J Appl Physiol
89: 2117–2122, 2000.
Plasma vasopressin and aldosterone responses to oral
and intravenous saline rehydration
ROBERT W. KENEFICK,1 CARL M. MARESH,2–4 LAWRENCE E. ARMSTRONG,2–4
JOHN W. CASTELLANI,2 DEBORAH RIEBE,2 MARCOS E. ECHEGARAY,2 AND
STAVROS A. KAVOROUS2
1
Department of Kinesiology, The University of New Hampshire, Durham, New Hampshire 03824;
and Departments of 2Kinesiology, 3Physiology and Neurobiology, and 4Nutritional Sciences,
University of Connecticut, Storrs, Connecticut 06269-1110
Received 27 October 1999; accepted in final form 28 June 2000
without rehydration
(Rh) has been shown to induce a state of hyperosmotic
hypovolemia (5, 11, 26, 28) and increase plasma arginine vasopressin (AVP) (3, 8) and aldosterone (Ald) (3,
10, 14) concentrations. The response of these fluidregulating hormones has generally been shown to be
lower when subjects were rehydrated, either during or
after exercise (31), especially when electrolytes were
also given (3, 15). However, to our knowledge, the
response of AVP and Ald to various Rh methods, such
as intravenous (IV) infusion and oral drinking, has not
been fully investigated. Comparison of the responses of
these fluid-regulating hormones to differing methods of
Rh and, additionally, differing osmotic loads may help
to identify which may provide a more effective means
of Rh. These findings may have important applications
regarding the most efficacious method for Rh for athletes, laborers, and military personnel during subsequent exercise heat stress.
Moses et al. (22, 23) used dehydration (Dh) and IV
saline infusion to examine mediators of AVP release
and suggested that expansion of plasma volume (PV)
after infusion may serve to attenuate the osmotic stimulus for AVP secretion. Francesconi et al. (14) observed
reduced Ald responses in subjects who received water
or an electrolyte solution before or during exercise.
However, the responses of fluid-regulating hormones
to IV Rh remain unclear. We are unaware of any
investigations that have specifically compared the effects of IV infusion and oral ingestion on AVP and Ald.
Therefore, the primary purpose of the present study
was to address the following question: After exerciseinduced Dh (⫺4% body wt), what are the responses of
plasma AVP and Ald after Rh via different routes
(ingestion vs. infusion) of administration? In the
present study, Rh occurred over a 45-min period, followed by 55 min of additional standing rest. Given the
amount of time allowed for Rh and rest, we hypothesized that plasma AVP and Ald would be similar between these different routes of administration because
PV could likely be restored to a similar degree. Use of
the IV infusion methodology also permitted us to address a second question: After Dh, what are the responses of plasma AVP and Ald to Rh using different
osmotic loads (0.45 vs. 0.9% IV saline)? In this regard,
we hypothesized that the 0.9% IV saline treatment
would lead to higher plasma AVP and Ald concentra-
Address for reprint requests and other correspondence: R. W.
Kenefick, Dept. of Kinesiology, The Univ. of New Hampshire,
New Hampshire Hall, Durham, NH 03824 (E-mail: RWK@hopper.
unh.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.
arginine vasopressin; oropharyngeal; osmotic load
PROLONGED EXERCISE HEAT STRESS
http://www.jap.org
8750-7587/00 $5.00 Copyright © 2000 the American Physiological Society
2117
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Kenefick, Robert W., Carl M. Maresh, Lawrence E.
