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J Appl Physiol 97: 39-44, 2004. First published February 27, 2004; doi:10.1152/japplphysiol.00956.2003
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Effect of hydration status on thirst, drinking, and related hormonal responses during low-intensity exercise in the heat

C. M. Maresh,1,2,3 C. L. Gabaree-Boulant,1 L. E. Armstrong,1,2,3 D. A. Judelson,1 J. R. Hoffman,1 J. W. Castellani,1 R. W. Kenefick,1 M. F. Bergeron,1 and D. J. Casa1

1Human Performance Laboratory, Department of Kinesiology, 2Department of Physiology and Neurobiology, and 3Department of Nutritional Sciences, University of Connecticut, Storrs, Connecticut 06269

Submitted 4 September 2003 ; accepted in final form 20 February 2004


   ABSTRACT
TOP
 ABSTRACT
METHODS
 RESULTS
 DISCUSSION
 GRANTS
 ACKNOWLEDGMENTS
 REFERENCES
 
During exercise-heat stress, ad libitum drinking frequently fails to match sweat output, resulting in deleterious changes in hormonal, circulatory, thermoregulatory, and psychological status. This condition, known as voluntary dehydration, is largely based on perceived thirst. To examine the role of preexercise dehydration on thirst and drinking during exercise-heat stress, 10 healthy men (21 ± 1 yr, 57 ± 1 ml·kg–1·min–1 maximal aerobic power) performed four randomized walking trials (90 min, 5.6 km/h, 5% grade) in the heat (33°C, 56% relative humidity). Trials differed in preexercise hydration status [euhydrated (Eu) or hypohydrated to –3.8 ± 0.2% baseline body weight (Hy)] and water intake during exercise [no water (NW) or water ad libitum (W)]. Blood samples taken preexercise and immediately postexercise were analyzed for hematocrit, hemoglobin, serum aldosterone, plasma osmolality (Posm), plasma vasopressin (PAVP), and plasma renin activity (PRA). Thirst was evaluated at similar times using a subjective nine-point scale. Subjects were thirstier before (6.65 ± 0.65) and drank more during Hy+W (1.65 ± 0.18 liters) than Eu+W (1.59 ± 0.41 and 0.31 ± 0.11 liters, respectively). Postexercise measures of Posm and PAVP were significantly greater during Hy+NW and plasma volume lower [Hy+NW = –5.5 ± 1.4% vs. Hy+W = +1.0 ± 2.5% (P = 0.059), Eu+NW = –0.7 ± 0.6% (P < 0.05), Eu+W = +0.5 ± 1.6% (P < 0.05)] than all other trials. Except for thirst and drinking, however, no Hy+W values differed from Eu+NW or Eu+W values. In conclusion, dehydration preceding low-intensity exercise in the heat magnifies thirst-driven drinking during exercise-heat stress. Such changes result in similar fluid regulatory hormonal responses and comparable modifications in plasma volume regardless of preexercise hydration state.

aldosterone; osmolality; renin activity; vasopressin

CONTINUOUS EXERCISE IN THE heat challenges the body's thermoregulatory systems. Hypohydration, a potential result of exercise in the heat, also influences thermoregulation (31, 33), limiting effective temperature maintenance (35). The extent to which thermoregulation is adversely affected dictates the physiological responses, from decrements in physical performance to thermal injury and, in severe cases, even death (21).

Under resting conditions, hypohydration is normally balanced and prevented by increases in thirst-driven drinking, which adequately stimulates fluid intake (17). Physiologically, thirst results from increases in the osmotic pressure of extracellular fluid (37) and is closely tied to several fluid-regulating hormones. During exercise, however, the human thirst mechanism may be insufficient. Despite exercise-induced increases in extracellular osmotic pressure, blood osmolality, and angiotensin II [a powerful dipsogen (32)], enhanced thirst may not sufficiently promote fluid intake to maintain water balance, a phenomenon known as "voluntary dehydration" (42). Despite free access to fluids, exercising subjects voluntarily replace only 66–75% of their net water loss (5, 19, 22, 31).

