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100:442-450, 2006. First published Oct 6, 2005; doi:10.1152/japplphysiol.00187.2005J Appl PhysiolWilliam J. KraemerJorge A. Herrera-Soto, Timothy P. Scheett, James Stoppani, Gary W. Mack andStavros A. Kavouras, Lawrence E. Armstrong, Carl M. Maresh, Douglas J. Casa,

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, October 1,2007; 26(suppl_5): 542S-548S.J. Am. Coll. Nutr.B. MurrayHydration and Physical Performance

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Rehydration with glycerol: endocrine, cardiovascular, and thermoregulatory

responses during exercise in the heat

Stavros A. Kavouras,1,4 Lawrence E. Armstrong,1,2 Carl M. Maresh,1,2

Douglas J. Casa,1 Jorge A. Herrera-Soto,1 Timothy P. Scheett,1

James Stoppani,1

Gary W. Mack,3

and William J. Kraemer1,2

1 Human Performance Laboratory, Department of Kinesiology, and 2Departments of Physiology and Neurobiology and of

Nutritional Sciences, University of Connecticut, Storrs; 3The John B. Pierce Laboratory, Yale University School of Medicine,

New Haven, Connecticut; and4 Laboratory of Nutrition and Clinical Dietetics, Harokopio University, Athens, Greece

Submitted 15 February 2005; accepted in final form 29 September 2005

Kavouras, Stavros A., Lawrence E. Armstrong, Carl M. Maresh,

Douglas J. Casa, Jorge A. Herrera-Soto, Timothy P. Scheett, JamesStoppani, Gary W. Mack, and William J. Kraemer. Rehydration withglycerol: endocrine, cardiovascular, and thermoregulatory responses dur-ing exercise in the heat. J Appl Physiol 100: 442450, 2006. Firstpublished October 6, 2005; doi:10.1152/japplphysiol.00187.2005.Theimpact of rehydration with glycerol on cardiovascular and thermoregu-latory responses during exercise in the heat was studied in eight highlytrained male cyclists. Each subject completed three dehydration-rehydra-tion experimental trials that differed only in the rehydration treatment,each separated by 7 days. Before each experimental day, subjects dehy-drated to4% of their body weight by exercise and water restriction. Theexperimental treatments were as follows: no fluid (NF), glycerol bolus (1g/kg body wt) followed by water (G), and water alone (W). Rehydration(3% body weight) was given over an 80-min period. After rehydration,subjects cycled (74% peak O2 uptake) to exhaustion in a hot and wet(37C and 48% relative humidity) environment. For G, plasma volumewas expanded (P 0.05) during rehydration and remained higher thanW (P 0.05) during exercise. Exercise time to exhaustion during G(33 4 min)was longer(P 0.05) compared with both W (27 3 min)and NF (19 3 min). Cutaneous vascular conductance was significantlyelevated (P 0.05) during G, but G provided no other thermoregulatory

or cardiovascular benefits compared with W and NF. Fluid-regulatinghormones (vasopressin, aldosterone, atriopeptin, and plasma renin activ-ity) decreased during rehydration and increased during exercise (exceptatriopeptin), but there were no differences between G and W. These dataindicated that glycerol had little or no major effect on fluid-regulatingfactors during rehydration or exercise, and the improved exercise capac-ity in G was likely due to a greater plasma volume during exercise.

fluid balance; plasma volume; osmoregulation; cycling; vasopressin

IT IS WELL ESTABLISHED THAT intense physical exercise in the heatincreases the risk of heat illnesses and decreases exerciseperformance, whereas significant dehydration can augmentthese responses (4, 17, 38, 43). Additionally, since the 1940s,

scientists have observed that, when people exercise in the heat,they become dehydrated, even if they have free access to water(38). It is generally accepted that dehydration is difficult toprevent during heavy training or competition in the heat (7). Inprolonged events and in some individuals with high sweatingrate, total body water loss may be as much as 8% of initialbody weight (3). This phenomenon has been described asinvoluntary dehydration (18). On the other hand, rapid fluid

and electrolyte restoration after exercise is a slow process thatrequires at least 3 h and 100% of fluid losses, along with asignificant amount of electrolytes (45).

However, ingesting a large volume of fluids, even in dehy-drated subjects, rapidly decreases arginine vasopressin (AVP),even before plasma volume or osmolality have been restored,leading to increased urinary output (12). Additionally, thirst

sensation decreases in response to plasma volume and osmo-lality restoration, mouth wetness, and oral-pharyngeal stimu-lation (33). For these reasons, rehydration is a major part of therecovery process after exercise, especially when individualsmust undertake repeated bouts of exercise-heat stress.