Armstrong, John W. Castellani, Deborah Riebe, Marcos E. Echegaray, and Stavros A. Kavorous. Plasma
vasopressin and aldosterone responses to oral and intravenous saline rehydration. J Appl Physiol 89: 2117–2122,
2000.—This investigation examined plasma arginine vasopressin (AVP) and aldosterone (Ald) responses to 1) oral and
intravenous (IV) methods of rehydration (Rh) and 2) different
IV Rh osmotic loads. We hypothesized that AVP and Ald
responses would be similar between IV and oral Rh and that
the greater osmolality and sodium concentration of a 0.9% IV
saline treatment would stimulate a greater AVP response
compared with a 0.45% IV saline treatment. On four occasions, eight men (age: 22.1 ⫾ 0.8 yr; height: 179.6 ⫾ 1.5 cm;
weight: 73.6 ⫾ 2.5 kg; maximum O2 consumption: 57.9 ⫾ 1.6
ml 䡠 kg⫺1 䡠 min⫺1, body fat: 7.7 ⫾ 0.9%) performed a dehydration (Dh) protocol (33°C) to establish a 4–5% reduction in
body weight. After Dh, subjects underwent each of three
randomly assigned Rh (back to ⫺2% body wt) treatments (0.9
and 0.45% IV saline, 0.45% oral saline) and a no Rh treatment during the first 45 min of a 100-min rest period. Blood
samples were obtained pre-Dh, immediately post-Dh, and at
15, 35, and 55 min post-Rh. Before Dh, plasma AVP and Ald
were not different among treatments but were significantly
elevated post-Dh. In general, at 15, 35, and 55 min post-Rh,
AVP, Ald, osmolality, and plasma volume shifts did not differ
between IV and oral fluid replacement. These results demonstrated that the manner in which plasma AVP and Ald
responded to oral and IV Rh or to different sodium concentrations (0.9 vs. 0.45%) was not different given the degree
of Dh (⫺4.5% body wt) and Rh and amount of time after Rh
(55 min).
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HORMONES AND REHYDRATION
tions because of a higher plasma sodium and osmolality (Osm) compared with the 0.45% IV saline treatment.
METHODS
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Subjects. Eight men, unacclimatized to heat, volunteered
to participate in this investigation. Physical characteristics
were as follows: age, 22.1 ⫾ 0.8 (SE) yr; height, 179.6 ⫾
1.5 cm; weight, 73.6 ⫾ 2.4 kg; maximal O2 consumption
(V̇O2 max), 57.9 ⫾ 1.6 ml 䡠 kg⫺1 䡠 min⫺1; percent body fat, 7.7 ⫾
0.9%. 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 approved all procedures. Subjects were given a
stipend for their participation.
Preliminary measures. V̇O2 max was determined by using a
continuous treadmill running test as previously described
(6). The hydrostatic weighing technique described by Katch
and Katch (20) was utilized to determine body density. Body
fat was calculated from the formula of Brozek et al. (4).
Measurement of residual lung volume was made by using a
nitrogen washout technique (32) on a pulmonary analysis
system (model 1070, Medical Graphics, St. Paul, MN).
Experimental design. Testing involved four treatments,
each consisting of two stages: 1) exercise-induced Dh and 2)
Rh. The Rh treatment protocols were randomly assigned and
separated by at least 14 days. The treatments were as follows: 0.9% IV infusion (0.9% IV); 0.45% IV infusion (0.45%
IV); 0.45% saline oral ingestion (0.45% Oral); and no Rh [no
fluid (NF)]. Subjects were asked to maintain similar diets
during the 3 days before each experimental trial and to
maintain a 3-day dietary record. These food diaries were then
analyzed for kilocalorie, carbohydrate, fat, protein, sodium,
and potassium content (Food Processor II, ESHA Research,
Salem, OR). Subjects were asked to refrain from any recreational or exercise training for 24 h before experimental
testing. They were also instructed to drink 450 ml of water
the night before testing and 450 ml of water the morning of
testing and to abstain from eating for 12 h before each
experimental treatment.
Experimental treatments. On arrival at the laboratory
(0700), subjects provided a urine sample for determination of
urine specific gravity (USG) (model A 300 CL, Spartan Refractometer). A USG of 1.023 ⫾ 0.006 (1) was used to verify
that the subject was adequately hydrated before each trial.
Hydration status was additionally verified by a pre-Dh
plasma Osm value of ⱕ286 ⫾ 3 mosmol/kgH2O (1). Subjects
were then fitted with a heart rate monitor (UNIQ heartwatch, Computer Instrument, Hempstead, NY), and a flexible thermistor (series 401, Yellow Springs Instruments, Yellow Springs, OH) was inserted 10 cm beyond the external
anal sphincter to monitor rectal temperature (Tre). A Teflon
catheter was then inserted into a superficial forearm vein,
and a male luer adapter (model 5877, Abbott Hospital, Chicago, IL) was inserted into the catheter port for acquisition of
subsequent blood samples. The catheter port and male luer
adapter were kept patent with heparin lock flush solution.
