Thirst Sensations and AVP Responses at Rest and during Exercise-Cold Exposure : Medicine & Science in Sports & Exercise

Journal Logo

BASIC SCIENCES: Original Investigations

Thirst Sensations and AVP Responses at Rest and during Exercise-Cold Exposure


Author Information
Medicine & Science in Sports & Exercise 36(9):p 1528-1534, September 2004. | DOI: 10.1249/01.MSS.0000139901.63911.75
  • Free


KENEFICK, R. W., M. P. HAZZARD, N. V. MAHOOD, and J. W. CASTELLANI. Thirst Sensations and AVP Responses at Rest and during Exercise-Cold Exposure. Med. Sci. Sports Exerc., Vol. 36, No. 9, pp. 1528–1534, 2004.


The purpose of this study was to 1) determine the effect of hypohydration (HYPO) on thirst sensations during moderate exercise in the cold and 2) determine a possible mechanism for a cold-induced decline in thirst.


In the first phase of the study, eight males walked on four occasions, in T-shirts, shorts, and shoes, at 50% V̇O2max, for 60 min in either a 4°C (cold) or 27°C (temperate) environment in a state of HYPO or euhydration (EU). In the second phase, nine males in states of EU or HYPO randomly performed four trials consisting of 30 min standing at 27°C, followed by 30 min of standing and 30 min of treadmill exercise at 50% of V̇O2max, in either 4°C or 27°C air.


In phase 1, thirst sensations were lower throughout 60 min of exercise (P < 0.05) in both HYPO and EU conditions during the cold trials. In phase 2, despite elevated plasma osmolality (P < 0.05), perception of thirst and plasma arginine vasopressin [AVP] similarly decreased (P < 0.05) after 30-min standing rest and 30-min exercise in the HYPO-cold trial, compared with the HYPO-temperate, EU-cold, and EU-temperate trials.


When either euhydrated or hypohydrated, cold exposure attenuated thirst by up to 40% at rest and during moderate-intensity exercise. The attenuated thirst when hypohydrated during cold exposure was associated with lower plasma [AVP] despite an elevated plasma osmolality. This decline in thirst and AVP in the cold may be the result of peripheral vasoconstriction, mediating an increase in central blood volume and stimulation of central volume receptors.

Fluid balance often relies upon the stimulation of thirst, resulting in voluntary fluid intake and renal conservation or excretion of water, mediated by fluid-regulating hormones such as plasma arginine vasopressin (AVP). These systems are activated when fluid deficits (hypohydration) occur at rest and during exercise, especially when individuals are exposed to hot environments. Hypohydration also occurs in the cold (10,13,17). Fluid deficits of 3–8% of body mass have been reported in individuals working in cold environments (10), due to cold-induced diuresis, reduction in voluntary fluid intake, an increase in insensible sweat loss and in respiratory fluid loss (10,13). In fact, voluntary dehydration has been noted as a major problem with exercise in a cold environment (17,21) and one cause of mountaineering failures (11).

Thirst and drinking behavior appear to be altered while at rest when exposed to a cold environment. Rats exposed to cold (5°C) air significantly reduced voluntary water ingestion, despite the availability of water and high serum osmolality (9). When these animals were transferred to temperate (26°C) air, drinking began within 15 min and lasted for up to 1 h, suggesting that cold exposure inhibits fluid intake, independent of plasma osmolality. Similarly, dogs exposed to cold (+1°C to −8°C) air were observed to have an increase in the osmotic thirst threshold, perhaps secondary to a rise in central blood volume due to cold induced vasoconstriction (23). In humans, thirst sensations are lower during immersion in cold (~5°C and ~14°C) water after exercise heat stress, compared with resting in temperate air (5). However, the use of water immersion in this study confounds these finding, as it is difficult to separate the effect of cold from hydrostatic pressure redistributing blood volume to the central circulation. Thus, it is still not known what effect dehydration has on thirst sensations during rest and exercise in the cold.

This investigation was carried out in two phases; the purpose of the first phase was to determine the influence of dehydration and exercise on thirst sensations in the cold. The second phase sought to provide insight into the possible mechanism for alterations in thirst at rest and during exercise in the cold by observing responses of plasma AVP. It is well established that changes in plasma osmolality and blood volume mediate the response of fluid regulating hormones (19,24). We hypothesized that despite the presence of hypohydration and plasma hyperosmolality, cold-induced vasoconstriction would increase central blood volume and stimulate central volume receptors, inhibiting AVP release and leading to a decline in thirst.