In 1987, glycerol, used with water, was first shown to inducehyperhydration more efficiently than water alone, and thiseffect persisted for 4 h (40). More recently, the effect ofglycerol-induced hyperhydration on fluid-regulating hormoneswas investigated (14). The authors demonstrated a small,nonsignificant increase in plasma vasopressin and no change incirculating aldosterone (Aldo) or atrial natriuretic factor. Theyreported that there may have been a direct glycerol effect on

the kidneys that increased fluid reabsorption and induced apositive fluid balance.Glycerol is a safe agent that does not approach toxic levels

when administered orally in doses of5 g/kg body wt (47).Glycerol also is an attractive compound for use in studies thatinvolve fluid balance and exercise, because it is not a majorenergy source during intense exercise (15, 32, 34, 37). Fur-thermore, glycerol-induced hyperhydration has been suggestedto 1) increase overall exercise performance (2, 9, 19) or time toexhaustion (36) in both temperate (36) and hot (2, 9, 19)environments; 2) increase sweat rate (28); 3) decrease heartrate (HR) (36) and rectal temperature (Tre) during moderate-intensity cycling exercise (2); and 4) last for 3248 h afterdosing (23). However, several other studies have shown no

performance (20, 29, 31, 48) or thermoregulatory benefit (9,19, 25, 26, 31, 36) following glycerol-induced hyperhydration.

The purpose of the present investigation was to examine theeffect of partial oral rehydration with glycerol on a subsequentexhaustive exercise test in the heat. Surprisingly, althoughthere is a vast amount of information on the role of glycerol asa hyperhydration agent, very limited information is availableon its effect in rehydration (44). We hypothesized that glycerol

Address for reprint requests and other correspondence: S. A. Kavouras,Laboratory of Nutrition and Clinical Dietetics, Dept. of Nutrition and Dietetics,Harokopio Univ., 70 El. Venizelou Av., Athens 17671, Greece (e-mail:[email protected]).

The costs of publication of this article were defrayed in part by the paymentof page charges. The article must therefore be hereby marked advertisementin accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

J Appl Physiol 100: 442450, 2006.First published October 6, 2005; doi:10.1152/japplphysiol.00187.2005.

8750-7587/06 $8.00 Copyright 2006 the American Physiological Society http://www.jap.org442


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would stabilize cardiovascular function, reduce heat stress, andenhance exercise capacity after partial rehydration.

MATERIALS AND METHODS

Subjects

Eight endurance-trained male cyclists agreed to serve as subjects in

this study. Their mean (SE) characteristics were as follows: age,24 1 (range 19 29) yr; body mass, 70.1 1 (range 66.773.6) kg;height, 181 2 (range 174185) cm; fat-free mass, 56.6 0.4 (range52.661.7) kg; and peak O2 uptake (VO2 peak), 61.4 0.8 (range58.965.9) ml kg1 min1. Subjects were selected after their phys-ical activity and medical history questionnaires were reviewed, with-out regard to race or ethnic origin. These men were heat acclimatized,trained regularly, competed in road cycling or mountain bike races,were nonsmokers, and reported no previous history of endocrine,cardiovascular, renal, or thermoregulatory disorders. All athletes hadcompleted their competitive season at least 2 mo before the study andwere on their training season. The study was approved by theInstitutional Review Board for Studies Involving the Use of HumanSubjects at the University of Connecticut, and all volunteers gave theirwritten, informed consent after attending an informational meeting

that addressed the study purpose, methods, and attendant risks andbenefits.

Preliminary Testing

Body composition. The hydrostatic weighing technique was used todetermine body density. Each subject performed the measurement atleast 20 times, on 2 separate days, before the actual data werecollected. Before this measurement, residual volume was calculatedbased on the vital capacity measured with a hand-held spirometer.Calculation of the percentage of body fat from body density was basedon the Brozek equation (6).

V O2 peak test. VO2 peak was determined in a thermocomfortableenvironment (27C) using an incremental resistance exercise test on amechanically braked cycle ergometer (Monark ergomedic 818E,Stockholm, Sweden). The exercise test consisted of continuous cy-

cling at a constant cadence (90100 rpm), while resistance increasedby 0.5 kp every 2 min until volitional exhaustion. Breath-by-breathanalysis of the expired gases during the test was performed with anopen-circuit respiratory apparatus (model CPXD, MedGraphics Car-diopulmonary Exercise System, St. Paul, MN). Two of the followingthree criteria were used to verify the attainment of VO2 peak: 1) noincrease in oxygen uptake (VO2; 150 ml/min) with an increase inergometer resistance, 2) HR 90% of predicted maximal value (i.e.,220 age), and 3) respiratory exchange ratio 1.1. The averageduration of the VO2 peak test was 10.01 0.96 min.

