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Human Performance Laboratory and Department of Physiology and Neurobiology, University of Connecticut, Storrs, Connecticut 06269-1110
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
ACKNOWLEDGEMENTS
FOOTNOTES
REFERENCES
ABSTRACT 
Armstrong, Lawrence E., Carl M. Maresh, Catherine V. Gabaree, Jay R. Hoffman, Stavros A. Kavouras, Robert W. Kenefick, John
W. Castellani, and Lynn E. Ahlquist. Thermal and circulatory responses during exercise: effects of hypohydration, dehydration, and
water intake. J. Appl. Physiol. 82(6):
2028-2035, 1997.
This investigation examined the distinct and
interactive effects of initial hydration state, exercise-induced
dehydration, and water rehydration in a hot environment. On four
occasions, 10 men performed a 90-min heat stress test (treadmill
walking at 5.6 km/h, 5% grade, 33°C, 56% relative humidity).
These heat stress tests differed in pretest hydration [2
euhydrated (EU) and 2 hypohydrated (HY) trials] and water intake
during exercise [2 water ad libitum (W) and 2 no water (NW)
trials]. HY + NW indicated greater physiological strain than all
other trials (P < 0.05-0.001)
in heart rate, plasma osmolality
(Posm), sweat sensitivity
(g / °C · min), and rectal temperature.
Unexpectedly, final HY + W and EU + W responses for rectal temperature,
heart rate, and Posm were similar,
despite the initial 3.9 ± 0.2% hypohydration in HY + W. We
concluded that differences in pretest
Posm (295 ± 7 and 287 ± 5 mosmol/kg for HY + W and EU + W, respectively) resulted in greater
water consumption (1.65 and 0.31 liter for HY + W and EU + W,
respectively), no voluntary dehydration (0.9% body mass increase), and
attenuated thermal and circulatory strain during HY + W.
temperature regulation; body temperature; plasma; fluid shifts; rehydration
INTRODUCTION STUDIES SPANNING 50 years have demonstrated that
hypohydration effects an increased core temperature (27) subsequent to reduced blood volume, hyperosmolality, skin blood flow, and sweat rate
(21, 27); an increased cardiovascular strain associated with body water
loss, hypovolemia, peripheral vasodilation, tachycardia, decreased
venous return, and decreased stroke volume (6, 25); and a decreased
capacity to perform submaximal endurance exercise (25). Similarly, it
has been documented that minor dehydration (i.e., Furthermore, it is widely recognized that active humans do not
voluntarily replace all the water lost during prolonged exercise in
heat (14). Known as voluntary dehydration (14, 28), this behavior is
complex, involves psychological (i.e., alliesthesia) and physiological
components, and results in increased core temperature and
cardiovascular strain even when test subjects begin exercise in the
euhydrated state. The exact means by which extracellular tonicity
affects voluntary dehydration is not known, but it may be due to the
fact that plasma osmolality (normal mean: 287 mosmol/kg) does not rise
to the threshold (295 mosmol/kg) for thirst (30) until late in the
exercise period (14). This hypothetically suggested that, if humans
began exercise in a HY state with an elevated plasma osmolality
(Posm) and an activated thirst
drive, exercise-heat exposure would involve greater total water intake (vs. EU) and perhaps attenuated physiological strain. Therefore, the
second purpose of this study was to determine the differential effects
of initial HY and EU states on ad libitum water consumption, fluid
balance, and physiological responses.
METHODS
1 to
2% of body weight) augments core temperature and cardiovascular
strain (13, 19, 23, 26), that the increase in these variables is
directly related to the magnitude of dehydration accrued during
prolonged exercise (18, 20, 26), and that the optimal rate of
rehydration approximates the rate of sweat production (19). Although
numerous studies have replaced sweat losses with
carbohydrate-electrolyte formulations, few investigations have examined
the effects of pure water replacement during exercise on thermal and
circulatory responses (7), despite the fact that water is the most
common replacement fluid in athletic, industrial, and military
settings. Also we are unaware of any previous study that has isolated
the effects of hypohydration, dehydration, and water rehydration as
they influence temperature regulation and physiological strain during
prolonged upright exercise (15, 23). This is significant because
rehydration during exercise maintains sweating and/or skin
blood flow (7), thereby preserving the ability to dissipate heat, and
reduces cardiovascular strain (19). Therefore, the first purpose of
this investigation was to determine the distinct effects of preexercise
hypohydration (HY, 3.6 ± 0.2 and 3.9 ± 0.2% body
mass) and euhydration (EU), with ad libitum water intake (W) or no
water intake (NW) during exercise, on thermoregulatory, fluid balance,
and circulatory responses. The interactions of HY, EU, W, and NW also
were of interest, because combinations of these factors may
differentially affect the nature and magnitude of responses to
exercise-heat stress (6, 16). Ten test subjects performed four tests
(EU + W, EU + NW, HY + W, and HY + NW) involving 90 min of graded treadmill walking in a hot environment. Because exercise-induced strain
is directly related to the level of hypohydration (18, 20, 26), we
hypothesized that the magnitude of physiological perturbations in the
four experimental conditions would be ranked in the following order: HY + NW > HY + W > EU + NW > EU + W.