Eight men, not heat or cold acclimated, volunteered to participate in phase 1 of this investigation. Physical characteristics (mean ± SEM) were: age, 35.1 ± 2.7 yr; height, 175.5 ± 3.1 cm; weight, 73.3 ± 2.6 kg; V̇O2max57.2 ± 2.6 mL·kg−1·min−1; percent body fat, 19.6 ± 2.4%; and BMI, 23.8 ± 0.9 kg·m−2. In phase 2 of the study, a different subject pool of nine men, not heat or cold acclimated, volunteered to participate. Physical characteristics (mean ± SEM) were: age, 21.3 ± 1 yr: height, 177.5 ± 2.3 cm; weight, 75.8 ± 4.3 kg; V̇O2max 55.5± 2.9 mL·kg−1·min−1; percent body fat, 9.9 ± 1.8%; BMI, 24.1 ± 0.8 kg·m−2. For both phases, each subject completed a written informed consent document and a medical history questionnaire after being informed of the purpose of the experiment and possible risks. The Committee on the Use of Human Subjects in Research at the University of New Hampshire approved all procedures.

Preliminary measures.

Body mass was determined for each subject using an electronic scale (General GE510, Cape Coral, FL), followed by measures of maximal oxygen uptake (V̇O2max mL·kg 1·min−1), via a modified Costill-Fox (6) treadmill test. Body density was determined via a hydrostatic weighing technique previously described (12), and body fat was calculated from the formula of Brozek et al. (4). Vital capacity was measured via spirometry and residual lung volume was estimated from these values (28).

Experimental design.

Subjects in phase 1 and subjects in phase 2 performed four experimental exercise-testing sessions. Each session occurred in one of two hydration states, hypohydrated (HYPO) or euhydrated (EU), and in one of two environmental conditions, 4°C, 74% RH (cold) or 27°C, 38.5% RH (temperate). On the day previous to each experimental exercise-testing session, subjects performed an exercise-induced dehydration protocol in 37°C air, to reduce body weight by ~3–4% (Tables 1 and 2). To maintain consistency, on the days before the EU trials, subjects performed the dehydration protocol but matched sweat losses with water replacement during the protocol. On the following morning, subjects in phase 1 performed experimental trials of 60 min of walking exercise at ~50% of V̇O2max when either euhydrated or hypohydrated in cold or temperate environments (Fig. 1A). The morning after the dehydration protocol, subjects in phase 2 performed an experimental protocol including 30 min standing in 27°C, followed by 60 min in a cold or temperate environment. This 60-min period included 30-min standing rest followed by 30-min of treadmill exercise at 50% of V̇O2max (Fig. 1B). Subjects in phase 1 and 2 performed all dehydration and experimental treatments in shorts, a T-shirt, and running shoes, and in front of fans set at a wind speed of 6 m·s−1. Subjects were asked to maintain similar diets during the 3 d before each experimental trial and to refrain from activity other than the dehydration protocol 24 h before experimental testing.

Hydration variables pre- and postdehydration and preexercise in cold or temperate environments for phase 1 and 2 experiments. (mean ± SE).
Core temperature (Tre) and mean weighted skin temperature (Tsk) values in cold (4°C) or temperate (27°C) environments for phase 1 and 2 experiments (mean ± SE)
Experimental protocols for phase 1 (A; N = 8) and phase 2 (B; N = 9); each subject performed four trials at random, in a state of EU or HYPO and in the cold (4°C) or temperate (27°C) environments.

Exercise-induced dehydration.