Experimental Protocol

Each subject completed three experimental trials, which differedonly with regard to rehydration. The rehydration treatments were asfollows: no fluid (NF), which served as a control; glycerol followed by

water (G), and water alone (W). To ensure double-blind design, anoncaloric, nonsodium, flavored powder (Kool-Aid, White Plains,NY) was added to both G and W drinks. The experimental treatments

were presented in a random sequence to avoid order effect and wereseparated by a minimum of 1 wk to prevent a carryover effect.Subjects were asked to maintain similar eating and training habitsduring the 3 days before each trial, verified by 3-day dietary intakeand physical training records.

Euhydration baseline. Subjects reported to the laboratory between1000 and 1200 in a euhydrated state, having ingested at least 30 ml/kgof their body weight of water (or other noncaffeinated fluids) duringthe previous day. After each subject emptied his bladder, urinespecific gravity (USG) was determined by refractometry to verifygood hydration status (1.020), and baseline euhydrated body weightwas recorded to 50 g (SRI, Instruments Precision Scales, Tonawanda,NY). Hydration status also was verified by plasma (Osm P 285295mosmol/kgH2O) and urine osmolality (Osmu 900 mosmol/kgH2O).The subjects entered the environmental chamber (model 2000, MinusEleven, Malden, MA; ambient temperature, 36.7 0.2C; relativehumidity, 48.0 1.2%) and sat for 20 min before a blood sample wastaken without stasis using a 20-gauge butterfly needle.

Dehydration. Following euhydration baseline, and for the remain-der of the day, subjects underwent fluid restriction and consumed foodlow in fluid content for lunch and dinner. Additionally, during theafternoon and evening of this day, subjects performed 2 h of low-

intensity cycling exercise to induce a body fluid loss equivalent to 4%of body weight. Dehydration baseline. The subject arrived at the laboratory 12 h

postprandial, emptied his bladder, and had body weight measured toverify the degree of dehydration. If dehydration was 3.5 or 4.5%,the experiment was canceled for that day (see Table 1). USG also wasrecorded to verify hypohydration. A 20-gauge, 32-mm indwellingTeflon catheter was inserted in an antecubital vein, and an extensiontube with a stopcock was attached to the catheter port for acquisitionof serial blood samples. The catheter was kept patent by flushingisotonic saline solution containing 20 heparin units/ml of solution.From that point on, the subject remained seated in a wheelchair.Subjects were taken into the environmental chamber (36.7 0.2C),and, after 20 min of equilibration, a blood sample (25 ml) was taken.

Rehydration. The subject, remaining in the wheelchair, was taken

from the environmental chamber and remained in a comfortableenvironment (27.3 0.3C) for 20 min to allow body fluids toequilibrate. A blood sample was then taken, and one of the threerandomly assigned, double-blind experimental trials began [i.e., NF(control), G, and W]. One-third of the rehydrating fluid was admin-istered during the first 15 min. The remaining two-thirds of the fluidwere administered in equal doses every 10 min, from minute 20 to 80of the rehydration period. The first dose for G consisted of a 20%glycerol and water solution (Penta Manufacturing, Livingston, NJ)that was administered as 1 g glycerol/kg body wt. For W, the first doseconsisted of aspartame-flavored water to mimic the sweetness of theglycerol solution. All other doses in G and W were identical andconsisted of water. A noncaloric, nonsodium, flavored powder (Kool-Aid) was added to both G and W to provide consistent sweetness,flavor, and color. All fluids were served chilled (10C). The total fluid

ingested was equal to 3% of the euhydrated body weight for eachsubject and was designed to partially rehydrate the subjects. Tenminutes following rehydration, subjects were taken back into the

Table 1. Indexes of fluid-electrolyte status during dehydration and rehydration

Trial

Euhyd Dhy-Base Rhy

Weight, kg USG Osmp, mosmol/kgH2O Weight, kg Dehydration, % USG Osmp, mosmol/kgH2O Fluid intake, ml

No fluid 71.31.3 1.0050.001 279.42.4 68.51.3 3.910.26 1.0280.02 289.42.4 0Glycerol 70.81.3 1.0050.001 280.11.6 68.01.2 3.860.17 1.0290.01 289.31.6 2,14830Water 71.81.1 1.0050.002 284.01.0 68.91.1 4.000.35 1.0290.01 291.61.0 2,14240

Values are means SE. Euhyd, euhydrated baseline; USG, urine specific gravity; Dhy-Base, dehydrated baseline; Osmp, plasma osmolality; Rhy, rehydration.

443REHYDRATION WITH GLYCEROL

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environmental chamber (36.7 0.2C) and sat quietly in the wheel-chair for 20 min before another 25-ml blood sample was obtained.

