***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: This investigation determined the manner in which the cardiovascular system copes with the dehydration-induced reductions in cardiac output ( Q ) during prolonged exercise in the heat . On two separate occasions , seven endurance-trained subjects ( maximal O2 consumption 4.70 + /- 0.41 l/min )  cycled in the heat ( 35 degrees C ) for 2 h , beginning at 62 + /- 2 % maximal O2 consumption . During exercise , they r and omly received either 0.2 liter of fluid and became dehydrated by 4.9 + /- 0.2 % of their body weight [ i.e. , dehydration trial ( DE ) ] or 3.6 + /- 0.4 liter of fluid and replaced 95 % of fluid losses [ i.e. , euhydration trial ( EU ) ] . During the 10- to 120-min period of EU , Q , mean arterial pressure ( MAP ) , systemic vascular resistance ( SVR ) , cutaneous vascular resistance ( CVR ) , and plasma catecholamines did not change while esophageal temperature stabilized at 38.0 + /- 0.1 degrees C. Conversely , after 120 min of DE , Q and MAP were reduced 18 + /- 3 and 5 + /- 2 % , respectively , compared with EU ( P < 0.05 ) . This was associated with a significantly higher SVR ( 17 + /- 6 % ) and plasma norepinephrine concentration ( 50 + /- 19 % , P < 0.05 ) . In addition , CVR was also significantly higher ( 126 + /- 16 vs. 102 + /- 6 % of 20-min value ; P < 0.05 ) during DE despite a 1.2 + /- 0.1 degrees C greater esophageal temperature ( P < 0.05 ) . In conclusion , significant reductions in Q are accompanied by significant increases in SVR and plasma norepinephrine and a slight although significant decline in MAP . The cutaneous circulation participates in this systemic vasoconstriction as indicated by increases in CVR despite significant hyperthermia This study examined the effects of rehydration ( Rehy ) with fluids of varying tonicities and routes of administration after exercise-induced hypohydration on exercise performance , fluid regulatory hormone responses , and cardiovascular and thermoregulatory strain during subsequent exercise in the heat . On four occasions , eight men performed an exercise-dehydration protocol of approximately 185 min ( 33 degrees C ) to establish a 4 % reduction in body weight . Following dehydration , 2 % of the fluid lost was replaced during the first 45 min of a 100-min rest period by one of three r and om Rehy treatments ( 0.9 % saline intravenous ; 0.45 % saline intravenous ; 0.45 % saline oral ) or no Rehy ( no fluid ) treatment . Subjects then stood for 20 min at 36 degrees C and then walked at 50 % maximal oxygen consumption for 90 min . Subsequent to dehydration , plasma Na(+ ) , osmolality , aldosterone , and arginine vasopressin concentrations were elevated ( P < 0.05 ) in each trial , accompanied by a -4 % hemoconcentration . Following Rehy , there were no differences ( P > 0.05 ) in fluid volume restored , post-rehydration ( Post-Rehy ) body weight , or urine volume . Percent change in plasma volume was 5 % above pre-Rehy values , and plasma Na(+ ) , osmolality , and fluid regulatory hormones were lower compared with no fluid . During exercise , skin and core temperatures , heart rate , and exercise time were not different ( P > 0.05 ) among the Rehy treatments . Plasma osmolality , Na(+ ) , percent change in plasma volume , and fluid regulatory hormones responded similarly among all Rehy treatments . Neither a fluid of greater tonicity nor the route of administration result ed in a more rapid or greater fluid retention , nor did it enhance heat tolerance or diminish physiological strain during subsequent exercise in the heat Abstract . The aim of this study was to compare the cardiovascular responses to prolonged submaximal cycling and running .  Eleven males [ maximal oxygen uptake ( V˙O2max ) : 3.58±0.15 l min–1 for running and 3.84±0.16 l min–1 for cycling ; mean±SE ]  either cycled ( C ) or ran ( R ) for 90 min at 60 % of mode-specific V˙O2max , on two r and omly assigned occasions . Cardiac output declined after 85 min of exercise in C ( –1.9±0.5 l min–1 , P<0.01 ) but not in R , as a result of a more pronounced decrease in stroke volume in the former exercise mode ( –22.7±3.8 ml beat–1 vs –14.3±1.9 ml beat–1 , P<0.01 ) since heart rate did not differ between trials . Stroke volume responses were despite a higher level of dehydration ( –3.3±0.2 % in R vs –2.8±0.2 % in C , P<0.05 ) and hyperthermia in R ( 39.6±0.1 vs 38.8±0.1 ° C in C at 90 min , P<0.01 ) . Finally , mean skin blood flow was