In each phase, subjects performed a HYPO trial first to determine the length of time needed to achieve a 3–4% loss in body mass during dehydration exercise. This time was held constant for the following three treatments, all of which were randomly assigned and separated by at least 6 d. Upon arrival at the laboratory in the afternoon, subjects provided a urine sample for determination of urine specific gravity (USG; Spartan Refractometer, model A 300 CL, Japan), and body weight was measured. A USG of less than 1.023 (1) was used to verify that the subject was adequately hydrated. Subjects were then fitted with a heart rate monitor and a flexible thermistor (Yellow Springs Instruments, series 401, Yellow Springs, OH) was inserted 10 cm beyond the anal sphincter to monitor rectal temperature (Tre). The mean ambient temperature and percent relative humidity in the environmental chamber (Harris Environmental Systems, Andover, MA) was 37 ± 0.1°C and 65 ± 2.0% rh, respectively. Airflow (6.1 m·s−1, 13.6 mph), generated by two fans, was directed at the subject to enhance evaporative sweat cooling.

The dehydration protocol for phase 1 consisted of alternating treadmill walking (1.6 ± 0.1 m·s−1; 8.6 ± 0.5% grade; Quinton, Seattle, WA) and cycle ergometry (117 ± 9 W; Model 818E, Monark, Varberg, Sweden) at a 25-min: 5-min ratio (exercise:rest) for each modality. In phase 2, subjects performed treadmill walking (1.6 ± 0.1 m·s−1; 8.0 ± 1.0% grade) at a 25-min:5-min ratio (exercise:rest). The %V̇O2max for the four dehydration trials ranged from 47 to 51%. Body weight was measured during each rest interval. It was during the rest interval that sweat losses were matched with water replacement on the days before the EU trials. Urine was collected throughout the dehydration stage and was included as part of the weight loss. The mean exercise time for the dehydration protocol in phase 1 was ~78 min and for phase 2 was ~94 min.

After the dehydration session and before departure from the lab, each subject was given overnight dietary instructions. To induce an additional 1% loss in body mass overnight during HYPO treatments, subjects were instructed to consume only dry foods and to refrain from fluid intake. Subjects were permitted to have a usual intake of food and fluid overnight during EU treatments.

Experimental exercise testing.

After the dehydration protocol on the previous afternoon, the next morning subjects arrived at the laboratory between 0600 and 0700 h, and provided a urine sample for determination of USG, and had body weight measured. A light breakfast (bagel, fruit, juice) was then provided for each subject. Subjects were then fitted with a heart rate monitor and a flexible thermistor to monitor Tre, and skin thermistors (Yellow Springs Instruments, series 401) were placed on the upper arm, chest, upper thigh, and calf of the subject’s left side for measurement of mean weighted skin temperatures (Tsk) (15). In phase 1, subject entered the environmental chamber where the conditions were set for either the cold (4°C) or temperate (27°C) testing session and began the 60 min experimental treadmill exercise session. In phase 2, after breakfast, a cannula was inserted into an antecubital vein for blood collection during the session. After standing for 30 min in 27°C, each subject entered the environmental chamber set at 4°C or 27°C for 30 min of standing followed by 30 min of treadmill exercise at 50% V̇O2max.

Physiological and perceptual measures.

During the dehydration protocol, the subject’s heart rate and oxygen uptake (V̇O2, L·m1) were measured every 8 min. During experimental exercise testing in phase 1, HR, Tsk, V̇O2, and thirst sensation (1: not thirsty to 9: very thirsty) (8) were measured preexercise and at min 20, 40, and 60 during exercise. In phase 2, these variables and additional blood variables were measured at three, 30-min time points: after standing in 27°C (postequilibration); after standing rest in the chamber set at 4°C or 27°C (post 4°C or 27°C); and after treadmill exercise (postexercise). At these 30-min time points, a 10-mL venous blood draw was made from the cannula for measurements of hematocrit, plasma osmolality (Posm), and plasma AVP concentrations. To ensure subject safety, Tre was monitored continuously throughout the dehydration protocol and experimental exercise testing.

Analysis of blood samples.