Exercise test. Following the blood sample, subjects sat on amechanically braked cycle ergometer (Monark ergomedic 818E). Seatheight was the same for all trials, and toe clips were used. Theexercise test (time to exhaustion expressed in minutes) consisted ofsteady-state cycling (74.0 1.1% VO2 peak) at 80100 rpm. Subjectscontinued cycling until one of the following criteria for termination

were met: inability to maintain cadence (decrease by 20 rpm),increase in Tre to 39.5C for 5 min, or signs or symptoms of heatexhaustion. The following ambient conditions were maintained in theclimatic chamber during exercise: 36.8 0.1C, 48.1 1.6% relativehumidity, and wind speed by fan of 2.54 m/s. All clocks and stop-watches were removed from subject view.

Tre and skin temperatures (Tsk) were recorded every 4 min,whereas HR was obtained at 2-min intervals during exercise. Arterialblood pressure, forearm skin blood flow (SkBF), VO2, carbon dioxideproduction (VCO2), respiratory quotient (R), respiratory rate (RR),pulmonary ventilation (VE), and cardiac output (Q) were measured at0, 5, 15, 30, 45, and 60 min of exercise. Blood samples (5 ml) weretaken at 0, 5, 15, 30, 45, and 60 min of exercise, and a final bloodsample (25 ml) was drawn immediately after the end of exercise.

Thermoregulatory measurements. Tre was measured by using a

rectal thermistor (model 401, Yellow Springs Instruments, YellowSprings, OH) inserted 10 cm past the external anal sphincter. T sk wererecorded via skin thermistors (model 409, Yellow Springs Instru-ments) at four sites: chest, triceps, thigh, and calf. Mean-weighted T skwas calculated according to the equation of Ramanathan [T sk 0.2(Tchest Ttriceps) 0.3 (Tthigh Tcalf), where T is temperature] (39).Forearm SkBF was measured for 2 min with a laser Doppler flow-meter for microvascular perfusion (model Periflux PF2B, Perimed,Stockholm, Sweden). During the measurement, subjects rested theirforearm in a neutral position with 90 flexion of the elbow. Data wereexpressed as cutaneous vascular conductance (CVC) by dividingSkBF, in volts, over mean arterial pressure (MAP), in 100 mmHg.Whole body sweat rate during exercise was calculated from bodyweight changes, corrected for estimated respiratory water losses (35),blood sample volume, and urine output.

Cardiovascular variables. HR was measured by a lead I configu-ration, using a telemetric cardiotachometer (model Vantage XL, PolarElectro). Breath-by-breath analysis of the expired gases was per-formed with an open-circuit respiratory apparatus (model CPXD,MedGraphics Cardiopulmonary Exercise System) to determine VO2,VCO2, R, RR, and VE. Q was measured via CO2 rebreathing, employ-ing the exponential method (1, 10). VO2 and VCO2 were measured, asdescribed above, for 3 min before each rebreathing procedure. Tocalculate stroke volume (SV), HR was recorded just before the onsetof the rebreathing technique. Arterial systolic (SBP) and diastolicblood pressures (DBP) also were measured with an aneroid sphyg-momanometer and stethoscope. MAP was calculated as shown in thefollowing formula: MAP (SBP DBP)/3 DBP.

Blood collections. All blood samples were drawn without stasis atthe points described above. From the 5-ml blood samples, a 4-ml

aliquot was transferred to a test tube containing lithium heparin todetermine OsmP, plasma sodium concentration ([Na

]P), plasmapotassium concentration, plasma glucose concentration, plasma lac-tate concentration, total plasma proteins (TPP), and plasma Aldoconcentration ([Aldo]P). The remaining aliquot (1 ml) was analyzedimmediately for hematocrit (Hct) and hemoglobin (Hb). From the25-ml blood sample, a 5-ml aliquot was treated as just described.From the remaining sample, a 7-ml aliquot was transferred into anEDTA-treated test tube for plasma AVP ([AVP]P) and glycerol([Glyc]P) analysis. A separate 5-ml aliquot was transferred into achilled EDTA-treated test tube that contained 2,000 kallikrein-inhib-itor units of aprotinin (Sigma Diagnostics, St. Louis, MO) for plasmaatriopeptin ([AP]P) analysis. An 8-ml aliquot was transferred into achilled EDTA-treated tube for plasma renin activity (PRA) analysis.

These samples were centrifuged immediately at 1,800 g and 4C for12 min. Plasma samples for hormonal assays were refrigerated at80C for later analysis.