O2 max) was 57.1 ± 1.5 ml · kg
1 · min1.
O2 max was determined
by a continuous treadmill running test (5) verified by a plateau of
oxygen uptake (<150 ml O2)
with an increase in exercise intensity. Subsequently, subjects
completed four consecutive days of preliminary exercise-heat exposure.
The purposes of these exposures were to enhance cardiovascular
stability, reduce the risk of heat illness, reduce between-subject
variability in measurements, and determine whether any subject probably
would not be able to complete daily 90-min tests (13). These
preliminary sessions involved cycle ergometer exercise at 47 ± 2%
O2 max in an
environmental chamber (33 ± 1°C, 64 ± 8% relative
humidity, 0.1 ± 0.1 m/s air speed). Ambient conditions were
monitored during all tests by two instruments: a thermohygrometer
(model 3309-60, Cole-Parmer Instrument, Chicago, IL) and a
thermoanemometer (model 9850, Alnor Instrument, Skokie, IL). Water was
consumed ad libitum. Subjects wore shorts, T-shirt, socks, and athletic
shoes. Exercise lasted 80 ± 2 min, unless terminated by
predetermined end points of heart rate (HR) >180
beats/min for 5 min, a rectal temperature
(Tre) >39.5°C, or
clinical signs and symptoms of heat exhaustion.
Within 20 ± 1 days of the conclusion of this preliminary program,
each subject had completed four experimental heat stress tests (HST) in
a hot environment (33 ± 1°C, 56 ± 5% relative humidity, 0.1 ± 0.1 m/s air speed); for most subjects 3-4 days of rest
were allowed between HST. The four HST differed in pretest hydration (2 EU and 2 HY trials) and whether subjects consumed chilled water (~10-15°C) during exercise (2 W and 2 NW trials): EU + W, EU + NW, HY + W, and HY + NW. To reduce the likelihood of an order effect,
the sequence of treatments was randomized and HST were separated by 
3
days. Subjects began each HST at the same time of day and wore the same
clothing (i.e., shorts, T-shirt, socks, and athletic shoes) during all
trials. Each HST lasted 90 min (treadmill walking, 5.6 km/h, 5% grade,
36 ± 2%
O2 max),
unless terminated by the predetermined end points described above.
Preparation for HY and EU sessions.
Before all HST, subjects abstained from strenuous exercise for 24 h and
consumed no food for 4 h. The preexercise hydration status of each
subject was verified within 30 min of the start of all HST by
triplicate measurements of urine specific gravity (refractometer,
Spartan) and body mass and was later confirmed by
Posm (osmometer, model 5004, Precision Instruments, Natick, MA) (2).
A baseline body mass was determined for each subject from the average
of three to five preprandial morning measurements taken on the days
between preliminary exercise-heat exposures and HST. Before HY + NW and
HY + W, the subjects dehydrated to 3.4 ± 0.2 and 3.6 ± 0.2%, respectively, of the baseline body mass. This was
accomplished via various forms of mild-to-moderate exercise (i.e.,
jogging, cycling, weight lifting) while the subjects wore a cotton
sweat suit over the clothing items described above. Dehydration was
accomplished in 3.0 ± 0.5 (HY + NW) and 3.3 ± 0.4 h (HY + W). After the subjects had achieved the desired body mass, they were instructed to consume no fluids before the HST, which began on the
next day 17 ± 1 (HY + NW) and 18 ± 1 h (HY + W)
later. This resulted in additional overnight body mass losses of 0.2% for HY + NW and 0.3% for HY + W, increasing the total mass losses (immediately before HST) to 3.6 ± 0.2% for HY + NW and
3.9 ± 0.2% for HY + W. Before EU + NW and EU + W, subjects
underwent no programmed dehydration and consumed four large glasses of
water (>470 ml total) in excess of their normal dietary fluid intake: two glasses before going to sleep on the night before testing and two
on awakening on the morning of testing.