Approximately 2 mL of whole blood was drawn off each 10-mL blood sample and transferred into a heparinized tube for measures of hematocrit and Posm. To measure hematocrit, microcapillary tubes were filled in triplicate and spun in the centrifuge (Micro Hematocrit Centrifuge Damon/IEC Division, Needham Heights, MA) for 4 min at 9500 ×g. Hematocrit was read on a Micro-capillary reader (Damon/IEC Division, Need-ham Heights, MA). The remains of the 2-mL sample in the tube were then spun for 10 min at 9500 ×g, and approximately 50 μL of plasma was extracted in triplicate for measures of Posm (mmol·kg 1 of H2O) via freezing point depression (micro-osmometer model 3MO, Advanced Instruments, Needham Heights, MA). The remainder of the 10-mL blood sample was then transferred to tubes containing EDTA for measures of plasma AVP. Samples were centrifuged (Marathon 12KBR Refrigerated Centrifuge, Fisher Scientific, Pittsburgh, PA) for 10 min at 4°C after which the plasma was drawn off and stored at −80°C for later analysis. Upon analysis, a radioimmunoassay kit (Diasorin, Peninsula Laboratories, Inc., San Carlos, CA) was used to determine plasma AVP via extraction of AVP onto silica columns. AVP measures were corrected for plasma volume shifts using hematocrit values (26).

Statistical analysis.

An analysis of variance (time × condition) with repeated measures was used to compare differences among the trials. A Newman-Keuls post hoc analysis was used to determine significant differences within and between conditions. The P < 0.05 level of significance was employed and all data are presented as means ± SE.


Each subject completed all four experimental treatments. Dietary intake in kilocalories per day, and percentages of fat, protein, carbohydrate, and sodium were not significantly different over the 3 d before each experimental treatment. There were no significant differences among treatments in exercise intensity (range 47–51% V̇O2max) during the dehydration exercise sessions or during the experimental exercise session (range 48–51% V̇O2max).

Hydration state.

Table 1 provides hydration indices for the four tests in phases 1 and 2. In general, EU and HYPO treatments were similar for cold and temperate trials. There were no significant differences in hydration state based upon predehydration values of body mass (kg), Posm, and USG. In phases 1 and 2, HYPO resulted in a 4% decrease in body weight versus EU and a significant elevation in preexercise USG and POsm (phase 2). To maintain euhydration during the dehydration protocol for subsequent EU trials, subjects drank 1286 ± 153 mL and 1364 ± 118 mL of H2O for the EU-cold and EU-temperate sessions, respectively.

Perceived thirst sensations.

In phase 1 of the study, thirst sensations in the EU condition were rated lower at minutes 40 and 60 in the cold compared with the temperate trials. In the HYPO condition thirst sensations were lower in the cold trials at the preexercise and 20-, 40-, and 60-min time points compared with the temperate trials (Fig. 2A). In phase 2 of the study, thirst sensations in the EU condition were rated lower at the post 30-min exercise time point in the cold compared with the temperate trials. In the HYPO condition, thirst sensations were lower in the cold trials after 30 min rest and after 30 min exercise compared with the temperate trials (Fig. 2B).

Perceived thirst sensations vs exercise time (min) for phase 1 (A) and phase 2 (B) during EU-cold (•), HYPO-cold (ˆ), EU-temperate (▪), and HYPO-temperate (□) trials. Values are means ± SE. * EU-cold and HYPO-cold significantly different (P < 0.05) from corresponding EU-temperate and HYPO-temperate time points.

Plasma AVP and plasma osmolality.

In the HYPO-cold trial of phase 2, values of plasma AVP significantly declined from 5.9 ± 0.5 pg·mL−1, after 30-min equilibration at 27°C, to 2.0 ± 0.3 pg·mL−1 after 30 min of standing rest at 4°C and 30 min of exercise. Plasma AVP values were significantly lower (P < 0.05) at the 30-min rest and 30-min postexercise time points for both the EU and HYPO-cold trials compared with the EU and HYPO-temperate trials, respectively (Fig. 3A). In both the cold and temperate environments, Posm was higher (P < 0.05) in the HYPO treatments than corresponding EU values (Fig. 3B).

Plasma AVP concentrations (A) and plasma osmolality (B) vs time during EU-cold (•), HYPO-cold (ˆ), EU-temperate (▪), and HYPO-temperate (□) trials. Values are means ± SE. * EU-cold and HYPO-cold significantly different (P < 0.05) from corresponding HYPO-temperate and EU-temperate time points. + Post 30-min rest and post 30-min exercise significantly different (P < 0.05) from post 27°C equilibration time point within the HYPO-cold trial. # HYPO-cold and HYPO-temperate significantly different (P < 0.05) than corresponding EU-cold and EU-temperate at respective time points.