Blood and urine analyses. USG and TPP were measured byrefractometer (model A300CL, Spartan). Hct was determined intriplicate from whole blood by the microcapillary technique, follow-ing centrifugation for 4 min at 9,500 g. No corrections were made fortrapped plasma or for peripheral venous sampling. Hb was measured

in triplicate from whole blood with the cyanmethemoglobin technique(Sigma Diagnostics). Percent changes in plasma volume were calcu-lated with the following formula (11):

PV 100HbB/HbA1 HctA/100/1HctB/100 100

where PV is percent change of plasma volume, subscript B is before(control), and subscript A is after (experimental). OsmP and OsmUwere determined in duplicate by freezing point depression the sameday (model 3DII, Advanced Digimatic Osmometer, Norwood, MA).[Na]P and plasma potassium concentration were determined byion-sensitive electrodes on fresh plasma samples (model 984-S, AVLScientific, Roswell, GA). Plasma glucose and lactate concentrationswere determined in triplicate with an enzymatic technique (model2003, Yellow Springs Instruments). [Glyc]P was measured in dupli-

cate with a colorimetric technique (Sigma Diagnostics). [AVP]P wasdetermined by a commercially available radioimmunoassay kit (Ni-chols Institute, San Juan Capistrano, CA). The within- and between-assay coefficients of variation for [AVP]P at midrange (13 pg/ml)were 1.8 and 5.8%, respectively. The sensitivity of the assay and theaverage extraction recovery were 1.3 pg/ml and 63.8%, respectively.PRA was evaluated in duplicate by radioimmunochemical determina-tion of plasma angiotensin I, generated during 1 h of incubation at pH6.0 (Incstar, Stillwater, MN). The within- and between-assay coeffi-cients of variation of this assay at midrange (1.2 ng l1 s1) were 4.6and 4.8%, respectively. The sensitivity of the assay was 0.05ng l1 s1. [AP]P was determined by a radioimmunoassay technique(Peninsula Laboratories, Belmont, CA), after extraction on octadecyl-silane C18 cartridges (Sep-Pak C18, Waters Associates, Milford, MA).The coefficient of variation of the assay was 5%. [Aldo]P was

determined with a radioimmunoassay technique (Coat-A-Count, Di-agnostic Products, Los Angeles, CA) that had a within-assay coeffi-cient of variation for the mid- (395 pmol/l) and the high-range (1,020pmol/l) of 3.3 and 1.9%, respectively. The sensitivity of the assay was44 pmol/l. To reduce interassay variations, each subjects plasmasamples were analyzed within the same assay run. All hormonalanalyses were performed in duplicate.

Statistical Analysis

Statistical evaluation of the data was accomplished with atwo-way analysis of variance with repeated measures (treatment time). Significant differences between the means were determined byNewman-Keuls post hoc test. Statistical differences were determinedat the P 0.05 level of confidence. All values were reported asmeans SE.

RESULTS

Hydration indexes, hydration status, and amount of fluidingested by the subjects are presented in Table 1. The euhy-drated body weight and fluid status of subjects before eachtrial, the degree of dehydration achieved, pretest USG, andOsmP after dehydration did not differ significantly (P 0.05).The amount of fluid ingested during G and W was almostidentical. During rehydration, urine output for the NF, G, andW were 0, 138 63, and 523 93 ml, respectively. It shouldbe noted that, during G, only two subjects were able to urinate.As a result of the urine output, although the amount of fluid

444 REHYDRATION WITH GLYCEROL



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intake was the same, hydration levels before the beginning ofexercise were 4.06, 0.89, and 1.37% for NF, G, and W,respectively. No statistically significant differences were foundin urine output or level of hydration between G and W beforethe beginning of exercise. The dehydration levels at the end ofthe exercise were greater in NF (5.5 0.3%) compared withG (3.3 0.4%) and W (3.4 0.4%), whereas no differ-

ences were found between G and W. Because volunteersexercised more during G, it seems that the rate of dehydrationis likely reduced during the G trial. Urine output after exercisefor NF (118 20 ml) was significantly lower (P 0.05) thanfor G (205 32 ml) and W (336 112 ml), but was notdifferent between G and W.

None of our subjects reported nausea, headache, or gastro-intestinal problems during, or the 24 h following, G. Onesubject was stopped by the investigators during the G exercisetest (time: 51 min and 45 s), as his core temperature reached39.5 for 5 min (see criteria for termination in ExperimentalProtocol section).

Exercise time to exhaustion during G (32.5 3.8 min) was19% longer than during W (27.1 3.3 min) and 72% longerthan during NF (18.9 2.7 min). Whereas seven out of theeight subjects exercised longer in G than in W, all subjectsexercised longer in G and W than in NF. However, no differ-ences were observed among the three trials for VO2, R, VE, orRR, both at rest and during exercise (Table 2).

