| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
Human Performance Laboratory, Department of Kinesiology and Health Education, The University of Texas at Austin, Austin, Texas 78712
 |
ABSTRACT |
|---|
 TOP
 ABSTRACT
 INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
We determined
whether the deleterious effects of dehydration and hyperthermia on
cardiovascular function during upright exercise were attenuated by
elevating central blood volume with supine exercise. Seven trained men
[maximal oxygen consumption
(
O2 max) 4.7 ± 0.4 l/min (mean ± SE)] cycled for 30 min in the heat
(35°C) in the upright and in the supine positions
(O2 2.93 ± 0.27 l/min) while maintaining euhydration by fluid ingestion or while being dehydrated by 5% of body weight after 2 h of upright exercise. When
subjects were euhydrated, esophageal temperature
(Tes) was 37.8-38.0°C
in both body postures. Dehydration caused equal hyperthermia during
both upright and supine exercise
(Tes = 38.7-38.8°C).
During upright exercise, dehydration lowered stroke volume (SV),
cardiac output, mean arterial pressure (MAP), and cutaneous vascular
conductance and increased heart rate and plasma catecholamines
[30 ± 6 ml, 3.0 ± 0.7 l/min, 6 ± 2 mmHg, 22 ± 8%, 14 ± 2 beats/min, and 50-96%, respectively;
all P < 0.05]. In contrast,
during supine exercise, dehydration did not cause significant
alterations in MAP, cutaneous vascular conductance, or plasma
catecholamines. Furthermore, supine versus upright exercise attenuated
the increases in heart rate (7 ± 2 vs. 9 ± 1%) and
the reductions in SV (13 ± 4 vs. 21 ± 3%) and cardiac output
(8 ± 3 vs. 14 ± 3%) (all P < 0.05). These results suggest that the decline in cutaneous vascular
conductance and the increase in plasma norepinephrine concentration,
independent of hyperthermia, are associated with a reduction in central
blood volume and a lower arterial blood pressure.
skin circulation; stroke volume; central blood volume; catecholamines
| |
INTRODUCTION |
|---|
|
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
DEHYDRATION during prolonged upright exercise in the heat causes progressive hyperthermia that is associated with reductions in skin blood flow and mean arterial blood pressure (MAP) and increases in plasma norepinephrine levels (8, 9). Cardiac output declines with dehydration and hyperthermia because of the larger reductions in stroke volume (SV; 19-27%) compared with the parallel increases in heart rate (5-10%) (8-11, 21-23, 29, 31). Blood flow to the exercising skeletal muscles also declines significantly (8).
Therefore, the combined effects of dehydration and hyperthermia during upright exercise cause a severe deterioration in cardiovascular function. The effects of dehydration amounting to 4% of body weight (i.e., ~3,000 ml) on reducing skin blood flow is not caused simply by the characteristic 200- to 300-ml reduction in plasma volume, because Montain and Coyle (21) have shown that plasma volume expansion during dehydration failed to prevent reductions in forearm blood flow or to attenuate hyperthermia. It is likely that this amount of plasma volume expansion did not have a very large effect on central blood volume, even though it prevented hypovolemia and partially restored SV (21).
The present study has used exercise in the supine position as a method to more effectively raise central blood volume in dehydrated subjects. Dehydration and hyperthermia are thought to reduce central blood volume during exercise in the upright position. Alterations in central blood volume can influence both cardiopulmonary and arterial baroreceptors, which have the potential to alter sympathetic response to exercise as well as vascular conductance to skin and other organs (19, 28, 32). Therefore, the main purpose of this study was to determine whether large increases in central blood volume, achieved by supine exercise, prevent the reduction in cutaneous vascular conductance (CVC) and MAP and the increase in plasma norepinephrine that are characteristic of dehydration and hyperthermia during upright exercise.
| |
METHODS |
|---|
|
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
Subjects.
The seven endurance-trained male cyclists participating in this study
had a mean (±SD) age of 27.6 ± 1.9 yr, weight of 74.0 ± 10.7 kg, height of 178.3 ± 5.4 cm, maximal heart rate of 186 ± 5 beats/min, and maximal oxygen consumption
(O2 max) of 4.7 ± 0.4 l/min. This study was approved by the Institutional Review Board at
the University of Texas at Austin, and written informed consent was
obtained. During the preliminary testing,
O2 max was first
determined during upright cycling using an incremental protocol. The
subjects were well acclimated to the heat by bicycling outdoors at
ambient temperatures 
35°C. To adapt to exercise in the supine
position, each subject completed at least twelve to fifteen 30-min
bouts of supine cycling in a 3-wk period. Before the experimental
trials were begun, a sweating rate was determined during 2 h of cycling
(~60% O2 max) in
the heat.
Experimental design.