Temperature responses.

Core temperatures (Tre) and mean weighted skin temperatures (Tsk) are presented in Table 2. In phase 1, rectal temperatures did significantly rise throughout the 60 min of exercise in all conditions. However, core temperate responses were not different (P > 0.05) at each corresponding time point between the experimental) conditions. In phase 2, Tre increased significantly (P < 0.05after each 30-min period during the HYPO-cold and EU-cold treatments. However, there were no differences in Tre between the experimental conditions at each corresponding time point.

In phase 1, mean weighted skin temperature values were not different between EU and HYPO trials in the cold condition. In the temperate trials, mean skin temperatures were also not different between the EU and HYPO trials. As expected, skin temperatures during exercise were lower during exercise in cold versus temperate environment. Again, in phase 2, mean weighted skin temperatures were not different between the EU and HYPO conditions in either the temperate or cold environments. Mean weighted skin temperature values were lower (P < 0.05) in the cold when compared with temperate treatments at rest and during exercise.

Heart rate.

Heart rate values in both the cold and temperate environments for phase 1 and 2 experiments are presented in Table 3. Preexercise (phase 1) and post equilibration (phase 2) heart rate values were lower (P < 0.05) than those during exercise. In both phase 1 and 2, HYPO-temperate heart rate values during exercise were greater (P < 0.05) than HYPO-cold, EU-cold, and EU-temperate values at corresponding time points.

Heart rate values in cold (4°C) or temperate (27°C) environments for phase 1 and 2 experiments (mean ± SE).


The major findings of the present study were: 1) thirst sensations were attenuated at rest and during exercise in the cold when euhydrated or hypohydrated; 2) when resting or exercising, plasma AVP responses were reduced during cold exposure when subjects were either euhydrated or hypohydrated; and 3) the reduction in plasma AVP in the cold occurred despite a hyperosmotic state.


Previous research in the cold has reported a decline in fluid intake at rest (17) and during exercise (7,17,30), which implies a reduction in thirst sensation with cold exposure. In the present study thirst sensations were significantly lower at rest and during exercise by up to 40% in both the EU-cold and HYPO-cold conditions. Despite the presence of hypohydration and a significant rise in osmolality, thirst sensations were lower in the HYPO-cold treatment when compared with temperate treatments. A strong relationship between plasma osmolality and thirst sensation has been well defined (14,25). However, in the present study, this relationship does not seem to be borne out with cold exposure. Figure 4A, which compares thirst sensations to plasma osmolality, illustrates these findings. Similar observations have been reported with the use of head-out water immersion, a technique that also increases central blood volume, which has been shown to lower thirst perception (P < 0.05) in hypohydrated subjects, despite a rise in Posm (18,27).

Perceived thirst sensations vs plasma osmolality (A) and plasma AVP concentrations vs plasma osmolality (B) at the post 27°C equilibration (1), post 30-min rest (2), and post 30-min exercise (3) time points during EU-cold (•), HYPO-cold (ˆ), EU-temperate (▪), and HYPO-temperate (□) trials.

Plasma AVP.

Acute cold stress inhibits AVP (3,20,29). Wittert et al. (29) reported significantly lower (P < 0.01) plasma AVP levels in six euhydrated male subjects after 10 min of exposure to 4°C. These values then returned to baseline after 15 min of exposure to 22°C air (30). The present study provides additional evidence of a decline in plasma AVP during cold exposure when normally hydrated. Plasma AVP was significantly lower in EU-cold when compared with corresponding temperate treatments, both at rest and during exercise. Interestingly, in the HYPO-cold trial, plasma AVP declined by 66% after 30 min of cold exposure despite an elevated plasma osmolality. This is the first study to report a decrease in AVP with cold exposure in the presence of hypohydration and increased plasma osmolality (Fig. 4B).