Plasma Responses

Glycerol ingestion significantly increased (P 0.05)[Glyc]P by 100 times (from 0.06 0.01 to 9.94 0.23

mmol/l) above NF (from 0.06 0.01 to 0.08 0.02 mmol/l)and W (from 0.06 0.01 to 0.11 0.04 mmol/l). Glycerolrehydration induced a higher level of OsmP than W at 0, 10,and 15 min of exercise and immediately postexercise (Fig. 1).However, [Na]P was lower (P 0.05) during G than W.[Na]P during exercise was significantly higher for NF (P 0.05) than both G and W (Fig. 1). TPP also was higher before

and during exercise during NF (vs. G and W). Rehydrationwith glycerol significantly increased plasma volume (vs. Wand NF; P 0.05), and those differences were maintainedthroughout the exercise test (Fig. 1). Plasma glucose did notchange significantly during any of the trials (Table 2), but washigher than the 15-min value during all trials. However, at 15min of exercise and immediately postexercise, plasma glucosewas significantly higher during NF compared with G and W.During NF, plasma lactate was higher than G and W at 15 minof exercise, whereas immediately postexercise this was trueonly compared with G (Table 2).

Cardiovascular Responses

Q

was maintained to a similar level from 5 min (NF: 21.0 0.8, W: 20.6 0.9, and G: 21.4 0.8 l/min) to 15 min ofexercise (NF: 20.0 0.7, W: 21.0 0.9, and G: 20.5 0.8l/min) for all trials. HR responses during exercise (Fig. 2) werenot different between the G and W trials (P 0.05). However,during the first 15 min of NF, HR was significantly higher thanboth the G and W values. HR at the end of the exercise test didnot differ among trials. The SV at 15 min of exercise (Fig. 2)for NF was significantly (P 0.05) lower than the G and W.During the G, there was a slight trend to maintain a higher SV

Table 2. Selected measurements at Dhy-Base, preexercise, and 5, 15, and 30 min of exercise

Variable Title Dhy-Base Preexercise 5 min 15 min

End (Post-Ex for

Glucose, Lactate, and Glycerol)

VO2, l/minNo fluid 0.450.03 3.170.12 3.130.12 3.170.12Glycerol 0.530.06 3.190.11 3.250.10 3.200.11Water 0.470.03 3.210.12 3.230.11 3.200.12

RNo fluid 0.810.04 0.970.02 0.990.02 0.980.02Glycerol 0.800.05 0.970.02 0.970.02 0.970.02Water 0.810.04 0.990.02 0.960.02 0.980.02

VE, l/minNo fluid 14.01.2 91.45.3 108.06.5 99.25.1Glycerol 15.72.5 86.74.5 98.44.7 95.34.1Water 14.81.6 93.05.5 103.26.5 99.15.8

MAP, mmHgNo fluid 84.01.7 89.63.1 90.73.5 90.53.1Glycerol 82.42.7 90.02.1 88.02.8 85.82.9

Water 85.62.0 92.23.7 89.13.8 87.63.8RR, breaths/min

No fluid 172 424 524 464Glycerol 172 373 454 444Water 172 404 484 454

Plasma glucose, mmol/lNo fluid 4.90.2 4.80.1 4.90.2 6.40.4 8.00.5Glycerol 4.80.1 5.00.1 4.90.2 5.40.4* 6.80.8*Water 5.00.1 4.70.1 4.90.1 5.50.4* 7.00.5

Plasma lactate, mmol/lNo fluid 1.00.1 1.00.0 5.11.0 8.82.0 7.91.7Glycerol 1.00.1 1.30.1 4.50.9 6.81.3* 6.81.5*Water 1.00.1 1.10.1 5.21.0 7.31.9* 7.51.8

Values are means SE. VO2, oxygen uptake; R, respiratory quotient; VE, pulmonary ventilation; MAP, mean arterial pressure; RR, respiratory rate; End, endof exercise; Post-Ex, postexercise. Significantly different from *no fluid and preexercise value: P 0.05.




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than for W, but the difference was not statistically significant.We were unable to collect enough Q data after 15 min, sinceseveral subjects stopped exercising before the 30-min mark.

Thermoregulatory Responses

Tre (Fig. 3) was significantly elevated (P 0.05) during NFcompared with G and W at 0, 4, 8, and 12 min of exercise. Tsk(Fig. 3) was significantly higher before the beginning ofexercise in NF, but not different during exercise. SkBF andCVC were similar among the three experimental trials imme-

diately before the exercise test (Fig. 4). During exercise,however, both SkBF and CVC were significantly higher (P 0.05) during G vs. W and NF. Sweating was higher ( P 0.05)during G and W (G: 1,426 152 ml and W: 1,395 128 ml)than NF (798 72 ml).