Repeated days of prolonged low-intensity exercise in a hot, humid environment represent a real-life occupational or recreational scenario for many adults. In examining this situation, our laboratory previously reported that preexercise hypohydration and the corresponding elevations in plasma osmolality (Posm) resulted in a substantial water intake during exercise that increased body mass by 0.9% and attenuated the rise in rectal temperature (Tre) via favorable changes in Posm and sweat sensitivity (4). Although research has examined the relationship between hormonal response to exercise-heat stress and hydration status (6, 7, 14, 24), the relationships among thirst, fluid intake, and hydration status (12), and the relationship between plasma volume (PV) and hormonal response to exercise-heat stress (16, 34), none has considered all these factors simultaneously. Therefore, the purpose of this study was to examine the effect of hydration status on perceived thirst, drinking, plasma volume, and hormonal responses during low-intensity exercise in the heat. Measures of circulatory and thermal strain obtained concomitant with this study have been published elsewhere (4). We hypothesized that fluid deprivation would stimulate thirst-driven drinking during exercise, favorably altering hormonal and circulatory measures of exercise-heat stress.


   METHODS
TOP
 ABSTRACT
 METHODS
RESULTS
 DISCUSSION
 GRANTS
 ACKNOWLEDGMENTS
 REFERENCES
 
Subjects and prestudy requirements.   Ten healthy men participated in this study [age = 21 ± 1 yr, height = 174.5 ± 2.1 cm, mass = 72.7 ± 1.1 kg, percent body fat = 12.8 ± 1.0%, maximal aerobic power (O2 max) = 57 ± 1 ml·kg–1·min–1] that was approved by the University of Connecticut Institutional Review Board and conformed to 45CRF46. Subjects were nonsmokers with no history of endocrine and/or thermoregulatory disorders. Before beginning the study, subjects were briefed on potential risks and benefits, signed a written informed consent, and completed a medical history and allergy questionnaire. Additionally, body mass (model 700M, SR Instruments, Tonawanda, NY), height (GPM, Zurich, Switzerland), skinfold thickness (11), and O2 max were determined. The O2 max protocol was a modification of that described by Costill and Fox (9). Briefly, after a 3-min warm-up (5.6 km/h), subjects ran at 12.1 km/h; every 2 min, treadmill grade was increased 2% until the subject reached volitional exhaustion. Specific criteria ensured attainment of O2 max (38).

To reduce individual variability associated with exercise-heat exposure, subjects exercised on 4 consecutive days in a hot environment (preliminary exercise-heat exposure sessions) before (5.5 ± 0.6 days) the experimental trials (4). During these sessions, subjects cycled (model 818E, Monark, Stockholm, Sweden) at 47 ± 2% O2 max for ~90 min in hot conditions (33 ± 1°C, 64 ± 8% relative humidity). Heart rate (HR) (UNIQ, Computer Instrument, Hempstead, NY) and Tre were continuously measured via a lead I configuration and a thermistor (model 43TF, 400 series probe, Yellow Springs Instruments, Yellow Springs, OH) inserted 10 cm beyond the external anal sphincter, respectively. Drinking was permitted ad libitum and encouraged. During each session, subjects wore shorts, T-shirt, socks, and running shoes. If a subject's HR or Tre exceeded 180 beats/min or 39.5°C, respectively, for 5 min, exercise was stopped. Even if exercise ceased, subjects remained in the chamber for the full 90 min.

Experimental design.   Subjects completed four experimental trials differing in preexercise hydration status [euhydrated (Eu) or hypohydrated (Hy)] and water intake during exercise [water ad libitum (W) or no water (NW)]. Trial order was randomized; a minimum of 72 h separated each trial. All sessions for a given subject were standardized for time of day. For Eu trials, euhydration was ensured by instructing subjects to drink 474 ml of water the evening before and 474 ml water the morning of those trials (4). For Hy trials, subjects dehydrated (–3.5 ± 0.2% body weight) the day before by several hours (3.2 ± 0.4 h) of intermittent exercise (cycling and/or walking) while wearing a cotton sweat suit and running shoes. Body masses were obtained immediately before and routinely throughout the dehydration protocol. Once the desired reduction in body mass (–3%) was attained, subjects refrained from fluid consumption until permitted to drink the next day. Additionally, subjects refrained from eating during the 4 h preceding trials. The 17.5 ± 1.1-h period between the dehydration protocol and the subsequent experimental trial amply allowed for equilibration of body fluids (4). During one Eu and one Hy trial, subjects drank water ad libitum during exercise (Eu+W and Hy+W, respectively); during the other Eu and Hy trial, drinking was prohibited (Eu+NW and Hy+NW, respectively). All four experimental trials for each subject were completed within 20.0 ± 1.0 days of his last preliminary exercise-heat exposure session.