The subject then entered the environmental chamber (33°C;
model 2000, Minus-Eleven, Malden, MA) and stood quietly
for a 20-min equilibration period. A 26-ml blood sample
(baseline) was taken, and subjects then consumed a standard
breakfast of one bagel, one banana, and 240–350 ml (depending on body wt) of fruit juice.
For each of the four experimental trials, subjects performed an exercise-induced Dh protocol (33°C) to reduce body
weight by ⬃4%. The Dh protocol consisted of alternating
cycle ergometry (model 818E, Monark) and treadmill walking (Quinton, Seattle, WA) at an exercise-to-rest ratio of 25 to
5 min for each modality. Body weight was measured during
each rest interval. Urine was collected throughout the Dh
stage and was included as part of the weight loss. Subjects
continued exercising until the desired weight loss was
achieved. The last exercise mode before the ⫺4% weight loss
was always walking to ensure an upright posture. The time
to achieve the 4% decrease in body weight before each of the
four treatments was consistent for each individual subject.
The mean %V̇O2 max for the four Dh trials ranged from 49.8 to
51.1%. The mean ambient temperature and percent relative
humidity were 33.0 ⫾ 0.1°C and 47.6 ⫾ 0.5%, respectively.
Airflow (2.3 m/s) was generated by a fan directed at the
subject.
After Dh, a 26-ml blood sample was taken (post-Dh), and
the subject exited the chamber to a 25.5 ⫾ 0.2°C environment. Subjects assumed a recumbent position, and after a
15-min rest period received one of the three Rh treatments or
NF over a 45-min period. An experienced IV nurse, using a
butterfly catheter (1.5 in., 16 gauge; Abbott Laboratories,
North Chicago, IL), administered the IV infusions in the arm
opposite to the indwelling venous cannula. During the 0.45%
Oral and NF trials, a cannula was not placed in the opposite
arm during the Rh period. The rate of IV infusion was 0.56
ml 䡠 kg⫺1 䡠 min⫺1. 0.45% Oral consisted of 4 g of a commercial
sugar-free flavored beverage (Kool-Aid) dissolved in 889 ml of
0.45% NaCl and 111 ml of distilled deionized water. 0.45%
Oral was chilled to 4°C for palatability and was consumed in
equal volumes every 5 min over the 45-min period. The
composition of 0.45% Oral was 78.6 ⫾ 1.0 meq Na⫹/l, 0.96 ⫾
0.02 meq K⫹/l, and 2.54 ⫾ 0.07 meq Ca2⫹/l and 145.6 ⫾ 1.1
mosmol/kgH2O. Fluid intake was 25 ml/kg of pre-Dh body
weight. This volume has been shown to be the upper range
for fluids orally ingested after exercise-induced Dh (24). Immediately after Rh, subjects assumed a standing posture for
a 55-min period. Blood samples were taken 15, 35, and 55
min post-Rh.
Physiological measures. During all Dh bouts, the subject’s
heart rate and Tre were measured every 15 min to monitor
physiological strain. Heart rates that exceeded 180 beats/min
for 5 min terminated testing, as did a Tre of ⬎39.5°C. Oxygen
consumption was measured once every 30 min during the Dh
protocol for a 7- to 10-min period. Expired gas samples were
analyzed by using an on-line breath-by-breath metabolic
system (Medical Graphics CPX-D system).
Analysis of blood samples. Blood was transferred to tubes
containing EDTA, lithium heparin, or SST gel and clot activator for serum separation, depending on the specifications
for each blood variable. Serum or plasma was separated from
each sample and stored at ⫺80°C for later analysis. Samples
of whole blood were taken for analysis of Hb and hematocrit
(Hct). After centrifugation, plasma was separated and analyzed for Osm, sodium (Na⫹), and potassium (K⫹).