On two separate occasions, subjects first cycled for 2 h on an
ergometer (Jaeger ERGOTEST), rested for 45 min in a thermoneutral environment (23°C), and then performed two counterbalanced,
randomly assigned 30-min bouts of cycling, one in the upright and
another in the supine position. These bouts were interspaced by 45 min of rest in a 23°C environment (Fig. 1).
All the exercise was performed in the heat (35°C dry bulb; 50%
relative humidity, wind speed 2 m/s) and at an intensity of 62 ± 2% of upright
O2 max (220 ± 12 W; 80-90 rpm).
|
, and 3 mM
K+) during both euhydration and
dehydration trials so that the same hydration status observed after the
2-h bout of exercise was maintained. In the euhydration trials, the
subjects' body weight after cycling in the upright and the supine
positions was only 0.20 ± 0.01 kg (0.3 ± 0.1%) below the
initial baseline body weight. On the other hand, in the dehydration
trials, the subjects' body weight after cycling in the upright and the
supine positions was 3.30 ± 0.42 kg (4.7 ± 0.2%) lower than
the initial body weight. The trials were separated by 5-7 days.
On the day before the experimental testing, the hydration status of the
subjects was standardized by having them adopt the same diet, exercise
bout (i.e., 1 h of low-intensity cycling), and fluid intake. They
also ingested 200-300 ml of fluid 2 h before arriving at the
laboratory. On arrival on the experimental testing day, subjects' nude
body weights (i.e., baseline values) were recorded, and rectal and
esophageal temperature thermistors were inserted. The subjects then put
on shorts, socks, and cycling shoes, entered the environmental chamber
(35°C), and sat quietly in an armchair for 15 min. During this
time, a heart rate monitor was attached and a Teflon catheter was
inserted into an antecubital vein for blood sampling. After 15 min of
seated rest, a 6-ml blood sample was withdrawn for later determination
of baseline hematocrit, hemoglobin (Hb) concentration, serum
osmolality, and electrolytes. The subject then mounted the cycle
ergometer and started cycling in the upright position for 120 min at 62 ± 2% O2 max.
Physiological responses of the same subjects with and without
dehydration during this first 2-h exercise bout have been published
previously (9).
On completion of the first 2 h, the instrumentation and clothing were
rapidly removed from the subject, who then toweled dry, and
postexercise body weight was recorded. The subject then voided his
bladder to determine the volume of urine formed during exercise. Next,
the subject redressed in dry clothing and rested for 45 min in a
thermoneutral environment (23°C) in front of a fan to return core
temperature to the baseline level. After this rest period, a 30-min
bout of cycling in either the upright or supine position was performed.
During supine exercise, the subjects lay on a table while secured with
straps around the shoulders. The table was set ~50 cm
below the center of the ergometer crank arms. During supine exercise,
an additional fan, apart from the frontal one used during exercise in
both body positions, was placed 1.5 m above the subjects to offset the
diminished heat dissipation from the back so as to maintain a similar
core temperature during supine and upright exercise. Before subjects
exercised in either body position, skin thermistors, a
mercury-in-Silastic strain gauge, and a laser Doppler probe (left
forearm) were attached. The mercury-in-Silastic strain gauge and the
laser Doppler probe remained in place throughout exercise as well as
during the 45-min resting period between exercise bouts.
During each 30-min exercise bout,
O2 was determined from 3 to
18 min of exercise and during each determination of cardiac output.
Cardiac output was determined in quadruplicate from 20 to 28 min of
exercise, using a CO2 rebreathing
technique. Blood pressure was determined during each determination of
cardiac output. Heart rate, esophageal temperature
(Tes), rectal temperature, and
skin temperature were recorded continuously. Forearm blood flow was
measured 8-10 times at rest and after 13-18 min of exercise using venous occlusion plethysmography. Cutaneous blood flow was measured at rest and after 10-12 min and 28-30 min of
exercise (laser Doppler flowmetry). In a follow-up study, cutaneous
blood flow was measured continuously. A 10-ml blood sample was
withdrawn at 30 min of exercise. A rating of perceived exertion was
recorded at 30 min of exercise (2).
Analytic techniques.
A more detailed description of the analytic methods can be found
elsewhere (9). O2 was
measured using computerized open-circuit spirometry. Cardiac output was
determined using a computerized version of the
CO2 rebreathing technique of
Collier (3) and adjusted for Hb concentration (20). Heart rate was
measured using a heart rate monitor (Uniq CIC Heartwatch). SV was
calculated as cardiac output divided by heart rate. Systolic blood
pressure and diastolic blood pressure were measured on the left arm
using an automatic blood pressure monitor (STBP-680; Colin Medical
Instruments). MAP was calculated as [(2 × diastolic blood pressure) + systolic blood pressure]/3. Systemic
vascular resistance was calculated as MAP divided by cardiac output and
expressed as peripheral resistance (in
mmHg · l1 · min).