Experimental protocol.   On arrival to the laboratory, subjects provided a urine sample and body mass was measured (wearing shorts and socks). To assess hydration status, urine specific gravity was determined in triplicate via refractometer (model A300CL, Spartan, Tokyo, Japan) and later verified by the preexercise Posm value. A urine specific gravity <1.020 and Posm between 280 and 287 mosmol/kgH2O indicated euhydration (3). A 20-gauge Teflon cannula (Critikon, Tampa, FL) was then inserted into a superficial forearm vein and a male luer-adaptor (model 5877, Abbott Hospital, Chicago, IL) was attached to the cannula to acquire subsequent blood samples. The cannula was kept patent with isotonic saline. After placement of the cannula, subjects stood quietly for 20 min in the environmental chamber, after which the first experimental blood sample (Pre) was drawn.

Subjects then walked on a motor-driven treadmill for 90 min at 5.6 km/h at 5% grade in hot conditions (33 ± 0°C and 55.6 ± 2.7% relative humidity). Treadmill speed was repeatedly verified by application of a tachometer (model 8204–20, Cole-Parmer Instrument, Chicago, IL) to the moving treadmill belt. Several circulatory and thermoregulatory measures were also obtained during exercise; details of these findings have been reported elsewhere (4).

At the completion of exercise, body mass was measured. Immediately (IP; within 1 min) after exercise completion, blood samples were drawn. All blood samples were obtained without stasis and transferred to plain, chilled EDTA, or chilled heparinized tubes. Hematocrit (Hct), hemoglobin (Hb), and Posm were evaluated immediately after blood sampling. All other blood samples were centrifuged, aliquoted, and frozen (–90°C) until subsequent analysis.

Thirst scale.   Concomitant with blood draws (Pre and IP), subjects were asked to numerically identify their perceived thirst by using a 9-point thirst scale with verbal anchors ranging from 1 ("not thirsty at all") to 9 ("very, very thirsty") (23).

Blood analysis.   Hct was assessed in triplicate via microcapillary technique after 4 min of centrifuging at 9,500 g. Values were not corrected for trapped plasma. Hb was ascertained in duplicate via an enzymatic, photometric technique (Reflotron, Boehringer Mannheim Diagnostics, Indianapolis, IN). Percent changes in PV were calculated from Hct and Hb values (10). Posm was evaluated in duplicate via freezing-point depression (model 5004, Precisions Systems, Natick, MA).

After extraction on silica columns (Incstar, Stillwater, MN), plasma arginine vasopressin (PAVP) was determined in duplicate via a commercially available radioimmunoasssay kit (Incstar). Extraction recovery was 91.3%. Assay sensitivity was 0.65 x 10–3 fmol/l. The within- and between-assay coefficients of variation were 5.6 and 12.7%, respectively. Plasma renin activity (PRA) was ascertained in duplicate via radioimmunochemical determination of plasma angiotensin I generated during 1 h of incubation at pH 6.0 (Incstar). Assay sensitivity was 0.018 ng·100 µl–1·h–1. The within- and between-assay coefficients of variation were 4.1 and 10.9%, respectively. Serum aldosterone (SAld) was evaluated in duplicate via radioimmunoassay (Diagnostics Products, Los Angeles, CA). Assay sensitivity was 44.4 pmol/l. The within- and between-assay coefficients of variation were 4.2 and 8.3%, respectively.

Statistics.   Data were analyzed via a repeated-measures analysis of variance (condition x time). Significant F-ratios were further evaluated with a Fisher's post hoc test. Statistical significance was set at P < 0.05. Values reported are means ± SE.


   RESULTS
TOP
 ABSTRACT
 METHODS
 RESULTS
DISCUSSION
 GRANTS
 ACKNOWLEDGMENTS
 REFERENCES
 
Body mass, Posm, perceived thirst, water intake, sweat loss, and PV.   Body mass data are shown in Table 1. The dehydration protocol successfully decreased body mass, as preexercise body mass measures before the exercise protocol during Hy trials were significantly lower than corresponding Eu trials. During Eu+NW, Eu+W, and Hy+NW, body mass significantly fell from pre- to postexercise. During Hy+W, however, body mass significantly increased during the exercise, causing the postexercise body mass to be statistically greater after Hy+W than after Hy+NW.