Hormonal Responses

[AVP]P was significantly decreased after rehydration duringG and W, but increased (P 0.05) in response to exercise forall of the trials. The postexercise level of vasopressin for NFwas significantly higher (P 0.05) than for G and W (Fig. 5).[AP]P level was similar before rehydration and did not changeduring rehydration and exercise (Fig. 5).

Fig. 1. Plasma osmolality (OsmP), plasma sodium concentration ([Na]P),total plasma proteins (TPP), and percent change of plasma volume (PV) atdehydrated baseline (Dhy-Base), during, and immediately postexercise (Post-Ex). Rhy, rehydration. Values are means SE. Significantly different from*no fluid and water: P 0.05.

Fig. 2. Heart rate (HR) and stroke volume (SV) responses during exercise.Values are means SE. *Significantly different from no fluid: P 0.05.




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PRA (Fig. 6) decreased during rehydration for G and W andincreased significantly (P 0.05) at the end of exercise (vs.preexercise) in all experimental conditions. No differenceswere found among the different trials. [Aldo]P was greater(P 0.05) after exercise (vs. preexercise) for all trials. At theend of exercise, [Aldo] was lower (P 0.05) in NF than W andG (Fig. 6).

DISCUSSION

This study examined the endocrine, thermoregulatory, andcardiovascular responses to exercise in the heat after oral

rehydration with glycerol. We hypothesized that rehydrationwith glycerol (G trial) would prolong exercise time to exhaus-tion, elicit greater cardiovascular stability, and lower thermo-regulatory strain compared with NF or W trials. Rehydrationwith glycerol did prolong exercise time to exhaustion in theheat. However, this improved exercise capacity in the heat withglycerol rehydration was not associated with any clear thermo-regulatory or cardiovascular advantage compared with rehy-dration with water only. Although glycerol rehydration re-sulted in a higher SkBF during exercise in the heat, theenvironmental conditions prevented any heat loss by radiationor convection. As such, the improved SkBF had no thermo-regulatory impact.

Similar improvements in exercise time to exhaustion havebeen observed in the only other study in which glycerol wasused as a rehydration agent (44), as well as in a hyperhydrationstudy (36). Increase in exercise performance has been observedin some studies that utilized glycerol-induced overhydrationbefore exercise (2, 9, 19), whereas others reported no perfor-mance improvement (20, 29, 31, 48). Although previous glyc-

erol-induced overhydration studies have reported gastrointes-tinal discomfort, headaches, or even blurred vision (9, 25, 26),in our study, none of the subjects experienced any of thosesymptoms during G or the 24 h following the study. Theabsence of side effects has been also shown by others (27, 36,40), and it has been speculated that high-concentration glycerolsolutions (i.e., 50%) are likely to induce these symptoms.

Although rehydration during G did not induce a statisticallysignificant better fluid balance compared with W, the smalldifference in hydration (due to smaller urinary output) mayhave provided physiologically greater body water availabil-ity during the glycerol trial. Furthermore, since volunteersexercised more during G but sweated similarly with W, wefound that the rate of dehydration was reduced. Glycerol, onthe other hand, is a solute that increases the tonicity of blood,and, although 2 liters of water were consumed, the 100-fold

Fig. 4. Skin blood flow (SkBF) and cutaneous vascular conductance (CVC) inthe forearm. Values are means SE. Significantly different from *no fluid,water, and 0-min value: P 0.05.

Fig. 3. Rectal temperature (Tre) and mean weighted skin temperature (Tsk)during exercise. Values are means SE. Significantly different from *no fluid

trial and 0-min value: P 0.05.




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increase in plasma glycerol (Table 2) led to maintenance of thedehydration-induced elevation of Osmp. This osmotic effect,along with a slight improvement in hydration level, couldinduce the increased plasma volume observed during G com-pared with W. A similar response of plasma volume has beenreported in other glycerol studies when plasma volume changeswere calculated from Hct and Hb values, like in the presentstudy (21, 29, 37, 44), or with Evans blue dilution technique (21).

Both Montner et al. (36) and Anderson et al. (2) indicatedthat glycerol-induced hyperhydration maintained HR at a lowerlevel than a placebo. In the present study, although plasma

volume for G was always greater than that for W, HR, V O2,blood pressure, and SV were not significantly different (G vs.W), although SV showed a nonsignificant trend to be higherduring G (Fig. 2). It should be noted that we were unable tomeasure SV for all subjects after 15 min of exercise, since fewof the volunteers managed to reach the 30-min time point atwhich the CO2 rebreathing maneuver was performed for theSV estimation (NF: 1, G: 5, and W: 3 subjects). We speculatethat SV would have been higher in the G compared with W andNF at a later exercise stage, when cardiovascular strain waslikely greater. Based on the first 15 min of exercise, our dataare in agreement with a previous study by Latzka et al. (26), inwhich glycerol-induced hyperhydration before uncompensable

exercise-heat stress offered no cardiovascular advantage com-pared with water-induced hyperhydration.