Measurements.
HR and Tre were recorded at 10-min
intervals, during each of the four preliminary exercise-heat exposures
and four HST, to monitor physiological strain. Chest surface electrodes
(lead I configuration) transmitted HR to an external digital receiver (Computer Instrument, Hempstead, NY).
Tre was monitored by using a
thermistor (series 400, Yellow Springs Instruments, Yellow Springs, OH)
inserted 10-12 cm beyond the anal sphincter and connected to a
thermistor thermometer (model 08402, Cole-Parmer Instrument). The
Tre was graphed against time (29),
allowing computation of the area under the heating curve (i.e., the
integral °C · min). Skin temperature was obtained
at the chest, forearm, and calf by placing an infrared temperature
scanner (Ototemp 3000, Exergen, Newton, MA) on the skin surface, and
mean weighted skin temperature (
sk)
was calculated (4).
Body mass was determined on a precision electronic balance (model 700M,
SR Instruments, Tonawanda, NY) to an accuracy of ±45 g. Total body
sweat rate was calculated from body mass loss (immediate preexercise to
postexercise) and was adjusted for water intake, urine output, and
evaporative water loss from the respiratory tract (16). Sweat
sensitivity was calculated by dividing the sweat loss (g) by the area
under the heating curve (°C · min, see above).
Heat storage (HS) in body tissues
(W/m2) was calculated (16) from
the formula
|
(1) |
1 · kg1 · °C1),
BWpre is the preexercise body mass (kg),
(b post b pre) represents the increase in mean body temperature during the 90-min exercise bout (°C), SA is the
DuBois surface area (m2) of the
body (10), and t is the elapsed time
(h). The effect of ingesting cool water on body temperature was
calculated by using the specific heat of water and of the human body
(see above). Radiant heat exchange
(R) with the environment
(W/m2) was calculated according
to the linear approximation equation published by Mitchell and
colleagues (17)
![<IT>R</IT> = [&sfgr;&egr;<SUB>sk</SUB>(<IT>A</IT><SUB>r</SUB> /<IT>SA</IT>)(<OVL>T</OVL> <SUB>sk</SUB><SUP>4</SUP> − <OVL>T</OVL> <SUB>sur</SUB><SUP>4</SUP>)]](/content/vol82/issue6/fulltext/2028/img003.gif)
|
(2) |
is the Stefan-Boltzmann constant (5.67 × 108
W · m2 · °K4),
sk is the emissivity of the
skin (assumed to be 0.99),
Ar is the surface
area (m2) of the body that
radiates heat, SA is the total surface
area (m2) of the body (10), the
quantity
(Ar /SA)
was measured as 0.88, sk is
the mean weighted skin temperature (°K), and
sur is
the mean temperature of the surrounding surfaces (°K). Evaporative heat loss (W/m2) was calculated
by multiplying sweat production (liters) by the appropriate factor (580 kcal/l sweat) and was corrected by calculating the percentage of sweat
that dripped to the floor. Under these environmental and exercise
conditions, an iterative computation indicated that 30% of sweat did
not evaporate on the skin surface (R. R. Gonzalez, personal
communication). Evaporative heat loss was added to radiant heat
exchange to derive the total heat dissipation by evaporation and
radiation (W/m2).
Expired oxygen, carbon dioxide, and ventilatory volume were determined
by using open-circuit spirometry. Subjects breathed through a two-way
valve (model single J, Collins, Braintree, MA), and expired gases were
analyzed with an on-line breath-by-breath system (series 2000, Medical
Graphics, St. Paul, MN). This metabolic system was calibrated with
standard gases before each test. Oxygen consumption was recorded at
30-s intervals during the
O2 max test, between
10-15 and 40-45 min of preliminary exercise-heat exposures,
and between 45-50 and 85-90 min of each HST. Metabolic heat
production was calculated from oxygen consumption data (4.8 kcal/l
O2) (3). We also assumed that
80% of metabolic energy evolved as heat (26).
