***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: 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 PURPOSE To determine the effect of a 48-h period of either fluid restriction ( FR ) , energy restriction ( ER ) , or fluid and energy restriction ( F + ER ) on 30-min treadmill time trial ( TT ) performance in temperate conditions . METHODS Thirteen males participated in four r and omized 48-h trials ( mean + /- SD : age , 21 + /- 3 yr ; VO2max 50.9 + /- 4.3 mL x kg(-1 ) x min(-1 ) ) . Control ( CON ) participants received their estimated energy ( 2903 + /- 199 kcal x d(-1 ) ) and water ( 3912 + /- 500 mL x d(-1 ) ) requirements . For FR , participants received their energy requirements and 193 + /- 50 mL x d(-1 ) water to drink , and for ER , participants received their water requirements and 290 + /- 20 kcal x d(-1 ) . F + ER was a combination of FR and ER . After 48 h , participants performed a 30-min treadmill TT in temperate conditions ( 19.7 + /- 0.6 degrees C ) . A separate investigation ( N = 10 ) showed the TT to be highly reproducible ( CV 1.6 % ) . RESULTS Body mass loss ( BML ) was 0.6 + /- 0.4 % ( CON ) , 3.2 + /- 0.5 % ( FR ) , 3.4 + /- 0.3 % ( ER ) , and 3.6 + /- 0.3 % ( F + ER ) . Compared with CON ( 6295 + /- 513 m ) , less distance was completed on ER ( 10.3 % ) and F + ER ( 15.0 % : P < 0.01 ) . Although less distance was completed on FR ( 2.8 % ) , this was not significantly different from CON . CONCLUSIONS These results show a detrimental effect of a 48-h period of ER but no significant effect of FR on 30-min treadmill TT performance in temperate conditions . Therefore , these results do not support the popular contention that modest hypohydration ( 2 - 3 % BML ) significantly impairs endurance performance in temperate conditions This investigation determined the effect of different rates of dehydration , induced by ingesting different volumes of fluid during prolonged exercise , on hyperthermia , heart rate ( HR ) , and stroke volume ( SV ) . On four different occasions , eight endurance-trained cyclists [ age 23 + /- 3 ( SD ) yr , body wt 71.9 + /- 11.6 kg , maximal O2 consumption 4.72 + /- 0.33 l/min ] cycled at a power output equal to 62 - 67 % maximal O2 consumption for 2 h in a warm environment ( 33 degrees C dry bulb , 50 % relative humidity , wind speed 2.5 m/s ) . During exercise , they r and omly received no fluid ( NF ) or ingested a small ( SF ) , moderate ( MF ) , or large ( LF ) volume of fluid that replaced 20 + /- 1 , 48 + /- 1 , and 81 + /- 2 % , respectively , of the fluid lost in sweat during exercise . The protocol result ed in grade d magnitudes of dehydration as body weight declined 4.2 + /- 0.1 , 3.4 + /- 0.1 , 2.3 + /- 0.1 , and 1.1 + /- 0.1 % , respectively , during NF , SF , MF , and LF . After 2 h of exercise , esophageal temperature ( Tes ) , HR , and SV were significantly different among the four trials ( P < 0.05 ) , with the exception of NF and SF . The magnitude of dehydration accrued after 2 h of exercise in the four trials was linearly related with the increase in Tes ( r = 0.98 , P < 0.02 ) , the increase in HR ( r = 0.99 , P < 0.01 ) , and the decline in SV ( r = 0.99 , P < 0.01 ) . LF attenuated hyperthermia , apparently because of higher skin blood flow , inasmuch as forearm blood flow was 20 - 22 % higher than during SF and NF at 105 min ( P < 0.05 ) . There were no differences in sweat rate among the four trials . In each subject , the increase in Tes from 20 to 120 min of exercise was highly correlated to the increase in serum osmolality ( r = 0.81 - 0.98 , P < 0.02 - 0.19 ) and the increase in serum sodium concentration ( r = 0.87 - 0.99 , P < 0.01 - 0.13 ) from 5 to 120 min of exercise . In summary , the magnitude of increase in core temperature and HR and the decline in SV are grade d in proportion to the amount of dehydration accrued during exercise 1 . The present study examined whether the blood flow to exercising muscles becomes reduced when cardiac output and systemic vascular conductance decline with dehydration during prolonged exercise in the heat . A secondary aim was to determine whether the upward drift in oxygen consumption ( VO2 ) during prolonged exercise is confined to the active muscles . 