Vol. 89, Issue 4, 1302-1309, October 2000
Postexercise rehydration: effect of Na+ and volume
on restoration of fluid spaces and cardiovascular function
J. B.
Mitchell,
M. D.
Phillips,
S. P.
Mercer,
H. L.
Baylies, and
F. X.
Pizza
Exercise Physiology Laboratory, Department of Kinesiology,
Texas Christian University, Fort Worth, Texas 76129
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ABSTRACT |
Our
purpose was to study the interaction between Na+ content
and fluid volume on rehydration (RH) and restoration of fluid spaces
and cardiovascular (CV) function. Ten men completed four trials in
which they exercised in a 35°C environment until dehydrated by 2.9%
body mass, were rehydrated for 180 min, and exercised for an additional
20 min. Four RH regimens were tested: low volume (100% fluid
replacement)-low (25 mM) Na+ (LL), low volume-high (50 mM)
Na+ (LH), high volume (150% fluid replacement)-low
Na+ (HL), and high volume-high Na+ (HH). Blood
and urine samples were collected and body mass was measured before and
after exercise and every hour during RH. Before and after the
dehydration exercise and during the 20 min of exercise after RH,
cardiac output was measured. Fluid compartment (intracellular and
extracellular) restoration and percent change in plasma volume were
calculated using the Cl
and hematocrit/Hb methods,
respectively. RH was greater (P < 0.05) in HL and HH
(102.0 ± 15.2 and 103.7 ± 14.7%, respectively) than in LL
and LH (70.7 ± 10.5 and 75.9 ± 6.3%, respectively). Intracellular RH was greater in HL (1.12 ± 0.4 liters) than in all other conditions (0.83 ± 0.3, 0.69 ± 0.2, and 0.73 ± 0.3 liter for LL, LH, and HH, respectively), whereas extracellular
RH (including plasma volume) was greater in HL and HH (1.35 ± 0.8 and 1.63 ± 0.4 liters, respectively) than in LL and LH (0.83 ± 0.3 and 1.05 ± 0.4 liters, respectively). CV function (based
on stroke volume, heart rate, and cardiac output) was restored equally
in all conditions. These data indicate that greater RH can be achieved
through larger volumes of fluid and is not affected by Na+
content within the range tested. Higher Na+ content favors
extracellular fluid filling, whereas intracellular fluid benefits from
higher volumes of fluid with lower Na+. Alterations in
Na+ and/or volume within the range tested do not affect the
degree of restoration of CV function.
fluid replacement; plasma volume; extracellular and intracellular
fluid
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INTRODUCTION |
THE RAPID
RESTORATION of body fluids is necessary after activities that
lead to significant dehydration, particularly when additional physical
exertion is to be conducted on the same day. Previous research has
shown that to achieve complete rehydration, a volume of fluid greater
than that lost should be consumed (9, 11, 20). In
addition, an oral rehydration solution should contain enough
Na+ to prevent excessive urine production. Maughan and
Leiper (8) and others have suggested that the amount of
Na+ ingested should be similar to the amount lost, since
extracellular fluid balance and Na+ balance are closely
linked (17, 21). By simultaneously varying the volume and
Na+ concentration of the fluid ingested, it is possible to
gain insight into the interaction between these two important
rehydration variables.
Although a number of investigations have been conducted to examine
postexercise rehydration (5, 7, 10, 11, 15), few studies
have included an assessment of function after a fluid replacement
regimen. Among others, cardiovascular responses are negatively affected
by dehydration (12, 14); thus a major determinant of the
efficacy of a rehydration protocol would be the restoration of the
dehydration-induced alterations in cardiovascular function. Costill and
Sparks (2) found that the heart rate response to exercise
was normalized with only 62% replacement, even in the face of
incomplete plasma volume restoration. On the other hand, Nielsen et al.
(15) reported that submaximal exercise heart rates were
elevated after a fluid regimen that produced ~75% rehydration and,
in some conditions, a positive percent change in plasma volume.