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  		Table 1. Body mass measurements before and after the dehydration and exercise protocols

 
Posm and perceived thirst responses are presented in Fig. 1. Pre Posm and perceived thirst were higher in both Hy conditions (Hy+NW: Posm = 296 ± 3 mosmol/kgH2O, perceived thirst = 5.47 ± 0.76; Hy+W: Posm = 295 ± 2 mosmol/kgH2O, perceived thirst = 6.65 ± 0.65) than Eu trials (Eu+NW: Posm = 287 ± 2 mosmol/kgH2O, perceived thirst = 2.00 ± 0.35; Eu+W: Posm = 287 ± 2 mosmol/kgH2O, perceived thirst = 1.59 ± 0.41). At IP, Posm and perceived thirst were greater in Hy+NW than all other treatments.



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  		Fig. 1. Group mean (± SE) plasma osmolality (A) and perceived thirst (B) responses. Eu, preexercise euhydration; HY, prexercise hypohydration to –3.8 ± 0.2% baseline body weight; NW, no water during exercise; W, water ad libitum during exercise; Pre, preexercise; IP, immediately postexercise. *Significant difference compared with all other values at the same time point and compared with corresponding Pre values, P < 0.05. {dagger}Significant difference compared with both Eu values at the same time point, P < 0.05.

 
During Hy+W, subjects drank more (1.65 ± 0.18 liters) and more frequently (3.5 ± 0.7 drinks) than during Eu+W (0.31 ± 0.11 liter and 1.5 ± 0.9 drinks, respectively). Sweat loss was stable and similar during all treatments (Hy+NW = 1.01 ± 0.05 kg, Hy+W = 0.96 ± 0.05 kg, Eu+NW = 0.94 ± 0.04 kg, Eu+W = 0.96 ± 0.04 kg). Hb, Hct, and changes in PV are shown in Table 2. The percent change in PV significantly decreased at IP in Hy+NW. For all other conditions, PV was stable and similar throughout.


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  		Table 2. Hemoglobin, hematocrit, and PV changes

 
Fluid-regulating hormones.   PAVP responses are presented in Fig. 2. Hy conditions showed a nonsignificant trend toward increased baseline PAVP. PAVP for Eu+W was statistically greater at IP (12.22 ± 5.83 x 10–3 fmol/l) than Pre (1.11 ± 0.42 x 10–3 fmol/l). A similar increase was seen in Hy+NW, where PAVP at IP was higher than all other conditions.



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  		Fig. 2. Group mean (± SE) plasma arginine vasopressin responses. *Significant difference compared with all other values at the same time point, P < 0.05. {dagger}Significant difference compared with corresponding Pre value, P < 0.05.

 
PRA and SAld responses are shown in Fig. 3. Baseline PRA was similar among conditions at Pre, significantly rising at IP for both NW trials. At IP, Hy+NW PRA was greater than both Eu treatments. SAld significantly increased from Pre to IP in all trials except Eu+W. Like PRA, Hy+NW SAld at IP was greater than the corresponding Eu conditions.



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  		Fig. 3. Group mean (± SE) plasma renin activity (A) and aldosterone (B) responses. ANG I, angiotensin I. *Significant difference compared with both Eu values at the same time point, P < 0.05. {dagger}Significant difference compared with corresponding Pre value, P < 0.05.

 

   DISCUSSION
TOP
 ABSTRACT
 METHODS
 RESULTS
 DISCUSSION
GRANTS
 ACKNOWLEDGMENTS
 REFERENCES
 
Considering that subjects completed the same exercise bouts during Hy+W and Eu+W, these results suggest that preexercise dehydration was primarily responsible for the differences in thirst and fluid intake. Although this relationship between dehydration and thirst has been seen at rest (12), a primary finding of this study was that the extended period of hypohydration before low-intensity exercise magnified the drive to drink such that the hormonal and circulatory measures of exercise-heat stress were indistinguishable from results obtained when exercise was initiated in a euhydrated state. Thus significant preexercise dehydration favorably modified the drinking response during this exercise-heat stress.