Hct was determined in triplicate by the microcapillary
technique after centrifugation for 4 min at 9,500 g. Values
were not corrected for trapped plasma. Hb was determined in
triplicate by the cyanomethemoglobin method (kit 525,
Sigma Chemical, St. Louis, MO). Percent change in PV
(%⌬PV) was calculated by using the equation of Dill and
Costill (13) from appropriate Hct and Hb values. All %⌬PV
values were calculated by using post-Dh as the initial time
point. Plasma Osm was measured in triplicate via freezingpoint depression (microosmometer model 3MO, Advanced
Instruments, Needham Heights, MA). Plasma and urine Na⫹
and K⫹ concentrations were determined in duplicate by se-
2119
HORMONES AND REHYDRATION
Table 1. Selected plasma and urine variables pre- and post-Dh
Pre-Dh
Post-Dh
0.45% IV
0.45% Oral
0.9% IV
NF
AVP, pg/ml
Ald, pg/ml
Osm, mosmol/kgH2O
Na⫹, meq/l
K⫹, meq/l
5.5 ⫾ 0.8
410 ⫾ 69
284 ⫾ 1
146 ⫾ 0.4
4.3 ⫾ 0.1
5.8 ⫾ 0.6
277 ⫾ 51
282 ⫾ 2
145 ⫾ 1.0
4.2 ⫾ 0.1
3.8 ⫾ 0.8
386 ⫾ 66
282 ⫾ 1
145 ⫾ 1.0
4.2 ⫾ 0.1
4.9 ⫾ 1.2
248 ⫾ 62
286 ⫾ 1
146 ⫾ 0.4
4.2 ⫾ 0.1
Osm, mosmol/kgH2O
Na⫹, meq/l
K⫹, meq/l
607 ⫾ 108
61 ⫾ 9
83 ⫾ 27
655 ⫾ 97
75 ⫾ 14
60 ⫾ 17
555 ⫾ 133
64 ⫾ 23
58 ⫾ 17
617 ⫾ 113
58 ⫾ 12
59 ⫾ 15
0.45% IV
0.45% Oral
0.9% IV
NF
20.0 ⫾ 1.9*
1,351 ⫾ 226*
294 ⫾ 2*
153 ⫾ 1.0*
4.9 ⫾ 0.1*
25.0 ⫾ 2.0*
996 ⫾ 190*
296 ⫾ 1*
151 ⫾ 1.0*
4.8 ⫾ 0.1*
15.4 ⫾ 1.9*
1,148 ⫾ 139*
294 ⫾ 2*
151 ⫾ 1.0*
4.7 ⫾ 0.1*
18.4 ⫾ 1.9*
1,054 ⫾ 147*
296 ⫾ 1*
151 ⫾ 1.0*
4.7 ⫾ 0.1*
403 ⫾ 101
63 ⫾ 7
65 ⫾ 25
432 ⫾ 94
52 ⫾ 6
57 ⫾ 16
Plasma
Urine
499 ⫾ 117
44 ⫾ 6
108 ⫾ 33
487 ⫾ 76
24 ⫾ 5*
108 ⫾ 40
Values are means ⫾ SE; n ⫽ 8 subjects. Pre- and Post-Dh, pre- and postdehydration; AVP, arginine vasopressin; Ald, aldosterone; Osm,
osmolality. Treatment groups are as follows: 0.9 and 0.45% intravenous saline infusion (0.9% IV and 0.45% IV, respectively), 0.45% saline
oral ingestion (0.45% Oral), and no rehydration [no fluid (NF)]. * Significant difference (P ⬍ 0.05) from corresponding Pre-Dh measure within
a treatment.
RESULTS
Pre-Dh. Pre-Dh dietary carbohydrate, sodium, and
total kilocalorie intakes were similar over the 3 days
before each experimental treatment. Pre-Dh body
weights were not different (P ⬎ 0.05) and were 75 ⫾ 2,
74 ⫾ 3, 74 ⫾ 3, and 74 ⫾ 3 kg for the 0.45% IV, 0.45%
Oral, 0.9% IV, and NF treatments, respectively.
Pre-Dh plasma and urine Osm, Na⫹, and K⫹ were not
different (P ⬎ 0.05) among treatments (Table 1).
Pre-Dh USG values were 1.018 ⫾ 0.002, 1.017 ⫾ 0.003,
1.018 ⫾ 0.004, and 1.014 ⫾ 0.004 for 0.45% IV, 0.45%
Oral, 0.9% IV, and NF, respectively, and were not
different among treatments.
Post-Dh plasma and urine values. Overall, post-Dh
values of plasma AVP and Ald were not different (Table 1). Similarly, plasma and urine Osm and electrolytes were similar among treatments pre- and post-Dh
(Table 1). In each treatment, post-Dh plasma AVP, Ald,
Osm, Na⫹, and K⫹ were significantly (P ⬍ 0.05) elevated above pre-Dh after the Dh protocol (Table 1).