Similarly, Heaps et al. (6) reported that 65% rehydration
did not restore cardiovascular function as indicated by the persistence
of elevated heart rate and decreased stroke volume, even though blood
volume had been restored. Furthermore, Montain and Coyle
(12) showed that, during exercise, fluid replacement of
80% is necessary to prevent large declines in stroke volume and
cardiac output. Thus there are discrepancies in the literature in this
area, and an analysis of the interaction between Na+ intake
and the volume of fluid consumed on cardiovascular function has not
been conducted.
The majority of rehydration studies have focused on whole body fluid
restoration, with less attention given to the measurement of
intracellular and extracellular fluid spaces. Nose et al.
(17) reported that when Na+ was administered
in capsule form (equivalent to ~77 mM) during an ad libitum
rehydration procedure, it produced an accelerated extracellular
recovery compared with plain water. This finding is similar to that
reported by Nielsen et al. (15) when a
high-Na+ (127 mM) solution was used. Both of these levels
of Na+ are higher than the recommended concentration for a
post- exercise oral rehydration solution (4) and may pose
a problem with beverage palatability. The use of different volumes of
fluid combined with Na+ content within recommended
concentrations provides an opportunity to investigate the influence of
these variables on the movement of fluid into the various body fluid spaces.
The purpose of this investigation was to examine the interaction
between Na+ content and volume ingested on the postexercise
whole body rehydration and the restoration of cardiovascular function
and fluid compartments. Specifically, using a two-by-two design, we
investigated the ingestion of fluid at 100 and 150% of body mass lost
with Na+ at 25 and 50 mM. It was hypothesized that the most
effective rehydration would occur with the 150%-50 mM treatment and
that this would selectively restore the extracellular space to a
greater extent than the other treatments. Furthermore, it was
hypothesized that the recovery of cardiovascular function would be
influenced by the level of rehydration.
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METHODS |
Subjects.
Ten moderately trained men capable of performing 90 min of cycling at
60% of their maximal O2 power
(
O2 max) were chosen as subjects. Their
age, weight, and O2 max were 27.5 ± 5.8 yr, 79.60 ± 11.9 kg, and 3.88 ± 0.47 l/min,
respectively. The subjects first completed a medical history
questionnaire and then read and signed an institutionally approved
informed consent form.
Experimental design.
The subjects were first tested for
O2 max by use of a standard graded
cycle ergometer test, the results of which were used to determine their
target submaximal workload during the experimental trials. Each subject
was then subjected to four rehydration conditions conducted in a
randomized counterbalanced design, with each trial separated by 1 wk.
The following conditions were imposed: 1) low volume (100%
of volume lost)-low (25 mM) Na+ (LL), 2) low
volume-high (50 mM) Na+ (LH), 3) high volume-low
Na+ (HL), and 4) high volume-high
Na+ (HH). The four conditions consisted of 90 min of
exercise-induced dehydration, a 30-min transition period, and 180 min
of rehydration. A 20-min steady-state ride was conducted after
rehydration to assess the recovery of cardiovascular function. During
the 24 h before each condition, diet, fluid intake, and exercise
were standardized.
Experimental testing.
Before exercise, a venous blood sample was taken after 30 min of seated
rest. The subjects emptied their bladders, and nude body mass was
measured using a digital scale accurate to 20 g. Subjects were
fitted with a rectal thermistor inserted to a depth of 12 cm, and a
telemetry heart rate monitor (Polar) was placed around the chest. The
90-min exercise bout was conducted in an environmentally controlled
chamber adjusted to 35°C and 55% relative humidity. Each subject
rode on a Monark cycle ergometer at ~60% of
O2 max until 2.5% of initial body
weight was lost or until a core temperature of 39°C was reached. Core
temperature was monitored continuously during exercise and recorded
every 15 min. During the first and last 10 min of exercise, a series of
three CO2 rebreathing maneuvers were conducted to determine cardiac output. During this same period, O2 uptake was
measured by analysis of expired gases collected in Douglas bags, and
heart rates were recorded. Sweat samples were obtained from an arm bag at 20, 50, and 80 min of the ride. The arm was rinsed thoroughly with
distilled water and dried with a clean towel before each collection.