We recognize that the exercise performed the day before the protocol to induce hypohydration for the Hy+NW and Hy+W trials was a potential weakness of the study design. Given the real-life applicability of low-intensity, prolonged exercise in the heat on consecutive days, however, we believe use of an exercise-dehydration model, as opposed to one offering more control (i.e., passive heating and/or diuretic usage), significantly improved the external validity of the present research. PV, Posm, and fluid regulatory hormones rapidly return to baseline or near-baseline values after low- to moderate-intensity exercise (i.e., <2 h), further supporting the present research design (25, 41). Additionally, the similar Pre hormonal and circulatory responses of Hy+W and Hy+NW support the contention that the exercise bout used to hypohydrate subjects was not responsible for the observed responses.

Posm, perceived thirst, and PV.   Normal values for Posm after prolonged dehydration and/or low-intensity exercise in the heat (280–295 mosmol/kgH2O) were seen at all times except for postexercise Hy+NW. Despite the 3–4% loss in body weight preceding the Hy trials, subjects were able to maintain normal Posm when allowed to drink water ad libitum (IP, Hy+W = 293 ± 3 mosmol/kgH2O) but not when denied fluids (IP, Hy+NW = 307 ± 3 mosmol/kgH2O). The further rise in Posm during Hy+NW (Fig. 1) likely resulted from the absence of fluid to counteract exercise-induced increases in sweat volume and a concomitant decrease in PV. Because a Posm of 295 mosmol/kgH2O is the putative osmolar threshold for thirst (40), the effectiveness of osmolar-driven thirst and drinking is reinforced.

Engell et al. (12) have shown a strong, direct relationship between the intensity of perceived thirst and degree of hypohydration before and after exercise in the heat. Additionally, they reported a direct correlation between fluid consumption during rehydration and the level of dehydration. The increased drinking frequency and fluid intake during Hy+W, complemented by the uniform responses in perceived thirst and Posm at Pre and IP, support these conclusions. This study extends the previous findings by showing that the relationship between hypohydration, thirst, and drinking holds true during low-intensity exercise in the heat.

The ability of thirst-driven drinking to prevent hypohydration during Hy+W disagrees, however, with the classic studies of Adolph (1) and Wolf (43), who proposed that thirst was an inadequate stimulus to maintain appropriate hydration. The dehydration work of Adolph (1), however, documented water intake during exercise initiated in a euhydrated state. Because subjects were required to maintain a hypohydrated state in both the Hy trials for several hours before the exercise trial, fluid intake during the 90-min exercise bouts may be better viewed as a function of rehydration than voluntary dehydration. Although the volume of fluid ingested during rehydration after a dehydration session is only ~50% of the fluid lost (12, 26, 30), studies examining this phenomenon have used rehydration sessions immediately after dehydration, in thermoneutral ambient conditions, and at rest. The addition of two strong dipsogenic factors (i.e., increased time without fluids and exercise-heat stress) may have contributed to the significantly increased fluid intake (~60% of prior fluid loss) seen during Hy+W.

Fluid-regulating hormones.   That Posm dictated PAVP responses during Hy+W and Eu+NW is not surprising, because Posm is the primary regulator of PAVP (42). However, two anomalies in our study deserve special note. First, significant differences in baseline Posm between Hy and Eu were not matched by significant decreases in PAVP. The trend toward an increased PAVP for preexercise Hy measures did not reach statistical significance likely because Posm never greatly exceeded 295 mosmol/kgH2O (40). Thus, although the increases in resting Posm may have been statistically significant, it can be argued that it was not physiologically relevant. Second, PAVP during Eu+W was significantly increased from Pre to IP despite no statistical change in Posm, which is contrary to most studies, which find no change in PAVP at exercise intensities <40% O2 max (8, 15, 27). In this case, the combination of exercise and heat stress may have induced a sympathetic nervous response, supplementing the nonsignificant stimulation of PAVP by Posm (8, 20). It is unclear why this only occurred in the Eu+W trial.