It was hypothesized that glycerol-related ergogenicity couldenhance thermoregulatory responses, despite the fact that moststudies have not reported thermoregulatory benefits (9, 19, 36,44). In the present study, because the environmental tempera-ture was always higher than the Tsk, sweat evaporation was the

only means of heat dissipation. In contrast to the work of Lyonet al. (28), which reported that glycerol-induced hyperhydra-tion increased sweating and decreased exercise core tempera-ture, no difference was found in the sweat rates of W and G.

Glycerol is a gluconeogenic substance that can be metabo-lized in the liver and provides energy. Studies in experimentalanimals have shown that rats fed with high doses of glycerolperformed better: they were protected from hypoglycemia andexhibited both liver and muscle glycogen sparing (46). Thisfinding was not reported for humans, during 90 min of contin-uous running (34), cycling to exhaustion for 90 min (15), oreven cycling to exhaustion (8092 min) following a 36-h fast(32). These data suggest that the human liver may not be ableto metabolize glycerol fast enough to provide sufficient energyduring intense exercise. Similarly, we found no differencesbetween G and W in plasma glucose, lactate, VO2, and R,indicating that glycerol did not contribute substantially as anenergy substrate.

Fig. 6. Plasma renin activity (PRA) and aldosterone concentration ([Aldo]P)responses to rehydration and exercise. Values are means SE. Significantlydifferent from *no fluid, Dhy-Base value, and preexercise value: P 0.05.

Fig. 5. Plasma arginine vasopressin concentration ([AVP]P) and atriopeptinconcentration ([AP]P) responses to rehydration and exercise. Values aremeans SE. Significantly different from *no fluid, Dhy-Base value, andpreexercise value: P 0.05.




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In the present study, glycerol ingestion (G) altered fluid-regulating hormone responses to exercise in the heat (AVP,AP, and Aldo) and PRA in ways that were not observed whenwater alone was consumed (W). Glycerol increased OsmP;therefore, we expected a consequent increase in plasma AVP(42) (i.e., osmoreceptors are potent stimulators of AVP), de-spite a plasma volume increase that could otherwise hamper

AVP secretion (41). We also considered the observation thatthe supraoptic and paraventricular nuclei of the hypothalamusare more sensitive to sodium than to substances like glycerol,glucose, or urea (14). At the end of exercise during the NF trial,however, AVP was approximately three times greater than Gand W, likely because of a dehydration-induced hyperosmotic-hypernatremic hypovolemia (22, 30).

AP tended to decrease with rehydration and increase inresponse to exercise (P 0.05). This may have occurredbecause plasma AP increases in response to atrial stretch (16).Freund et al. (13) reported an increased [AP]P as a result ofmaximal exercise in both trained and untrained subjects,whereas Kraemer et al. (24) reported that submaximal exercise(71% maximum VO2) did not alter [AP]P. In the present study,AP remained unchanged during exercise, suggesting that sub-maximal exercise in the heat, with or without glycerol, is not apotent secretory stimulus. In agreement with this finding,Freund et al. (14) showed that glycerol did not affect ANP andother fluid-regulating hormones.

PRA decreased during both rehydration conditions (P 0.05), whereas Aldo did not change significantly. In responseto exercise, both PRA and Aldo increased significantly aspreviously reported (8), but no changes were found among thetrials. Brandenberger et al. (5) also observed that the initialstate of hydration does not affect exercise-induced responses ofAldo and PRA.

In conclusion, this study supported the hypothesis that re-

hydration with glycerol increased exercise time to exhaustionduring intensive cycling in the heat, likely by maintaininggreater plasma volume. Glycerol did not provide significantcardiovascular or thermoregulatory advantages, although CVCwas significantly increased. Furthermore, glycerol did not havea significant effect on fluid-regulating hormones, before orduring exercise.

ACKNOWLEDGMENTS

The authors gratefully acknowledge the technical assistance of Frank T.Hacker Jr., Dr. Tabbatha Elliott, Dr. NiCole Keith, Dr. Melissa Roti, CostasAnastasiou, Timothy Bilodeau, David Blair, Sheri Huckleberry, Jeff Mace, andJason Sutherland. We also thank all of our subjects for their cooperation.

GRANTS

The study was partially supported by General Nutrition, Pittsburgh, PA; theUniversity of Connecticut Research Foundation, Storrs, CT; and NationalHeart, Lung, and Blood Institute Grant HL-39818.

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