Immediately after exercise, the subjects were removed to a normal room
temperature environment (23°C, 50% relative humidity). They rested
in a seated position for 30 min before rehydration to allow the
reversal of the exercise-induced plasma volume shift. At the end of
this transition period, a blood sample was taken from an antecubital
vein, a urine sample was collected and measured, and nude body mass was
obtained. Total dehydration was calculated at this point; thus
dehydration was based on the difference between the initial nude body
mass and the body mass at the end of the transition period.
After the transition period, subjects ingested the first drink of the
rehydration period, which was administered as a "priming dose" and
was 30% of the total to be ingested for the particular condition. The
subsequent volumes were administered at 30-min intervals and were
one-fifth of the remaining volume to be ingested for each condition
(14% of the total volume). In the LL and LH conditions, the total
volume consumed equaled the total loss in body mass. In the HL and HH
conditions, subjects consumed 1.5 times the body mass loss. The priming
dose in the LL and LH conditions averaged 683 ml, and the subsequent
volume was 319 ml for a total volume ingested of 2.28 liters. The
priming dose in the HL and HH conditions averaged 1,017 ml, and the
subsequent volume was 475 ml for a total volume of 3.39 liters. The
rehydration solution was a noncommercial beverage containing 50 g/l
maltodextrin and 25 or 50 mM Na+ for the low- and
high-Na+ conditions, respectively. A solution containing
carbohydrate was used to facilitate intestinal absorption. At 60, 120, and 180 min of rehydration, a blood sample was drawn and urine volume and body weight were measured.
After the 180-min rehydration protocol, the subjects returned to the
heat chamber and completed an additional 20 min of exercise at the same
intensity used for the dehydration exercise. After a steady state was
reached, the CO2 rebreathing maneuver was again conducted.
Heart rates were recorded, and respiratory gases were collected in
Douglas bags.
Blood and fluid analyses.
Whole blood samples were analyzed for hematocrit and Hb by use of the
microcapillary tube and cyanmethemoglobin methods, respectively. Plasma
samples were obtained and frozen for later analysis of osmolality
(freeze-point depression; Advanced Instruments, Norwood, MA),
electrolytes (Na+, K+, and Cl;
Nova V Analyzer), and antidiuretic hormone (ADH) by RIA (Diagnostic Products, Los Angeles, CA). Urine and sweat samples were collected, and
a sample was frozen for determination of urine electrolytes (Na+, K+, and Cl; Nova V Analyzer).
Calculations.
Percent dehydration was calculated as the difference between the
prerehydration and preexercise body mass divided by the preexercise body mass. Percent rehydration was calculated as the body mass gain
during rehydration divided by the total mass lost. Percent change in
plasma volume was calculated according to the method of Dill and
Costill (3). Sweat loss was calculated as the body mass
loss with adjustments made for respiratory water loss and metabolic
carbon loss. Na+ balance was determined by subtracting
absolute Na+ loss (sweat and urine volume multiplied by
their respective Na+ concentrations) from total
Na+ intake in the rehydration solutions. Changes in fluid
compartments during rehydration were calculated using the
Cl method described by Costill et al. (1)
and Nose et al. (17). A Donnan factor of 0.95 was used in
this calculation. Absolute plasma volume was assumed to be 7% of
preexercise body mass for the purposes of these calculations.
Statistical analyses.
A three-factor ANOVA for repeated measures was conducted for the
majority of the dependent variables. The first factor was "volume"
and had two levels (100 and 150%), the second factor was
"Na+" and also had two levels (25 and 50 mM), and the
third factor was "time" and had various levels depending on the
number of samples taken. Variables that were analyzed at only one time
point (percent dehydration, fluid compartment data, and Na+
balance) were analyzed using a two-factor ANOVA. Differences detected
by the ANOVA were analyzed further using a Newman-Keuls post hoc test.
Relationships between selected dependent measures were conducted using
Pearson product correlations. Significance was accepted at
P < 0.05.
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RESULTS |
Rehydration and urine volume results.
The level of rehydration was significantly greater in both high-volume
trials than in both low-volume trials (Fig.