The distinct responses of PRA and SAld vs. PAVP in the present study support a multifactorial drinking regulation system, as proposed by Greenleaf et al. (18). They described two general systems for the regulation of drinking: a sodium-Posm-PAVP system (2, 39) and a renin-angiotensin II-SAld system (13); the interaction of the two systems controls thirst and fluid replenishment. Greenleaf et al. have suggested that the renin-angiotensin II-SAld system, influenced by reductions in total body water and PV, is the predominant stimulus to thirst during exercise in the heat. In the present study, however, the combination of 1) the significantly higher Pre Posm in Hy trials (Hy+NW = 296 ± 3 mosmol/kgH2O, Hy+W = 295 ± 2 mosmol/kgH2O) than Eu trials (Eu+NW = 287 ± 2 mosmol/kgH2O, Eu+W = 287 ± 2 mosmol/kgH2O); 2) the comparable responses of Posm, PAVP, and thirst; and 3) the dissimilar patterns of PRA, SAld, and thirst indicate that thirst was more closely associated with Posm and PAVP than with PRA and SAld. Nose et al. (28) have found similar results, concluding that the sodium-Posm-PAVP system was the dominant influence in dictating thirst during rehydration, after a 2.3% decrease in body mass induced by an exercise-heat stress.

Our results may conflict with those of Greenleaf et al. (18) due to differences in the exercise heat stress (8 continuous days of 2 h of low-intensity exercise in the 39.8°C vs. a single 90-min bout of low-intensity exercise in 33°C) or the importance placed by Greenleaf et al. on reductions in total body water or PV to stimulate the renin-angiotensin II-SAld system. By allowing fluid balance to equilibrate between dehydration and exercise (17.5 ± 1.1 h), however, the full loss of body mass cannot be attributed to decreases in PV alone, especially considering that several studies have shown PV is selectively restored before intracellular and interstitial fluid compartments after dehydrating exercise in the heat (28, 29, 36). Although it can be assumed that PV remained lower in the Hy conditions compared with the Eu conditions (potentially increasing PAVP and thirst in and of itself), the decrease in PV may have been insufficient to maximally stimulate the renin-angiotensin II-SAld system. Additionally, during Hy+W, subjects showed no losses in PV during the exercise-heat stress; PV (+1.0%) and body masses (+0.9%) were greater after the trial than before, suggesting that the renin-angiotensin II-SAld system played a minor role vs. the sodium-Posm-PAVP system.

In conclusion, this investigation suggests that dehydration preceding low-intensity exercise in the heat magnifies thirst-driven drinking, effectively attenuating the negative influences of preexercise hypohydration on PV and fluid-regulatory hormonal measures. Furthermore, the data support the interaction of a minor renin-angiotensin II-SAld system and a dominant, highly responsive sodium-Posm-PAVP system in regulating thirst in this exercise-heat challenge.


   GRANTS
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 ABSTRACT
 METHODS
 RESULTS
 DISCUSSION
 GRANTS
ACKNOWLEDGMENTS
 REFERENCES
 
This study was supported in part by a grant from Evian, Incorporated.


   ACKNOWLEDGMENTS
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 ABSTRACT
 METHODS
 RESULTS
 DISCUSSION
 GRANTS
 ACKNOWLEDGMENTS
REFERENCES
 
The authors gratefully acknowledge a dedicated group of subjects and the technical assistance of Andrew Judelson, Daniel Hannon, Tamara Morrocco, and Michael Whittlesey.


   FOOTNOTES
 

Address for reprint requests and other correspondence: C. M. Maresh, Dept. of Kinesiology, 2095 Hillside Rd., U-1110, Storrs, CT 06269-1110 (E-mail: carl.maresh{at}uconn.edu).

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


   REFERENCES
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 RESULTS
 DISCUSSION
 GRANTS
 ACKNOWLEDGMENTS
 REFERENCES
 