Dh and Rh. There were no differences among treatments in exercise intensity (%V̇O2 max), exercise time,
urine volume, and percent weight loss during the Dh
protocol (Table 2). Also, there were no differences in
the volume of fluid given during infusion or ingestion.
Post-Rh percent weight loss (compared with the pre-Dh
body wt) was similar among the three treatment conditions (Table 2).
Plasma Osm. After Rh, ⌬Osm was greater (P ⬍ 0.05)
in the infusion and ingestion treatments vs. NF, with
no differences (P ⬎ 0.05) among 0.9% IV, 0.45% IV, and
0.45% Oral treatments (Fig. 1A).
Plasma sodium. At 15, 35, and 55 min post-Rh, the
⌬Na⫹ concentration was significantly greater (P ⬍
0.05) in 0.45% IV and 0.45% Oral vs. 0.9% IV and NF
(Fig. 1B).
⌬PV. %⌬PV was different (P ⬍ 0.05) at 15 min
post-Rh between the 0.45% Oral (⫹4 ⫾ 2%) and IV
infusions (⫹16 ⫾ 2 and ⫹11 ⫾ 3% for 0.9% IV and
Table 2. Selected Dh and Rh variables
⫺1
⫺1
Dh %V̇O2max, ml 䡠 kg 䡠 min
Exercise time, min
Post-Dh urine volume, liter
Rh fluid volume, ml
Post-Dh weight loss, %
Post-Rh weight loss, %
0.45% IV
0.45% Oral
0.9% IV
NF
51 ⫾ 2
190 ⫾ 12
0.34 ⫾ 0.12
1,890 ⫾ 45
4.4 ⫾ 0.07
2.1 ⫾ 0.10
50 ⫾ 2
182 ⫾ 8
0.45 ⫾ 0.15
1,856 ⫾ 65
5.1 ⫾ 0.14
2.3 ⫾ 0.07
50 ⫾ 3
179 ⫾ 12
0.44 ⫾ 0.11
1,889 ⫾ 62
4.5 ⫾ 0.07
2.1 ⫾ 0.10
51 ⫾ 2
180 ⫾ 10
0.48 ⫾ 0.09
4.6 ⫾ 0.07
4.3 ⫾ 0.04*
Values are means ⫾ SE; n ⫽ 8 subjects. %V̇O2max, percentage of maximum O2 consumption; Rh, rehydration. * Significant difference
(P ⬍ 0.05) from 0.9% IV, 0.45% IV and 0.45% Oral treatments.
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lective ion-sensitive electrodes (model 984-S, AVL Scientific,
Roswell, GA).
Endocrine measures. After extraction on silica columns
(DiaSorin, Stillwater, MN), plasma AVP was determined in
duplicate by a commercially available radioimmunoassay kit
(DiaSorin). AVP values were not corrected for extraction
recovery, which was 91.3%. Assay sensitivity was 7.042 ⫻
10⫺7 pg/ml. Serum levels of Ald were determined in duplicate
by radioimmunoassay (Diagnostics Products, Los Angeles,
CA). Assay sensitivity was 11.0 pg/ml. Within- and betweenassay coefficients of variability for both assays were ⬍5%.
Concentrations of AVP and Ald were not corrected for %⌬PV.
Statistical analysis. Analysis of variance (treatment ⫻
time) with repeated measures was used to compare differences among trials. A Newman-Keuls post hoc analysis was
employed to determine significant differences within and
between conditions. For the purpose of observing changes in
variables measured after Rh, all comparisons were made as
an absolute change (⌬) from the post-Dh values and analyzed
by using a two-way (treatment ⫻ time) analysis of variance
with repeated measures. The 0.05 level of significance was
selected. All data are presented as means ⫾ SE.
2120
HORMONES AND REHYDRATION
0.45% IV, respectively) (Fig. 2). However, at minutes 35
and 55 of post-Rh, no differences were observed. %⌬PV
was similar between 0.45% IV and 0.9% IV (Fig. 2).
Plasma AVP. The ⌬AVP was greater for infusion and
ingestion treatments (P ⬍ 0.05) vs. NF after Rh (Fig.
3A). No differences were observed among 0.45% Oral,
0.45% IV, and 0.9% IV.