1). This difference was present at all
three hourly time points. The restoration of plasma volume, expressed
as percent change, showed a main effect for Na+ with no
interaction with time or volume; however, the differences between the
LL and HL conditions compared with the LH and HH conditions appeared to
be present throughout the rehydration period (Fig. 2). The restoration of extracellular
fluid and the interstitial fluid volumes showed a main effect for
volume; thus the HL and HH conditions were greater than the LL and LH
conditions (Fig. 3). On the other hand,
the restoration of intracellular fluid volume showed a significant
Na+-by-volume interaction, such that the HL condition was
significantly greater than all others. Urine production demonstrated a
volume-by-time interaction, with the level of urine production
significantly greater in the HL and HH conditions than in the LL and LH
conditions at 2 and 3 h of rehydration (Fig.
4).
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Fig. 1.
Whole body rehydration. LL, low volume (100% fluid
replacement)-low (25 mM) Na+; LH, low volume-high (50 mM)
Na+; HL, high volume (150% fluid replacement)-low
Na+; HH, high volume-high Na+. * Significant
volume main effect. HH and HL are different from LL and LH at all 3 time points (P < 0.05).
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Fig. 2.
Percent change in plasma volume (% ). Pre,
preexercise; Post, postexercise.  Na+
main effect. LH and HH are different from LL and HL (P < 0.05).
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Fig. 3.
Fluid compartment restoration (in liters).
* Significant volume main effect. HH and HL are different from LH
and LL for extracellular fluid (ECF) and interstitial fluid (ISF).
a Na+ × volume interaction. HL is
different from all other conditions for intracellular fluid (ICF;
P < 0.05).
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Fig. 4.
Urine volume. Post Ex, after exercise.
c Significant volume × time interaction. HL and HH
are different from LL and LH at hours 2 and 3 (P < 0.05).
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Na+ results.
The amount of Na+ actually consumed varied because of the
manipulation of concentration and volume. These values were 65.6 ± 9.8, 117 ± 19.4, 95.4 ± 17.9, and 179 ± 30 mM for
the LL, LH, HL, and HH conditions, respectively. Plasma Na+
demonstrated only a main effect for time, with an elevation occurring at the postexercise time point for all conditions (Fig.
5). Plasma osmolality showed the same
pattern of significance as plasma Na+. Urine
Na+, however, showed an Na+-by-time interaction
such that the levels in the LH and HH conditions were greater than in
the LL and HL conditions but only at 2 and 3 h of rehydration
(Fig. 5). The calculated values of Na+ balance, expressed
as an Na+ deficit based on urine and sweat loss vs. intake,
showed a main effect for Na+ (Fig. 5). The deficit in the
LH and HH conditions was significantly less than in the LL and HL
conditions, with the deficit in the HH condition approaching zero.
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Fig. 5.
A: plasma Na+. B:
absolute urine Na+ loss. C: Na+
balance.  Significant time effect. Postexercise value
is different from all others in all conditions.
b Na+ × time interaction. LH and HH
are different from LL and HL at hours 2 and 3 (P < 0.05).
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Cardiovascular, temperature, and hormonal results.
All three cardiovascular variables showed a significant time effect,
with cardiac output and stroke volume decreasing significantly after
the dehydration exercise and then returning to preexercise levels after
rehydration (Fig. 6). Heart rate
demonstrated the opposite response. Core temperature increased in all
conditions at the end of the dehydration exercise and again at the end
of the 20 min of exercise that followed rehydration (Table
1). None of the conditions varied from
each other. ADH increased after exercise; however, none of the
conditions were significantly different from each other (Fig.
7).
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Fig. 6.
A: cardiac output. B: heart rate.
C: stroke volume. Rehyd, rehydration.
Significant time effect (P < 0.05).
Postexercise value is different from all others in all conditions.
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Fig. 7.
Antidiuretic hormone. Significant time
effect (P < 0.05). Postexercise value is different
from all others in all conditions.