Blood analyses.
Venous blood samples during each treatment were obtained before
exercise and immediately postexercise. A 20-gauge Teflon cannula (Critikon, Tampa, FL) was placed in a superficial forearm vein. The
cannula was kept patent with a 1.5-ml volume of isotonic saline solution at four to six points during each test (<10 ml total). The
preexercise blood samples were drawn after a 15-min equilibration period in the environmental chamber. All postexercise blood samples were drawn within 30 s of the conclusion of exercise. Hematocrit was
measured in triplicate via the microcapillary technique. Hemoglobin concentrations were determined in duplicate by reflectance photometry (Boehringer Mannheim Diagnostics, Indianapolis, IN). The percent changes in plasma volume and erythrocyte volume were calculated from
the appropriate hemoglobin and hematocrit values obtained at rest and
after exercise (9). Posm was
measured with the freezing-point depression method (model 5004, Precision Instruments). Selected hormonal responses during HST are
reported elsewhere (13).
Statistical analyses.
Evaluation of the data was accomplished by a treatment × time
analysis of variance (i.e., 4 × 2 for blood, 4 × 11 for
Tre and HR), with repeated
measures across time, using a commercial computer program (BMDP
Statistical Software, Los Angeles, CA). In the event of a significant
F ratio, Tukey's multiple comparison analysis was performed to determine specific differences among the
sample means. Regression analyses were utilized across treatments to
examine the thermoregulatory effects of hypohydration, dehydration, and
rehydration. Significance for all statistical tests was established at
P < 0.05, and all data are expressed
as means ± SE.
RESULTS
3 days. The
range of total body mass changes (i.e., day
1 to the end of HST) in all experimental trials
was 0.19 to 6.71%. Figure 1
presents comparisons of HR and Tre
in all treatments. The HY + NW test exhibited significantly greater HR
and Tre during all exercise
measurements beyond 10 min.
Table 1 presents fluid, cardiovascular, metabolic, and thermal variables. The volume of water consumed ad libitum during the HY + W test was 5.3 times greater than that consumed during the EU + W trial. The mean increases in HR per 1% loss of body mass were 38 ± 4, 40 ± 3, and 12 ± 1 beats/min for EU + W, EU + NW, and HY + NW, respectively, during HST. The mean increases in Tre per 1% loss of body mass were 0.6 ± 0.1, 0.8 ± 0.1, and 0.4 ± 0.1°C for EU + W, EU + NW, and HY + NW, respectively, during HST.
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Tre during exercise.
Figure 3 shows intratest differences in the
relationship between sweat loss and the area under the curve of
Tre plotted against time (the
integral °C · min).
Tre) and water intake during
EU + W and HY + W tests. Slopes of regression lines indicate that this
relationship shifted to right when pretest HY was induced.
Figure 4 illustrates the effect of water consumption on
Posm in EU and
HY conditions. Clearly, some subjects consumed ample water to maintain
or even decrease Posm. Figure
5 depicts the relationship between sweat
sensitivity (g / °C · min) and both total
body mass loss (n = 40) and
Posm
(n = 40) for all HST performed during
this investigation. Sweat sensitivity decreased as total body mass loss
and Posm increased.
Posm) and water intake in EU + W and HY + W states. Arrows, water intakes equal to fluid loss (0.96 liter) in both trials.
DISCUSSION
Few studies have examined the thermal and cardiovascular responses to pure water replacement during exercise (7) or the concurrent effects of hypohydration, dehydration, and water rehydration on temperature regulation and physiological strain during upright exercise (15, 23). This investigation examined the interactions of preexercise HY and EU with W and NW, because these factors may differentially affect the nature and magnitude of responses to exercise-heat stress (6, 16). Hypohydration was achieved in 3.0-3.3 h by voluntary food and fluid denial combined with physical exercise in a cool environment while subjects wore a cotton sweat suit. A recovery period of 17-18 h was spent in a comfortable environment to provide time for fluid compartments to equilibrate at the achieved hydration level. These dehydration-recovery procedures are consistent with those of previous investigations (26).
