell similarly from 84 + /- 2 % at rest to 73 + /- 1 % during the TT for both groups ( P < 0.05 ) , and on ALT10 O2 saturation fell more ( P < 0.02 ) for CHOS ( 91 + /- 1 to 76 + /- 2 % ) than for PLA ( 90 + /- 1 to 81 + /- 1 % ) . % SL Wpeak and O2 saturation were inversely related during the TT for both groups at ALT ( r > or = -0.76 ; P < or = 0.03 ) . It was concluded that , despite hypoxemia exacerbated by exercise , CHOS greatly improved TT performance at ALT in which there was a negative energy balance Objective We examined metabolic and endocrine responses during rest and exercise in moderate hypoxia over a 7.5 h time courses during daytime . Methods Eight sedentary , overweight men ( 28.6±0.8 kg/m2 ) completed four experimental trials : a rest trial in normoxia ( FiO2 = 20.9 % , NOR-Rest ) , an exercise trial in normoxia ( NOR-Ex ) , a rest trial in hypoxia ( FiO2 = 15.0 % , HYP-Rest ) , and an exercise trial in hypoxia ( HYP-Ex ) . Experimental trials were performed from 8:00 to 15:30 in an environmental chamber . Blood and respiratory gas sample s were collected over 7.5 h. In the exercise trials , subjects performed 30 min of pedaling exercise at 60 
    Output:
    
Conclusions Exposure to hypoxia did not induce a consistent change in the relative contribution of carbohydrate or fat to the total energy yield during exercise matched for relative intensities , compared with normoxia .
The direction of these responses appears to be mediated by the consumption of a pre-exercise meal and exercise intensity