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DISCUSSION |
The primary findings of this investigation were that when 25 mM
Na+ was compared with 50 mM Na+, the
Na+ content of the rehydration beverage did not influence
whole body rehydration; however, the ingestion of 150 vs. 100% of
fluid lost significantly improved the level of rehydration. On the
basis of these findings, no interaction between Na+ and
volume was observed for whole body rehydration. On the other hand, the
difference in Na+ content and volume did influence the
levels of extracellular vs. intracellular rehydration. Finally,
the degree of restoration of cardiovascular function was not affected
by the Na+ content or the volume of fluid ingested.
Rehydration.
A variety of rehydration protocols have been reported in the literature
over the past several years, many of which have been designed to
investigate the influence of electrolyte content and fluid volume on
rapid rehydration. Conflicting findings regarding the level of
Na+ and volume necessary to produce optimal rehydration
have been reported; however, variations in the rehydration protocols
employed may partially explain the discrepancies (2, 5, 7, 15, 17). Although many studies have employed serial feedings, the protocols typically employed by Maughan et al. (8-10)
and Shirreffs et al. (20) involve the ingestion of large
volumes of fluid (2-3 liters) in a relatively short (30-60
min) period of time. In the present study, the volume of fluid was
consumed over a 2.5-h period in serial feedings every 30 min. This
protocol more closely approximates ingestion patterns that might be
used in actual practice, since extreme stomach fullness would be
avoided. On the other hand, a significant strength of the studies by
Maughan et al. is that their subjects were followed for 5.5-6.0 h,
thus providing a more complete picture of the effect of the fluid
consumed on kidney function.
Previous work from our laboratory (11) and by Maughan et
al. (9) has shown that, to maximize rehydration, a volume
of fluid of 150% of that lost must be ingested. In addition, the solution must contain an amount of Na+ or other cation
sufficient to prevent significant urine production. When
Na+ levels are relatively low, even large volumes of fluid
do not appear adequate to produce rapid rehydration. With the ingestion of 14 mM Na+ (volume = 150% of fluid lost), Mitchell
et al. (11) achieved only 73% rehydration after 3 h
of rehydration, despite ingestion of 150% of fluid lost. Maughan and
Leiper (8) showed that, 5.5 h after ingestion of
150% of fluid lost at 26 mM Na+, subjects had retained
only 53% of that consumed, thus achieving ~80% rehydration. Even
with volumes of 150 and 200% of that lost, after 6 h, Shirreffs
et al. (20) reported that fluid balance was not achieved
with a 23 mM Na+ solution. These findings would suggest
that the optimal Na+ concentration is somewhere above 25 mM. Conversely, in the present investigation, increasing
Na+ concentration from 25 to 50 mM did not improve
rehydration, suggesting that no further benefits are gained by doubling
the concentration. It may be that the discrepancy can be explained by
the use of a 3-h protocol compared with a 5- or 6-h protocol; however,
direct comparisons are not possible, because the difference in the
ingestion pattern may influence urine production and the associated
percent rehydration. The final 2-4 h of the longer protocols by
Maughan and Leiper (8) produced relatively small changes in net fluid balance; thus the duration of the protocol may not be an issue. Furthermore, in general agreement with the present findings, Wemple et
al. (21) found that the increase in Na+ from
25 to 50 mM did not produce an enhanced whole body rehydration during a
3-h protocol.
The present findings are not in agreement with the concept that
Na+ replacement must occur to accomplish complete
rehydration (8). The relatively large Na+
deficit in the HL condition did not interfere with fluid
restoration, since 100% rehydration was achieved. Because of the
manipulation of volume and Na+ concentration, the LH
condition actually produced a smaller Na+ deficit than the
HL condition. This combination did not produce a significantly greater
fluid replacement than the other low-volume condition (LL), which
resulted in the largest deficit. Calculations of Na+
balance are, of course, influenced by sweat Na+
concentrations, which vary between subjects and according to the
sampling site. The use of arm bag sweat collection may have led to
relatively high sweat Na+ concentrations, thus exaggerating
the calculated deficit in all conditions. Regardless of the magnitude
of the Na+ deficit, however, the present data did not
produce a graded response that would indicate a relationship between
Na+ replacement and fluid gain.
Limited work has been conducted to investigate fluid compartment
restoration during postexercise rehydration; however, Nose et al.