Plasma Ald. The ⌬Ald for all four Rh treatments was
not different 15 min post-Rh (Fig. 3B). However, at
minutes 35 and 55, the ⌬Ald for the infusion and
ingestion treatments was significantly greater (P ⬍
0.05) compared with NF (Fig. 3). No differences were
observed among 0.45% Oral, 0.45% IV, and 0.9% IV.
DISCUSSION
In the present study, a ⫺4 to ⫺5% exercise-induced
Dh caused subjects to become hyperosmotic and hypovolemic, because of hypotonic sweat production. This,
in turn, enhanced circulating concentrations of vasopressin and Ald observed post-Dh. Additionally, as is
evident from PV and Osm data in the “no fluid” trial,
Fig. 2. Percent change in plasma volume as a function of time after
rehydration with NF, 0.9% IV, 0.45% IV, and 0.45% Oral. Postdehydration is considered the reference point. Pre Dehy, predehydration.
Values are means ⫾ SE. #0.45% Oral significantly different from
0.9% IV and 0.45% IV, P ⬍ 0.05. ⫹NF significantly different from
0.9% IV, 0.45% IV, and 0.45% Oral, P ⬍ 0.05.
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Fig. 1. Change in plasma osmolality (A) and sodium concentration
(B) as a function of time after no rehydration [no fluid (NF)] or
rehydration (Rehyd) with 0.9% intravenous (IV) saline (0.9% IV),
0.45% IV saline (0.45% IV), and 0.45% oral saline (0.45% Oral).
Postdehydration (Post Dehy) is considered the reference point. 15,
35, and 55-min Post values are postrehydration. Values are means ⫾
SE. ⫹NF significantly different from 0.9% IV, 0.45% IV, and 0.45%
Oral, P ⬍ 0.05. *NF and 0.9% IV significantly different from 0.45%
IV and 0.45% Oral, P ⬍ 0.05.
this state of hyperosmotic hypovolemia was maintained when body fluids were not restored. Consequently, concentrations of vasopressin and Ald remained elevated throughout the NF trial. These
responses are in agreement with other investigations
that have shown that Dh stimulates an increase in
these fluid regulatory factors (7, 10). However, it is
unknown how different Rh modes (oral vs. IV) or different IV fluids (osmotic stimulus) affect circulating
vasopressin or Ald concentrations after exercise-induced Dh. Our findings demonstrate that the manner
in which plasma AVP and Ald respond to different Rh
modes or sodium concentration (0.9 or 0.45%) was not
different, given the period of time allowed for Rh.
Infusion vs. drinking. The post-Rh ⌬AVP was not
different between the 0.45% IV and 0.45% Oral conditions. Additionally, there was no difference observed in
plasma Osm between these two treatments, which has
been demonstrated to be the major stimulus for AVP
release (19). PV has also been shown to be another
factor influencing AVP (19). In the present study,
%⌬PV was different at 15 min post-Rh between the
0.45% Oral and 0.45% IV treatments. Given the
greater time required for fluid to empty the gut, it
might be expected that the ⌬AVP might not be as great
in drinking compared with infusion. Although not statistically significant, however, ⌬AVP at 15 min post-Rh
fell to a greater extent in 0.45% Oral compared with
infusions, despite the lower %⌬PV. One mechanism
might be the residual effects of the oropharyngeal
reflex, which exerts its influence on plasma AVP concentrations almost immediately (18, 27). During oral
ingestion of fluid in animals and humans, the reduction in AVP release seems to be an anticipatory response to the absorption of water and the decrease in
plasma Osm after water intake (2, 18, 25, 27, 29, 30).
Collectively, these studies suggest that oropharyngeal
receptors may initiate a more rapid inhibition of AVP
before a decline in plasma Osm or PV is detectable. In
HORMONES AND REHYDRATION
humans, oropharyngeal receptors have been implicated in the rapid, transient fall in plasma AVP due to
drinking (18, 27). A comparable decrease in plasma
AVP may have occurred in 0.45% Oral; however, the
15-min post-Rh measure may have been too late to
observe this well-documented response.
The ⌬Ald was not different among any of the Rh
treatments at 15 min post-Rh. However, ⌬Ald was
different between the infusion and ingestion treatments and NF at 35 and 55 min post-Rh (Fig. 3).