We initially hypothesized that the magnitude of physiological
perturbations in the four experimental conditions would be ranked in
the following order: HY + NW > HY + W > EU + NW > EU + W. In partial support of this hypothesis, the HY + NW trial resulted in
greater HR and Tre
(P < 0.01-0.0001) than all
other experimental conditions from 20 to 90 min of the HST. HY + NW
also resulted in the greatest final HR, heat storage,
Posm,
Posm, and plasma volume change
(P < 0.05-0.001). Furthermore,
many significant differences (P < 0.05-0.001) were observed between the HY + W and HY + NW
trials, indicating that the consumption of water had a significant
influence on physiological responses when subjects were
hypohydrated.
However, the interpretation of responses in the HY + W and EU + W
trials was complicated by differences in the volume of water consumed
in these trials. For example, when subjects were euhydrated, ad libitum
water intake had no significant effect on measured variables (EU + W
vs. EU + NW). This outcome was influenced by the fact that four
subjects voluntarily drank little or no water during EU + W (Figs. 2
and 4), making their data equivalent to the EU + NW test. As a second
example, most HY + W responses were not different from those of EU + W,
and some (i.e., body mass and
Posm) were significantly
smaller. It is likely that this outcome resulted from the great
difference in ad libitum water intake between HY + W (1.65 liters) and
EU + W (0.31 liters) and not the preexercise hydration status per se,
because the responses of HY + NW differed greatly from those of EU + NW. If water intake in the HY + W and EU + W trials had been identical,
eliminating the possibility of studying voluntary dehydration and ad
libitum drinking, these findings may have been different.
body mass during HST, final
HR, heat storage, final
sk,
Tre, and final
Tre. It is likely that this resulted from the combined effects of preexercise hydration status and
fluid intake during exercise.
Physiologists have advised athletes to consume a volume of fluid that
approximates sweat loss (7, 16, 19, 23); this volume (0.96 liter) was
identical for EU + W and HY + W (Fig. 4, arrows). If this volume had
been consumed by our subjects, it would have resulted in a mean
decrease of 1 mosmol/kg during EU + W and a mean increase of 4 mosmol/kg during HY + W. This suggests that the above advice is correct
when athletes begin exercise in the euhydrated state. When athletes
begin exercise in a hypohydrated state, however, they should consume
water in excess of sweat loss to attenuate the detrimental influence of an increased Posm on sweat
sensitivity during prolonged exercise (6, 18, 20, 22, 29).
The present study also clarifies the influence of preexercise hydration
state on the relationship between water intake and Tre during exercise. The
regression lines for the EU + W and HY + W (Fig. 2) trials have similar
negative slopes, but the line representing HY + W is shifted to the
right of that representing EU + W. Therefore, for a given water intake
(i.e., 1.0 liter), Tre was higher
(~0.6°C) when subjects were hypohydrated (3.9% body
mass). These findings agree closely with previously published 2-h cycle
ergometry tests involving scheduled drinking (19) and indicate that
1.65 liters of additional water were required during HY + W (i.e., 5 times greater than EU + W) to produce a Tre that was equivalent to the
EU + W test.
Intrasubject drinking differences.
Two subjects consumed much less water than other subjects during the HY + W trial; they alone experienced a net loss of body mass, whereas the
other eight subjects had a mean body mass gain of 0.9% due to ad
libitum drinking. These two men were classified as reluctant drinkers
following the method of Szlyk et al. (28) and appear in Figs. 2 and 4
as the subjects with the smallest water intakes (i.e., within the range
of EU + W values) and the largest
Tre and
Posm. They also exhibited the
lowest sweat sensitivities concurrent with the greatest heat storage
rates, radiative heat losses, and final plasma glucose concentrations.
Their elevated plasma glucose concentrations are consistent with
decreased splanchnic blood flow combined with increased hepatic
metabolism (i.e., Q10 effect),
causing increased hepatic glycogenolysis and glucose release (24).
Clearly, these two test subjects exhibited greater strain than others
during HY + W, but it is unclear why their internal physiological state
did not stimulate greater drinking. Although increased circulating
catecholamines also could have increased hepatic glucose release,
analyses (13) indicated that the epinephrine and norepinephrine
concentrations of these two subjects were similar to the group mean
values.