  1. Adolph EF and Willis JH. Thirst. In: Physiology of Man in the Desert, edited by Adolph EF. New York: Interscience, 1947, p. 241–253.
  2. Andersson B, Olsson K, and Rundgren M. ADH in regulation of blood osmolality and extracellular fluid volume. JPEN J Parenter Enteral Nutr 4: 88–96, 1980.
  3. Armstrong LE, Herrera-Soto JA, Hacker FT, Casa DJ, Kavorous SA, and Maresh CM. Urinary indices during dehydration, exercise, and rehydration. Int J Sport Nutr 8: 345–355, 1998.
  4. Armstrong LE, Maresh CM, Gabaree CV, Hoffman JR, Kavorous SA, Kenefick RW, Castellani JW, and Ahlquist LE. Thermal and circulatory responses during exercise: effects of hypohydration, dehydration, and water intake. J Appl Physiol 82: 2028–2035, 1997.
  5. Boudou P, Fiet J, Laureaux C, Patricot MC, Guezennec CY, Foglietti MJ, Villette JM, Friemel F, and Haag JC. Changes in several plasma and urinary components in marathon runners. Ann Biol Clin (Paris) 45: 37–45, 1987.
  6. Brandenberger G, Candas V, Follenius M, and Kahn JM. The influence of the initial state of hydration on endocrine responses to exercise in the heat. Eur J Appl Physiol 58: 674–679, 1989.
  7. Brandenberger G, Candas V, Follenius M, Libert JP, and Kahn JM. Vascular fluid shifts and endocrine responses to exercise in the heat. Eur J Appl Physiol 55: 123–129, 1986.
  8. Convertino VA, Keil LC, Bernauer EM, and Greenleaf JE. Plasma volume, osmolality, vasopressin, and renin activity during graded exercise in man. J Appl Physiol 50: 123–128, 1981.
  9. Costill DL and Fox EL. Energetics of marathon running. Med Sci Sports Exerc 1: 81–86, 1969.
  10. Dill DB and Costill DL. Calculation of percentage changes in volumes of blood, plasma, and red cells in dehydration. J Appl Physiol 37: 247–248, 1974.
  11. Durnin JV and Womersley J. Body fat assessed from total body density and its estimation from skinfold thickness: measurements on 481 men and women aged from 16 to 72 years. Br J Nutr 32: 77–97, 1974.
  12. Engell DB, Maller O, Sawka MN, Francesconi RN, Drolet L, and Young AJ. Thirst and fluid intake following graded hypohydration levels in humans. Physiol Behav 40: 229–236, 1987.
  13. Fitzsimons JT. The physiological basis of thirst. Kidney Int 10: 3–11, 1976.
  14. Follenius M, Candas V, Bothorel B, and Brandenberger G. Effect of rehydration on atrial natruiretic peptide release during exercise in the heat. J Appl Physiol 66: 2516–2521, 1989.
  15. Freund BJ, Shizuru EM, Hashiro GM, and Claybaugh JR. Hormonal, electrolyte, and renal responses to exercise are intensity dependent. J Appl Physiol 70: 900–906, 1991.
  16. Grant SM, Green HJ, Phillips SM, Enns DL, and Sutton JR. Fluid and electrolyte hormonal responses to exercise and acute plasma volume expansion. J Appl Physiol 81: 2386–2392, 1996.
  17. Greenleaf JE. Problem: thirst, drinking behavior, and involuntary dehydration. Med Sci Sports Exerc 24: 645–656, 1992.
  18. Greenleaf JE, Brock PJ, Keil LC, and Morse JT. Drinking and water balance during exercise and heat acclimation. J Appl Physiol 54: 414–419, 1983.
  19. Greenleaf JE and Sargent F II. Voluntary dehydration in man. J Appl Physiol 20: 719–724, 1965.
  20. Hoffman JR, Maresh CM, Armstrong LE, Gabaree CL, Bergeron MF, Kenefick RW, Castellani JW, Ahlquist LE, and Ward A. Effects of hydration state on plasma testosterone, cortisol and catecholamine concentrations before and during mild exercise at elevated temperature. Eur J Appl Physiol 69: 294–300, 1994.
  21. Hubbard RW and Armstrong LE. The heat illnesses: biochemical, ultrastructural, and fluid-electrolyte considerations. In: Human Performance Physiology and Environmental Medicine at Terrestrial Extremes, edited by Pandolf KB, Sawka MN, and Gonzales RR. Indianapolis, IN: Benchmark, 1988, p. 305–359.
  22. Hubbard RW, Sandick BL, Matthew WT, Francesconi RP, Sampson JB, Durkot MJ, Maller O, and Engell DB. Voluntary dehydration and alliesthesia for water. J Appl Physiol 57: 868–873, 1984.