2 . Seven euhydrated , endurance-trained cyclists performed two bicycle exercise trials in the heat ( 35 C ; 40 - 50 % relative humidity ; 61 + /- 2 % of maximal VO2 ) , separated by 1 week . During the first trial ( dehydration trial , DE ) , they bicycled until volitional exhaustion ( 135 + /- 4 min , mean + /- s.e.m . ) , while developing progressive dehydration and hyperthermia ( 3.9 + /- 0.3 % body weight loss ; 39.7 + /- 0.2 C oesophageal temperature , Toes ) . In the second trial ( control trial ) , they bicycled for the same period of time while maintaining euhydration by ingesting fluids and stabilizing Toes at 38.2 + /- 0.1 C after 30 min exercise . 3 . In both trials , cardiac output , leg blood flow ( LBF ) , vascular conductance and VO2 were similar after 20 min exercise . During the 20 min-exhaustion period of DE , cardiac output , LBF and systemic vascular conductance declined significantly ( 8 - 14 % ; P < 0.05 ) yet muscle vascular conductance was unaltered . In contrast , during the same period of control , all these cardiovascular variables tended to increase . After 135 + /- 4 min of DE , the 2.0 + /- 0.6 l min-1 lower blood flow to the exercising legs accounted for approximately two-thirds of the reduction in cardiac output . Blood flow to the skin also declined markedly as forearm blood flow was 39 + /- 8 % ( P < 0.05 ) lower in DE vs. control after 135 + /- 4 min . 4 . In both trials , whole body VO2 and leg VO2 increased in parallel and were similar throughout exercise . The reduced leg blood flow in DE was accompanied by an even greater increase in femoral arterial-venous O2 ( a-vO2 ) difference . 5 . It is concluded that blood flow to the exercising muscles declines significantly with dehydration , due to a lowering in perfusion pressure and systemic blood flow rather than increased vasoconstriction . Furthermore , the progressive increase in oxygen consumption during exercise is confined to the exercising skeletal muscles AIM The purpose of this study was to investigate the effect of hypohydration ( HH ) on the lactate threshold ( LT ) in a hot and humid environment . METHODS Ten apparently healthy males ( age 25+/-3 yrs ; height 1.8+/-0.04 m ; mass 78+/-12 kg ; VO2peak 3.7+/-0.4 L/min ) underwent four r and omly assigned maximal treadmill tests . Two trials were at room temperature ( 22+/-1 degrees C ; RH = 50 % ) under two different hydration conditions : euhydrated ( EH-RM ) and hypohydrated ( HH-RM ) , and two trials were performed in a warm chamber ( 37+/-0.5 degrees C ; RH = 70 % ) under two different hydration conditions : euhydrated ( EH-HT ) and hypohydrated ( HH-HT ) . The desired HH level ( 2 - 4 % ) was accomplished in the 24 + hours before testing by fluid restriction . Mean HH was 2.6+/-1.0 % body weight . Capillary blood sample s were collected at the end of each stage and analyzed for lactic acid ( LA ) . LA concentrations were plotted for each exercise stage , and the LT was determined by visual inspection as the highest exercise stage at which blood LA concentration began to increase above each individual 's resting levels . LT and body temperature were analyzed with a two-way repeated measures ANOVA ( P < 0.05 ) . RESULTS During the trials in the warm chamber , the LT occurred at a significantly earlier stage compared to the thermoneutral environment ( 4.4+/-0.09 vs 5.8+/-0.10 ) and with a significantly lower oxygen consumption ( 2.38+/-0.09 L.min(-1 ) vs 2.86+/-0.13 L.min(-1 ) ) . Body temperature at the LT was significantly higher in the heat trials compared to room temperature ( 38.7+/-0.12 degrees C vs 37.6+/-0.14 degrees C ) . LT determination was not significantly altered by hydration . CONCLUSION These results suggest that during progressive incremental maximal treadmill exercise , moderate HH does not affect the LT , whereas exercise in a hot and humid environment induces a downward shift in the LT . The elevated body temperature during the heat trials suggests that body temperature may affect running performance associated with the LT CONTEXT Authors of most field studies have not observed decrements in physiologic function and performance with increases in dehydration , although authors of well-controlled laboratory studies have consistently reported this relationship . Investigators in these field studies did not control exercise intensity , a known modulator of body core temperature . OBJECTIVE To directly examine the effect of moderate water deficit on the physiologic responses to various exercise intensities in a warm outdoor setting . DESIGN Semir and omized , crossover