Recent investigations of drinking behavior have attempted to identify
why reluctant drinkers respond to internal cues differently from other
subjects, despite experiencing similar exercise-heat stress and fluid
losses (14, 28). The prevailing theory (11, 14) involves voluntary
dehydration, which originates with negative alliesthesia, an unpleasant
stimulus engendered by drinking that depends on the internal status of
the subject and characteristics of the fluid (i.e., odor, clarity,
palatability, temperature). Interestingly, during the EU + W trial, the
water intakes and physiological responses of reluctant drinkers were
similar to those of the other eight subjects. This demonstrates for the
first time that reluctant drinkers may not drink sparingly in all
situations and supports the theory of negative
alliesthesia.
Heat balance during HY + NW.
The mean preexercise Tre for all
treatments ranged from 37.1 to 37.4°C. At the end of exercise,
however, the HY + NW trial resulted in a mean
Tre that was 0.9-1.1°C
greater than that in the three other conditions
(P < 0.001). Heat production and
heat dissipation were analyzed to explain this finding. Oxygen
consumption values (range of means 19.9-21.2
ml · kg1 · min1)
indicated that there were no between-trial differences in aerobic heat
production normalized for surface area (range of means 202.4-210.8 W/m2). Although radiation was
limited by the environmental conditions (i.e., 6.5 W/m2 in 90 min), because the
ambient temperature (33°C) was similar to that of
sk
(34.6°C), radiative and evaporative heat losses were similar among
trials, with the latter accounting for 18-25 times more heat
dissipation than the former. Furthermore, considering the environmental
conditions during HST (33 ± 1°C, 56 ± 5% relative humidity), it is likely that convective and conductive heat losses (not
measured) were similar to the radiant heat losses in Table 1; it is
unlikely that they were solely responsible for the increased heat
storage in the HY + NW trial (1). Although other investigators have
concluded that dehydration increases heat storage during exercise
because dry heat loss is diminished (12, 18, 25), that response was not
observed in this investigation and may be specific to higher exercise
intensities (i.e., >60%
O2 max), where
increased systemic and cutaneous vascular resistance have been shown to
accompany dehydration and hyperthermia (12).
Although sweat rates were similar for all treatments, the body's
potential for evaporative cooling was not reached during HY + NW
because of a reduced sweat sensitivity. Had the sweat sensitivity
during HY + NW (11.2 g / °C · min) been
equal to the mean of the other three trials (21.3 g / °C · min), the 1.7°C rise in
Tre during HY + W could have been
offset by the evaporation of ~600 g of additional sweat. Tables 1 and
2 suggest the factors that may have influenced this change in sweat
sensitivity. For example, the HY + NW trial exhibited a significantly
greater plasma volume loss than EU + W and HY + W. Although this
suggests that plasma volume influenced sweat sensitivity, it has been
documented that increasing or reducing plasma volume does not
necessarily result in a systematic improvement or deterioration,
respectively, in temperature regulation (6, 7, 18, 27). It is also unlikely that either thermal input from the skin or plasma glucose concentration altered sweat sensitivity during HY + NW, because they
were similar during all treatments (Tables 1 and 2).
Posm, however, increased
significantly during HY + NW only (Table 2) and was inversely related
to sweat sensitivity (P < 0.02; Fig. 5, right). This observation agrees
with previous reports (6, 18, 20, 22, 29) that increased extracellular
osmolality (i.e., cell dehydration) diminishes thermal sweating in
exercising humans.
Summary.
Contrary to the paradigm of voluntary dehydration during exercise, the
3.9% body water deficit and elevated pretest
Posm resulted in a large water
intake during HY + W, a 0.9% body mass increase, and attenuation of
the rise in Tre via favorable
changes in Posm and sweat
sensitivity. This suggests that a large osmotic load in fluid or food
should be avoided during prolonged exercise-heat exposure and that
water consumption guidelines should be designed to minimize the
increase in Posm. When subjects
begin exercise in the hypohydrated state, this will be accomplished if
pure water is consumed at a rate that exceeds both the sweat rate and
the amount consumed when exercise is begun in a euhydrated state.
ACKNOWLEDGEMENTS
The authors gratefully acknowledge the technical and administrative contributions of Tamara Morocco, Daniel Hannon, Andrew Judelson, Angela Pasqualicchio, Dr. James M. Rippe, Dr. Ann Ward, Michael Whittlesey, and Dr. Richard Gonzalez.
FOOTNOTES
Address for reprint requests: L. E. Armstrong, University of Connecticut, Box U-110, 2095 Hillside Rd., Storrs, CT 06269-1110.
Received 17 July 1996; accepted in final form 12 February 1997.
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