Like that of thirst and plasma osmolality, a strong relationship between thirst and plasma AVP has been well documented (2,16). However, despite a rise in Posm during hypohydration, HYPO-cold plasma AVP concentrations and thirst sensations were significantly lower (P < 0.05) when compared with both temperate treatments. When a resting individual is hypohydrated and exposed to cold, thirst sensations are blunted to a greater degree than occurs in the other conditions. This response may be related to the fall in AVP. Further, during exercise in the cold when hypohydrated, AVP levels did not increase as occurs in the other conditions. As AVP levels are stimulated by a rise in plasma osmolality and decrease in blood volume, these data suggest that the decline in plasma AVP in the cold was due to volume factors, independent of changes in osmolality. This observation is further supported by the positive correlations between plasma osmolality and AVP in the HYPO-temperate (r = 0.90), EU-temperate (r = 0.99), and EU-cold (r = 0.71) and the negative correlation (−0.99) in the HYPO-cold condition. Plasma AVP values were not different between the HYPO-cold and EU-cold conditions after 30 min of exercise, despite different hydration states (Fig. 3A). After 30 min of exercise-cold exposure, it seems that central volume was increased in both the EU-cold and HYOP-cold states such that despite differences in hydration state, AVP levels were attenuated below that of the HYPO-and EU-temperate conditions.

Casa et al. (5) observed a decline in thirst sensations during immersion in cold water following exercise heat stress, compared with resting in temperate air. Further, Sagawa et al. (18) reported a decrease in plasma AVP during water immersion when hypohydrated, which coincided with a decrease in thirst sensation and voluntary intake of fluid even though plasma osmolality was elevated. They attributed these responses to changes in volume sensed by central baroreceptors overriding the impact of hypohydration and the rise in osmolality (18). Similar declines in plasma aldosterone and AVP were observed when subjects exercised at 40–100% of V̇O2peak during head-out water immersion (22).

The findings of this study indicate that when either euhydrated or hypohydrated, cold exposure attenuates thirst at rest and during moderate intensity exercise by up to 40%. Second, when hypohydrated at rest or during exercise, exposure to cold will attenuate plasma AVP responses regardless of elevated plasma osmolality. These responses may result from an increased central volume induced by peripheral vasoconstriction occurring in the cold. Attenuated thirst perception may further increase the risk of hypohydration in the cold since insensible fluid losses already occur in this environment (21).

The authors would like to thank the subjects who donated their time and effort in order to participate in this study. Further, the authors wish to thank Tara Foley, Timothy King, Jenny Klooster, Lisa Koning, Jamie Lessels, Julie Mullane, Ben Read, Sarah Wright, and Sandra Zurcher for their technical support. Lastly, the authors wish to thank Michael N. Sawka for his editorial assistance.

The views, opinions and/or findings in this report are those of the authors and should not be construed as official Department of the Army position, policy, or decision unless so designated by other official designation. All experiments were carried out in accordance to state and federal guidelines.