  23. Maresh CM, Herrera-Soto JA, Armstrong LE, Casa DJ, Kavorous SA, Hacker FT, Elliot TA, Stoppani J, and Scheett TP. Perceptual responses in the heat after brief intravenous versus oral rehydration. Med Sci Sports Exerc 33: 1039–1045, 2001.
  24. Melin B, Jimenez C, Savourey G, Bittel J, Cottet-Emard JM, Pequignot JM, Allevard AM, and Gharib C. Effects of hydration state on hormonal and renal responses during moderate exercise in the heat. Eur J Appl Physiol 76: 320–327, 1997.
  25. Melin B, Koulmann N, Jimenez C, Savourey G, Launay JC, Cottet-Emard JM, Pequignot JM, Allevard AM, and Gharib C. Comparison of passive heat or exercise-induced dehydration on renal water and electrolyte excretion: the hormonal involvement. Eur J Appl Physiol 85: 250–258, 2001.
  26. Miescher E and Fortney SM. Responses to dehydration and rehydration during heat exposure in young and older men. Am J Physiol Regul Integr Comp Physiol 257: R1050–R1056, 1989.
  27. Montain SJ, Laird JE, Latzka WA, and Sawka MN. Aldosterone and vasopressin responses in the heat: hydration level and exercise intensity effects. Med Sci Sports Exerc 29: 661–668, 1997.
  28. Nose H, Mack GW, Shi X, and Nadel ER. Role of osmolality and plasma volume during rehydration in humans. J Appl Physiol 65: 325–331, 1988.
  29. Nose H, Mack GW, Shi X, and Nadel ER. Shift in body fluid compartments after dehydration in humans. J Appl Physiol 65: 318–324, 1988.
  30. Nose H, Mack GW, Shi XR, and Nadel ER. Involvement of sodium retention hormones during rehydration in humans. J Appl Physiol 65: 332–336, 1988.
  31. Pitts GC, Johnson RE, and Consolazio FC. Work in the heat as affected by intake of water, salt and glucose. Am J Physiol 142: 253–259, 1944.
  32. Reid IA. Actions of angiotensin II on the brain: mechanisms and physiologic role. Am J Physiol Renal Fluid Electrolyte Physiol 246: F533–F543, 1984.
  33. Rothstein A and Towbin EJ. Blood circulation and temperature of men dehydrating in the heat. In: Physiology of Man in the Desert, edited by Adolph EF. New York: Interscience, 1947, p. 172–196.
  34. Roy BD, Green HJ, Grant SM, and Tarnopolsky MA. Acute plasma volume expansion in the untrained alters the hormonal response to prolonged moderate-intensity exercise. Horm Metab Res 33: 238–245, 2001.
  35. Sawka MN, Francesconi RP, Young AJ, and Pandolf KB. Influence of hydration level and body fluids on exercise performance in the heat. JAMA 252: 1165–1169, 1984.
  36. Stachenfeld NS, Gleim GW, Zabetakis PM, and Nicholas JA. Fluid balance and renal responses following dehydrating exercise in well-trained men and women. Eur J Appl Physiol 72: 468–477, 1996.
  37. Stevenson JAF. Neural control of food and water intake. In: The Hypothalamus, edited by Haymaker W, Anderson E, and Nauta WJH. Springfield, IL: Thomas, 1969, p. 524–605.
  38. Thoden JS, MacDougall JD, and Wilson BA. Testing of aerobic power. In: Physiological Testing of the Elite Athlete, edited by MacDougall JD, Wegner HA, and Green HJ. Ithaca, NY: Movement Publications, 1983, p. 39–54.
  39. Verney EB. The antidiuretic hormone and factors which determine its release. Proc R Soc Lond 135: 25–106, 1947.
  40. Vokes T. Water homeostasis. Annu Rev Nutr 7: 383–406, 1987.
  41. Wade CE and Claybaugh JR. Plasma renin activity, vasopressin concentration, and urinary excretory responses to exercise in men. J Appl Physiol 49: 930–936, 1980.
  42. Wade CE, Freund BJ, and Claybaugh JR. Fluid and electrolyte homeostasis during and following exercise: hormonal and non-hormonal factors. In: Hormonal Regulation of Fluid and Electrolytes: Environmental Effects, edited by Claybaugh JR and Wade CE. New York: Plenum, 1989, p. 1–44.
  43. Wolf AV. Thirst. In: Physiology of the Urge to Drink and Problems of Water Lack. Springfield, IL: Thomas, 1958.



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