(17) and Nielsen et al. (15) showed that high
Na+ concentrations favor extracellular refilling. In both
cases, the Na+ levels were quite high, with ~70 and 128 mM used by Nose et al. (18) and Nielsen et al.,
respectively. In the present investigation, the main effect for volume,
with no Na+-by-volume interaction, suggests that the
difference between 25 and 50 mM was not great enough to influence the
degree of extracellular restoration. Furthermore, it may be that 25 mM
is an adequate level of Na+, and once this level is
reached, the introduction of a greater volume of available fluid then
becomes a more powerful factor in extracellular rehydration. From a
practical point of view, extremely high Na+ concentrations
may present a palatability problem; thus the lower end of the
functional range would be preferable. Relative to intracellular rehydration, the findings differ from those of the extracellular compartment. The greater intracellular restoration in the HL condition suggests that when volume is high and Na+ is low, the cells
are able to take advantage of the greater fluid availability and the
absence of the Na+-induced osmotic forces that favor the
extracellular space. Of the combinations of Na+ and volume
tested in this study, none of which were specifically designed to
promote intracellular rehydration, the HL condition appears to be the
most effective for intracellular rehydration. Other combinations of
cations ingested with different volumes should be examined to determine
an optimal combination for maximizing intracellular restoration.
The Na+ main effect found for plasma volume restoration
suggests that, for the vascular space, Na+ was a more
significant factor than volume; however, complete restoration occurred
in all trials by 2 h of recovery. In fact, in the
high-Na+ conditions, there was actually an expansion of
plasma volume above the preexercise level, an effect that can probably
be attributed to the osmotic force created by the presence of
Na+. The selective restoration of plasma volume,
particularly in the presence of high Na+, has been reported
by others (2, 18, 21). Although it might be assumed that
Na+ intake would have an effect on plasma Na+
and/or osmolality, which in turn would affect plasma volume, neither
variable exhibited condition differences as a function of
Na+ concentration. This is likely due to the fact that the
restoration of plasma volume comes about in an attempt to normalize
plasma Na+ and osmolality; thus what we observed is the
outcome of the normalization process. It appears that the vascular
space is more sensitive to the influence of Na+ than the
extracellular fluid as a whole, since, in the latter, significant
increases occurred only in combination with higher volumes of fluid ingested.
Urine and hormonal results.
Numerous studies have shown that the primary obstacle to rapid
rehydration is the loss of large amounts of fluid in the form of urine.
As mentioned previously, if Na+ or some other cation is
added, kidney function and the concomitant hormonal responses may be
altered so that fluid is retained (8, 20). The poor
rehydration reported by Mitchell et al. (11) with a 14 mM
solution was due to high urine volumes. Shirreffs et al.
(20) also showed that urine production tended to be
greater with rehydration with 23 than with 61 mM Na+; thus
it was advantageous to increase Na+ above 25 mM. In the
present study, the urine results showed only a main effect for volume;
thus there was no advantage to increasing Na+ above 25 mM.
The activity of fluid-regulating hormones such as ADH is important in
providing a mechanism for the control of urine production. It is known
that ADH release is stimulated by increased osmolality, which is
detected by receptors in the hypothalamus (13, 16, 19).
Extracellular Na+ concentration plays a major role in
determining the osmolality; thus any dilution of the extracellular
space will signal the inhibition of ADH release, which, in turn,
promotes water loss via the increased permeability of the distal
tubule. This scenario explains the large urine production and poor
rehydration observed with the consumption of dilute oral rehydration
solutions. As expected, exercise-induced dehydration elicited an
increase in ADH levels in the present study; however, at 1 h of
rehydration, ADH levels were not significantly different from
preexercise levels. Physiologically significant elevations in some
conditions may have been detectable if blood samples had been taken
earlier in recovery. Plasma Na+ and plasma volume and ADH
were restored at approximately the same time. Although there was an
Na+-by-time interaction for absolute urine Na+
loss, the total amount of Na+ unloaded in the urine over
the 3-h period was relatively small (2-10 mM). Combined with the
Na+ balance calculation, which shows a fairly large deficit
in all but the HH condition, these data indicate that the majority of the Na+ ingested was retained, especially in the vascular
space, and probably in the extracellular space in general. The result
was removal of the stimulus to release ADH and possibly other hormones such as aldosterone and angiotensin. In the low-volume trials, therefore, there was not an excess of fluid that could be used to
overcome the increase in urine production that took place during the
2nd and 3rd h of rehydration. Because there was not an Na+
effect on urine volume or ADH levels, the increase from 25 to 50 mM did
not alter urine or hormonal dynamics.