1. Armstrong, L. E., C. M. Maresh, J. W. Castellani, et al. Urinary indices of hydration status. Int. J. Sport Nutr. 4:256–279, 1994.
2. Baylis, P. H., and G. L. Robertson. Plasma vasopression response to hypertonic saline infusion to assess posterior pituitary function. J. R. Soc. Med. 73:255–260, 1980.
3. Blume, F. D., S. J. Boyer, L. E. Braverman, A. Cohen, J. Dirkse, and J. P. Mordes. Impaired, osmoregulation at high altitude. JAMA 252:524–526, 1984.
4. Brozek, J., F. Grande, T. Anderson, and A. Keys. Densitometric analysis of body composition, revision of some quantitative assumptions. Ann. N. Y. Acad. Sci. 110:113–139, 1963.
5. Casa, D. J., J. M. McClung, J. C. Knight, et al. Body cooling between exercise sessions in the heat decreases thirst in the absence of rehydration (abstract). Med. Sci. Sports Exerc. 35(Suppl.):1728, 2003.
6. Costill, D. L., and E. L. Fox. Energetics of marathon running. Med. Sci. Sports Exerc. 1:81–86, 1969.
7. Dann, E. J., S. Gillis and R. Burstein. Effect of fluid intake on renal function during exercise in the cold. Eur. J. Appl. Physiol. Occup. Physiol. 61:133–137, 1990.
8. Engell, D. B., O. Maller, M. N. Sawka, R. N. Francesconi, L. Drolet, and A. J. Young. Thirst and fluid intake following graded hypohydration levels in humans. Physiol. Behav. 40:229–236, 1987.
9. Fregly, M. J. Thermogenic drinking: mediation by osmoreceptor and angiotensin II pathways. Fed. Proc. 41:2515–2519, 1982.
10. Freund, B. J., and M. N. Sawka. Influence of cold stress on human fluid balance. In:Nutrient Requirements for Work in Cold and High Altitudes, B. M. Marriott (Ed.). Washington, DC: National Academy of Sciences, 1995, pp. 161–180.
11. Guilland, J. C., and J. Klepping. Nutritional alterations at high altitude in man. Eur. J. Appl. Physiol. Occup. Physiol. 54:517–23, 1985.
12. Katch, F. I., and V. L. Katch. Measurement and prediction errors in body composition assessment and the search for the perfect prediction equation. Res. Q. Exerc. Sport 51:233–249, 1980.
13. O’Brien, C., A. J. Young, and M. N. Sawka. Hypohydration and thermoregulation in cold air. J. Appl. Physiol. 84:185–189, 1998.
14. Phillips, P. A., B. J. Rolls, J. E. G. Ledingham, M. L. Forsling, and J. J. Morton. Osmotic thirst and vasopressin release in humans: a double blind crossover study. Am. J. Physiol. 248:R645–R650, 1985.
15. Ramanathan, N. L. A new weighting system for mean surface temperature of the human body. J. Appl. Physiol. 19:531–533, 1964.
16. Robertson, G. L., R. L. Shelton and S. Athar. The osmoregu lation of vasopression. Kidney Int. 10:25–37, 1976.
17. Rogers, T. A., J. A. Setliff, and J. C. Klopping. Energy cost fluid electrolyte balance in subarctic survival situation. J. Appl. Physiol. 19:1–8, 1964.
18. Sagawa, S., K. Miki, F. Tajima, et al. Effect of dehydration on thirst and drinking during immersion in men. J. Appl. Physiol. 72:128–134, 1992.
19. Salata, R. A., J. G. Verbalis, and A. G. Robinson. Cold water stimulation of oropharyngeal receptors in man inhibits release of vasopressin. J. Clin. Endocrinol. Metab. 65:561–567, 1987.
20. Segar, W. E., and W.W. Moore. The regulation of antidiuretic hormone release in man: effects of change in position and temperature on blood ADH levels. J. Clin. Invest. 47:2143–2148, 1968.
21. Senay, L. C., and R. Kok. Effects of training and heat acclimatization on blood plasma contents of exercising men. J. Appl. Physiol. 43:591–599, 1977.
22. Sheldahl, L. M., F. E. Tristani, T. P. Connelly, S. G. Levandoski, M. M. Skelton and A. W. Cowley. Fluid-regulating hormones during exercise when central blood volume is increased by water immersion. Am. J. Physiol. 262:R779–R785, 1992.
23. Sobocinska, J., and S. Kozlowski. Osmotic thirst suppression in dogs exposed to low ambient temperature. Physiol. Behav. 40:171–175, 1987.
24. Szczepanska-Sadowska, E., J. Sobocinska, and B. Sadowski. Central dipsogenic effect of vasopressin. Am. J. Physiol. 242:R372–R379, 1982.
25. Thompson, C. J., J. M. Burd, and P. H. Baylis. The osmotic thresholds for thirst and vasopressin release are similar in healthy man. Clin. Sci. 71:651–656, 1986.
26. Van Beaumont, W. Evaluation of hemoconcentration from hematocrit measurements. J. Appl. Physiol. 32:712–713, 1972.
27. Wada, F., S. Sagawa, K. Miki, et al. Mechanism of thirst attenuation during head-out water immersion in men. Am. J. Physiol. 268:R583–R589, 1995.
28. Wilmore, J. H. Further simplification of a method for determination of residual lung volume. Med. Sci. Sports Exerc. 12:216–219, 1980.
29. Wittert, G. A., H. K. Or, J. H. Livesey, A. M. Richards, R. A. Donald and E. A. Espiner. Vasopressin, corticotrophin- releasing factor, and pituitary adrenal responses to acute cold stress in normal humans. J. Clin. Endocrinol. Metab. 75:750–755, 1992.
30. Wyant, K. W., and P. L. Caron. Water discipline and an arctic ration prototype. Mil. Med. 148:435–438, 1983.


©2004The American College of Sports Medicine