lower in R than C ( 72±8 vs 89±10 % ; P<0.05 ) . In conclusion , stroke volume and cardiac output decline was more pronounced in cycling than in running despite lower dehydration and rectal temperature in the former exercise mode Stearns , RL , Casa , DJ , Lopez , RM , McDermott , BP , Ganio , MS , Decher , NR , Scruggs , IC , West , AE , Armstrong , LE , and Maresh , CM . Influence of hydration status on pacing during trail running in the heat . J Strength Cond Res 23(9 ) : 2533 - 2541 , 2009-The purpose of this study was to determine the influence of hydration status on pacing of trail runners in the heat ( wet bulb globe temperature = 26.2 ± 1.8 ° C ) . A r and omized , crossover design was used and the participation occurred within a 2-week period . Seventeen competitive , well-trained distance runners ( 9 men , 8 women , age 27 ± 7 years , height 171 ± 9 cm , weight 64.2 ± 9.0 kg , body fat 14.6 ± 5.5 % ) completed the study . Subjects started maximum effort trials that were either hydrated ( HYR ) and dehydrated ( DHR ) . Each trial subjects ran three 4-km loops with a 4-minute rest between loops . Significance was set at p ≤ 0.05 . The DHR had a significantly greater body mass loss at the pre- and posttrial time points ( −2.05 ± 1.25 and −4.3 ± 1.25 % , respectively ) vs. HYR ( −0.79 ± 0.95 and −2.05 ± 1.09 % , respectively ) . Subjects ran the 12 km faster ( p < 0.001 ) in HYR ( 3,191 ± 366 seconds ) vs. DHR ( 3,339 ± 450 seconds ) . Differences between fastest and slowest loops during HYR ( 54 ± 40 seconds ) were significantly smaller than DHR ( 111 ± 93 seconds ; p = 0.041 ) . Additionally , loop times were slower for loop 1 ( HYR 1,039 ± 116 seconds vs. DHR 1,071 ± 123 seconds ; p = 0.028 ) , loop 2 ( HYR 1,066 ± 123 seconds vs. DHR 1,105 ± 148 seconds ; p = 0.01 ) and loop 3 ( HYR 1,081 ± 132 seconds vs. DHR 1,168 ± 189 seconds ; p = 0.003 ) when dehydrated . Percent of the race completed by loop as calculated by finishing time was significantly different at loop 2 between HYR ( 33.6 ± 0.36 % ) and DHR ( 33.1 ± 0.35 % , p = 0.002 ) and loop 3 ( 33.8 ± 0.75 % vs. 34.9 ± 1.35 % , respectively , p = 0.01 ) . Total variation from the mean pace for the duration of the HYR compared to the DHR approached significance ( p = 0.064 ) . Average percent of variance approached significance between trials ( p = 0.057 ) . Differences between the fastest and slowest loops between trials demonstrated an increased ability for hydrated individuals  to evenly pace themselves . While total variation from the mean pace was not significantly different , it could have practical applicability . These findings reveal that dehydration is associated with decreases in  a runners ' ability to evenly pace themselves during a competitive situation 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 We tested the hypothesis that , in humans , hypohydration attenuates hyperthermic hyperpnea during exercise in the heat . On two separate occasions , thirteen male subjects performed a fluid replacement ( FR ) and a no-fluid replacement ( NFR ) trial in r and om order . The subjects performed two bouts of cycle exercise ( Ex1 and Ex2 , 30 - 60 min ) at 50 % peak oxygen uptake ( Vo2 peak ) in 35 degrees C separated by a 70- to 80-min rest period , during which they drank water containing 25 mosmol/l sodium in the FR trial but not the NFR trial . The drinking in the FR trial nearly restored the body fluid to the euhydrated condition , so that the body fluid status differed between the trials before Ex2 ( the difference in plasma osmolality before Ex2 was 9.4 mosmol/kgH2O ; plasma volume was 7.6 % , and body weight was 2.5 % ) . The slopes of the linear relationships between ventilatory variables ( minute ventilation , ventilatory equivalents for oxygen uptake and carbon dioxide output , tidal volume , respiratory frequency , and end-tidal CO2 pressure ) and esophageal temperature ( Tes ) did not significantly differ between Ex1 and Ex2 , or between the FR and NFR trials . On the other h and , during Ex2 in the NFR trial , the Tes threshold for the onset of increased forearm vascular conductance ( FVC ) was higher , and the slope and peak values of the relationship between FVC and Tes were lower than during Ex1 in the NFR trial and during Ex2 in the FR trial . These findings suggest that hypoh 
    Output:
    
This increase in HR for every 1 % ΔBML exacerbates cardiovascular strain in exercising individuals , thus causing decrements in performance .