Cardiovascular responses.
Despite the differences in whole body rehydration produced by the
manipulation of volume ingested, the recovery of cardiovascular function was not affected by volume or by Na+ levels.
Cardiovascular drift, as indicated by increased heart rate and
decreased stroke volume, has been attributed to the degree of
dehydration induced during exercise (12). It is not known whether this same relationship holds true after multiple hours of
recovery in the presence of varying degrees of rehydration. An
additional consideration is the influence of hyperthermia on cardiovascular drift, especially when, as is usually the case, high
core temperatures are present in combination with dehydration. When a
rehydration model is used, the extended recovery period allows core
temperature to normalize. It is possible, therefore, to study the
effect of various levels of hydration on cardiovascular responses
independent of elevations in temperature and the concomitant increases
in subcutaneous blood flow, the latter having been associated with
decreases in stroke volume and elevations in heart rate (12, 14).
Although limited data are available on postrehydration responses, the
findings of Costill and Sparks (2), Heaps et al. (6), and Nielsen et al. (15) represent
conflicting findings relative to the recovery of cardiovascular
function after rehydration. The present findings are in general
agreement with those of Costill and Sparks, since all aspects of
cardiovascular function had returned to predehydration levels whether
rehydration was incomplete, as in the LL and LH conditions, or whether
it was at 100%, as in the HL and HH conditions. Our findings do not
agree with those of Heaps et al., since they reported continued
cardiovascular drift after 65% rehydration, even in the presence of
complete blood volume restoration. The present findings are, however,
in general agreement with those of Montain and Coyle (12),
since cardiovascular function was restored with ~71-76%
rehydration. These values fall between those of Heaps et al. and the
81% replacement reported to prevent extreme cardiovascular drift when
fluid is consumed during exercise (12). On the basis of
these percentages, a critical level of postexercise rehydration
necessary to restore cardiovascular function cannot be definitively
identified. The role of selective restoration of the vascular space in
the recovery of cardiovascular function may also be an important
factor; however, the conflicting findings from the few researchers who
have addressed this issue also preclude definitive conclusions.
Conclusion.
For whole body rehydration there was no benefit in adding
Na+ beyond the 25 mM level; however, as shown previously
(9, 11), greater rehydration can be achieved with large
volumes. On the other hand, for fluid compartment restoration, there
does appear to be an interaction between Na+ and volume,
particularly relative to the intracellular space. It is apparent that
plasma volume and, possibly, the entire extracellular space benefit
from the presence of Na+; however, it would be of interest
to examine the effects of different levels of the intracellular cation
K+ on fluid compartment restoration. Finally,
cardiovascular restoration was complete after 3 h of rehydration,
regardless of whether fluid or Na+ replacement was
complete; thus a minimum level of fluid replacement may be necessary to
restore cardiovascular function, particularly if it is accompanied by a
complete plasma volume restoration.
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FOOTNOTES |
Address for reprint requests and other correspondence: J. B. Mitchell, PO Box 297730, Texas Christian University, Fort Worth, TX
76129 (E-mail: J.Mitchell{at}tcu.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 5 October 1999; accepted in final form 9 May 2000.
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REFERENCES |
1.
Costill, DL,
Cote R,
and
Fink WJ.
Muscle water and electrolytes following varied levels of dehydration in man.
J Appl Physiol
40:
6-11,
1976[Abstract/Free Full Text].
2.
Costill, DL,
and
Sparks KE.
Rapid fluid replacement following thermal dehydration.
J Appl Physiol
34:
299-303,
1973[Free Full Text].
