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1 Department of Kinesiology, The University of New Hampshire, Durham, New Hampshire 03824; and Departments of 2 Kinesiology, 3 Physiology and Neurobiology, and 4 Nutritional Sciences, University of Connecticut, Storrs, Connecticut 06269-1110
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ABSTRACT |
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 TOP
 ABSTRACT
 INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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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 · kg
1 · min1, 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).
arginine vasopressin; oropharyngeal; osmotic load
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INTRODUCTION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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PROLONGED EXERCISE HEAT STRESS 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 fluid-regulating 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 exercise-induced 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 concentrations
because of a higher plasma sodium and osmolality (Osm) compared with
the 0.45% IV saline treatment.
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METHODS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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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
(
O2 max), 57.9 ± 1.6 ml · kg1 · min1; 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.
O2 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 
286 ± 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.
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 %O2 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 · kg1 · min1. 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+).
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 freezing-point
depression (microosmometer model 3MO, Advanced Instruments, Needham
Heights, MA). Plasma and urine Na+ and K+
concentrations were determined in duplicate by selective 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 × 107 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 between-assay
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.
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RESULTS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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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.
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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
(%O2 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).
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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).
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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 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).
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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.
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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.
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DISCUSSION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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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, 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 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.
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 sodium-chloride solution compared
with water after exercise-induced 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.
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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ACKNOWLEDGEMENTS |
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The authors thank Marie Kenefick, Mike Whittlesey, Stavros Kavouras, Dane McFarland, and Dean Aresco for technical support. We also thank the subjects for their participation. Additionally, the authors thank Deborah A. Podolin for editorial assistance.
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FOOTNOTES |
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This work was supported in part by a grant from the Proctor and Gamble Company and a grant from the University of Connecticut Research Foundation.
Present addresses: J. W. Castellani, Thermal and Mountain Medicine Division, US Army Research Institute of Environmental Medicine, Natick, MA 01760-5007; D. Riebe, Dept. of Physical Education, University of Rhode Island, Kingston, RI 02881; M. E. Echegaray, Dept. of Physiology, University of Puerto Rico, Rio, PR 00927.
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{at}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.
Received 27 October 1999; accepted in final form 28 June 2000.
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REFERENCES |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
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