design . SETTING Field setting . PATIENTS OR OTHER PARTICIPANTS Seventeen distance runners ( 9 men , 8 women ; age = 27 + /- 7 years , height = 171 + /- 9 cm , mass = 64.2 + /- 9.0 kg , body fat = 14.6 % + /- 5.5 % ) . INTERVENTION(S ) Participants completed four 12-km runs ( consisting of three 4-km loops ) in the heat ( average wet bulb globe temperature = 26.5 degrees C ) : ( 1 ) a hydrated , race trial ( HYR ) , ( 2 ) a dehydrated , race trial ( DYR ) , ( 3 ) a hydrated , submaximal trial ( HYS ) , and ( 4 ) a dehydrated , submaximal trial ( DYS ) . MAIN OUTCOME MEASURE(S ) For DYR and DYS trials , dehydration was measured by body mass loss . In the submaximal trials , participants ran at 
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However , no systematic approach has yet been used to determine how pre-exercise hypohydration , which imposes physiological challenges differing from those of a well-hydrated pre-exercise state , affects AEP and related components such as peak oxygen consumption (V˙O2peak)\documentclass[12pt]{minimal } \usepackage{amsmath } \usepackage{wasysym } \usepackage{amsfonts } \usepackage{amssymb } \usepackage{amsbsy } \usepackage{mathrsfs } \usepackage{upgreek } \setlength{\oddsidemargin}{-69pt } \begin{document}$$(\dot{V}{\text{O}}_{{2{\text{peak } } } } ) $ $ \end{document } and V˙O2\documentclass[12pt]{minimal } \usepackage{amsmath } \usepackage{wasysym } \usepackage{amsfonts } \usepackage{amssymb } \usepackage{amsbsy } \usepackage{mathrsfs } \usepackage{upgreek } \setlength{\oddsidemargin}{-69pt } \begin{document}$$\dot{V}{\text{O}}_{2}$$\end{document } at lactate threshold (V˙O2LT)\documentclass[12pt]{minimal } \usepackage{amsmath } \usepackage{wasysym } \usepackage{amsfonts } \usepackage{amssymb } \usepackage{amsbsy } \usepackage{mathrsfs } \usepackage{upgreek } \setlength{\oddsidemargin}{-69pt } \begin{document}$$(\dot{V}{\text{O}}_{2 } { \text{LT}})$$\end{document}. To determine , using a systematic approach with meta- analysis , the magnitude of the effect of pre-exercise hypohydration on AEP , V˙O2peak\documentclass[12pt]{minimal } \usepackage{amsmath } \usepackage{wasysym } \usepackage{amsfonts } \usepackage{amssymb } \usepackage{amsbsy } \usepackage{mathrsfs } \usepackage{upgreek } \setlength{\oddsidemargin}{-69pt } \begin{document}$$\dot{V}{\text{O}}_{{2{\text{peak}}}}$$\end{document } and V˙O2LT\documentclass[12pt]{minimal } \usepackage{amsmath } \usepackage{wasysym } \usepackage{amsfonts } \usepackage{amssymb } \usepackage{amsbsy } \usepackage{mathrsfs } \usepackage{upgreek } \setlength{\oddsidemargin}{-69pt } \begin{document}$$\dot{V}{\text{O}}_{2 } { \text{LT}}$$\end{document}. This was a systematic review with meta- analysis of well-controlled studies .
Compared with starting an exercise hypohydrated , it is respectively likely , possible and likely that AEP , V˙O2peak\documentclass[12pt]{minimal } \usepackage{amsmath } \usepackage{wasysym } \usepackage{amsfonts } \usepackage{amssymb } \usepackage{amsbsy } \usepackage{mathrsfs } \usepackage{upgreek } \setlength{\oddsidemargin}{-69pt } \begin{document}$$\dot{V}{\text{O}}_{{2{\text{peak}}}}$$\end{document } and V˙O2LT\documentclass[12pt]{minimal } \usepackage{amsmath } \usepackage{wasysym } \usepackage{amsfonts } \usepackage{amssymb } \usepackage{amsbsy } \usepackage{mathrsfs } \usepackage{upgreek } \setlength{\oddsidemargin}{-69pt } \begin{document}$$\dot{V}{\text{O}}_{2 } { \text{LT}}$$\end{document } benefit from a euhydrated state prior to exercise .
Pre-exercise hypohydration likely impairs AEP and likely reduces V˙O2LT\documentclass[12pt]{minimal } \usepackage{amsmath } \usepackage{wasysym } \usepackage{amsfonts } \usepackage{amssymb } \usepackage{amsbsy } \usepackage{mathrsfs } \usepackage{upgreek } \setlength{\oddsidemargin}{-69pt } \begin{document}$$\dot{V}{\text{O}}_{2 } { \text{LT}}$$\end{document } ( i.e. , the aerobic contribution to exercise was lower ) during running and cycling exercises ≤ 1 h across different environmental conditions ( i.e. , from 19 to 40 ° C ) .
Moreover , pre-exercise hypohydration possibly impedes V˙O2peak\documentclass[12pt]{minimal } \usepackage{amsmath } \usepackage{wasysym } \usepackage{amsfonts } \usepackage{amssymb } \usepackage{amsbsy } \usepackage{mathrsfs } \usepackage{upgreek } \setlength{\oddsidemargin}{-69pt } \begin{document}$$\dot{V}{\text{O}}_{{2{\text{peak}}}}$$\end{document } during such exercises