Changes in blood volume have been shown to be one of
the primary influences on Ald secretion (16). Additionally, plasma Ald concentrations have been demonstrated to be affected by circadian variation and dietary sodium and potassium intake (8, 17, 21, 31). The
Ald response in this study was primarily determined
by factors related to the maintenance of PV for the
following reasons. First, experimental testing occurred
at the same time of day for each trial. Second, dietary
sodium and potassium intake was similar for 3 days
before each treatment, and pre-Dh measures of plasma
sodium and potassium were not different (Table 1).
Third, with the exception of 15 min post-Rh, %⌬PV was
not different between infusion and ingestion, and the
amount of fluid restored during Rh was not different
among these treatments (Table 2).
We also hypothesized that PV shifts would not be
different among the Rh treatments because of the
consistent volume infused or orally ingested. Costill
and Sparks (12) reported that Rh with a glucose-electrolyte solution resulted in a better recovery of PV than
did tap water after thermal Dh. Nose et al. (24) reported a greater restoration of PV with a sodiumchloride solution compared with water after exerciseinduced Dh. In the present study, both the infused and
ingested solutions contained sodium chloride. Because
of the similar composition of the oral and IV fluids,
post-Rh %⌬PV tended not to be different. The only
difference in %⌬PV found among Rh treatments was at
15 min post-Rh. At this time point, the PV recovered to
a greater extent in both the 0.9% IV and 0.45% IV
trials compared with the 0.45% Oral treatment. By 35
min post-Rh, however, no differences in %⌬PV existed
among Rh treatments. The difference observed at 15
min post-Rh was likely due to limitations imposed by
gastric emptying (9) and transit compared with IV
administration. By 35 min post-Rh, the %⌬PV in 0.45%
Oral was not different compared with the IV treatments, and a greater amount of fluid had emptied from
the gut and entered the circulation.
0.9% IV vs. 0.45% IV. In the present study, Rh with
both 0.9% and 0.45% saline concentrations equally
blunted AVP and Ald responses. In previous studies in
which subjects received water or an electrolyte solution
before or during exercise in a warm environment,
plasma AVP and Ald were also reduced (3, 14, 15). We
reasoned that the 0.9% saline infusion used in this
study would increase the plasma sodium concentration
above that of the 0.45% saline treatment and subsequently continue to elevate plasma Osm after Rh and
stimulate AVP secretion. Although the sodium concentration in the 0.9% IV treatment was significantly
greater at 15, 35, and 55 min post-Rh, compared with
that in 0.45% IV, plasma Osm was not different
post-Rh between treatments, and ⌬AVP values were
not different. Plasma Osm in the present study did
parallel plasma sodium at each of the recovery time
points, as previously observed by Nose et al. (24). It is
possible that, whereas the volume or concentration of
IV saline infused was large enough to cause differences
in plasma sodium in the 0.9% IV treatment, it may not
have been large enough to cause differences in plasma
Osm between the 0.9% IV and 0.45% IV treatments. It
is also possible that the addition of 0.9% saline did, in
fact, temporarily raise plasma Osm. Because osmotic
forces cause water to move between intravascular and
interstitial compartments (24), this temporary increase might have caused a fluid shift from the interstitum into the vasculature, thereby reducing plasma
Osm and plasma AVP.
In brief, the results of the present investigation demonstrated that the manner in which fluid regulatory
hormones responded to different methods of Rh (IV or
oral) or sodium concentration (0.9 or 0.45%) was not
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Fig. 3. Change in plasma arginine vasopressin (A) and aldosterone
(B) as a function of time after rehydration with NF, 0.9% IV, 0.45%
IV, and 0.45% Oral. Postdehydration is considered the reference
point. Values are means ⫾ SE. ⫹NF significantly different from 0.9%
IV, 0.45% IV, and 0.45% Oral, P ⬍ 0.05.
2121
2122
HORMONES AND REHYDRATION
different. Clearly, the use of IV reinfusion offers no
advantage over oral Rh and is equally effective in
restoring fluid volume, given the degree of Dh (⫺4%
body wt) and time permitted for Rh (100 min). This
finding is important for individuals who exercise multiple times in 1 day, and our laboratory has shown (6)
that there is no performance or thermoregulatory advantage to rehydrating by using IV infusion before the
performance of subsequent exercise.
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The authors thank Marie Kenefick, Mike Whittlesey, Stavros
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We also thank the subjects for their participation. Additionally, the
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This work was supported in part by a grant from the Proctor and
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Research Foundation.
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