3.
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[Free Full Text].
4.
Gisolfi, CV,
and
Duchman SM.
Guidelines for optimal replacement beverages for different athletic events.
Med Sci Sports Exerc
24:
679-687,
1992[ISI][Medline].
5.
Gonzalez-Alonso, J,
Heaps CL,
and
Coyle EF.
Rehydration after exercise with common beverages and water.
Int J Sports Med
13:
399-406,
1992[ISI][Medline].
6.
Heaps, CL,
Gonzales-Alonso J,
and
Coyle EF.
Hypohydration causes cardiovascular drift without reducing blood volume.
Int J Sports Med
15:
74-79,
1994[ISI][Medline].
7.
Lambert, CP,
Costill DL,
McConell GK,
Benedict MA,
Lambert GP,
Robergs RA,
and
Fink WJ.
Fluid replacement after dehydration: influence of beverage carbonation and carbohydrate content.
Int J Sports Med
13:
285-292,
1992[ISI][Medline].
8.
Maughan, RJ,
and
Leiper JB.
Sodium intake and post-exercise rehydration in man.
Eur J Appl Physiol
71:
311-319,
1995.
9.
Maughan, RJ,
Leiper JB,
and
Shirreffs SM.
Restoration of fluid balance after exercise-induced dehydration: effects of food and fluid intake.
Eur J Appl Physiol
73:
317-325,
1996.
10.
Maughan, RJ,
Owens JH,
Shirreffs SM,
and
Leiper JB.
Post-exercise rehydration in man: effects of electrolyte addition to ingested fluids.
Eur J Appl Physiol
69:
209-215,
1994.
11.
Mitchell, JB,
Grandjean PW,
Pizza FX,
Starling RD,
and
Holtz RW.
The effect of volume ingested on rehydration and gastric emptying following exercise-induced dehydration.
Med Sci Sports Exerc
26:
1135-1143,
1994[ISI][Medline].
12.
Montain, SJ,
and
Coyle EF.
Influence of graded dehydration on hyperthermia and cardiovascular drift during exercise.
J Appl Physiol
73:
1340-1350,
1992[Abstract/Free Full Text].
13.
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[ISI][Medline].
14.
Nadel, ER,
Cafarelli E,
Roberts MF,
and
Wenger CB.
Circulatory regulation during exercise in different ambient temperatures.
J Appl Physiol
46:
430-437,
1979[Abstract/Free Full Text].
15.
Nielsen, B,
Sjogaard G,
Ugelvig J,
Knudsen B,
and
Dohlmann B.
Fluid balance in exercise dehydration and rehydration with different glucose-electrolyte drinks.
Eur J Appl Physiol
55:
318-325,
1986.
16.
Norsk, P.
Role of arginine vasopressin in the regulation of extracellular fluid volume.
Med Sci Sports Exerc
28:
S36-S41,
1996[ISI][Medline].
17.
Nose, H,
Mack GW,
Shi X,
and
Nadel ER.
Shift in body fluid compartments after dehydration in humans.
J Appl Physiol
65:
325-331,
1988[Abstract/Free Full Text].
18.
Nose, H,
Mack GW,
Shi X,
and
Nadel ER.
Role of osmolality and plasma volume during rehydration in humans.
J Appl Physiol
65:
318-324,
1988[Abstract/Free Full Text].
19.
Nose, H,
Mack GW,
Shi X,
and
Nadel ER.
Involvement of sodium retention hormones during rehydration in humans.
J Appl Physiol
65:
332-336,
1988[Abstract/Free Full Text].
20.
Shirreffs, SM,
Taylor AJ,
Leiper JB,
and
Maughan RJ.
Post-exercise rehydration in man: effects of volume consumed and drink sodium content.
Med Sci Sports Exerc
28:
1260-1271,
1996[ISI][Medline].
21.
Wemple, RD,
Morocco TS,
and
Mack GW.
Influence of sodium replacement on fluid ingestion following exercise-induced dehydration.
Int J Sport Nutr
7:
104-116,
1997[ISI][Medline].
J APPL PHYSIOL 89(4):1302-1309
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