1 · min1 · mmHg1).
CVC was calculated as cutaneous blood flow divided by MAP and expressed
as a percentage of the upright exercise value within a given trial
(euhydration or dehydration). Because the laser Doppler probe remained
in place during all the resting and exercise periods within a given
trial (euhydration or dehydration), this measure accurately detected
changes in skin blood flow and CVC between the upright and the supine
position. However, it did not allow direct comparisons of the laser
Doppler probe values of skin blood flow between dehydration and
euhydration trials, because measures were obtained on different days
and possibly on different skin surfaces. The laser Doppler probe only
measured the skin blood flow of a skin surface area of 1 mm2. To circumvent this
limitation, four subjects, two of them from the original group, were
first studied during upright and supine exercise when euhydrated and
then when dehydrated on the same day. The basic purpose of this
additional trial was to verify, with a design ideal for the laser
Doppler probe, that cutaneous blood flow and CVC were not significantly
different during supine exercise during euhydration and dehydration. In
this follow-up study, laser Doppler skin blood flow was recorded
continuously at a frequency of 10 Hz. Exercise time for the onset of
skin vasodilation was defined as the minute of a sustained increase of
skin blood flow. The Tes threshold
for the onset of vasodilation was defined as the
Tes at the time for the onset of
skin vasodilation.
Total sweat volume was estimated from the difference in body weight
(Acme Scale, FW 150 KAI) before and after exercise with correction for
respiratory water loss, saliva volume, body weight loss due to the
exchange of O2 and
CO2 (27), and urine volume collected after exercise. Percent dehydration was estimated from the
difference in body weight after each 30-min exercise bout in upright
and supine positions compared with the initial baseline body weight
obtained on arrival at the laboratory.
Tes was measured with a thermistor
(YSI 491) inserted through the nasal passage a distance equal to
one-quarter of the subject's standing height. Rectal temperature was
measured with a thermistor (YSI 401) inserted 15 cm past the anal
sphincter. Mean skin temperature was calculated from the skin
temperatures measured at six sites (i.e., upper arm, forearm, chest,
back, thigh, and calf) using the weighting method of Hardy and DuBois
(12).
The percent changes in blood volume and plasma volume were calculated
using the equations of Dill and Costill (4). Serum osmolality was
determined by the freezing point-depression technique (Advanced
Instruments 3MO). Serum sodium and chloride concentrations were
measured with an automated electrolyte analyzer (Nova 5). Serum glucose
concentration was determined with the glucose oxidase technique using a
YSI 23 glucose analyzer. Plasma lactate concentration was determined
using an enzymatic assay. Plasma norepinephrine and epinephrine
concentrations were determined using HPLC with electrochemical
detection (13).
Statistical analysis. Data were analyzed using a two-way ANOVA with repeated measures. When F values were significant, pairwise differences were identified using Tukey's honestly significant difference procedure. The significance level was set at P < 0.05. Data are presented as means ± SE.
| |
RESULTS |
|---|
|
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
Resting circulatory and thermoregulatory data.
Resting heart rate was similar in all conditions (79-81
beats/min), except during dehydration before upright exercise, when it
was significantly elevated above all other conditions (90 ± 3 beats/min; P < 0.05). Resting core
temperature was similar (36.8-36.9°C) before the 30 min of
exercise in all conditions, as was skin temperature (34.7-34.9°C). Resting forearm blood flow (2.8-3.2
ml · 100 ml1 · min1)
and FVC before the initial 120-min and subsequent 30-min bouts of
upright cycling were all similar. Before supine exercise, resting forearm blood flow was somewhat higher (4.1-4.6
ml · 100 ml1 · min1)
than that observed before upright exercise but again was not affected
by dehydration. When subjects were either euhydrated or dehydrated,
resting laser Doppler skin blood flow was not significantly different
before supine compared with upright exercise (0.2-0.3 ± 0.1 V).
Hydration status and oxygen consumption during exercise.
After the 30-min bouts of exercise were finished in either body
position, body weight was similar to preexercise baseline values during
euhydration (i.e., within 0.2 kg) but was reduced by 4.7% during
dehydration. O2 was identical
during exercise in either body position in the euhydration and
dehydration trials (2.93 ± 0.27 l/min).
Blood variables during exercise.
As expected, dehydration compared with euhydration resulted in a
significantly lower blood volume during exercise in both body
positions, largely because of plasma volume losses (i.e., ~200-300 ml lower as Hb concentration was 3.7-4.3%
higher). On the other hand, serum osmolality, serum sodium, and serum
chloride concentrations all reflected the hydration status, being
equally increased (P < 0.05) with
dehydration compared with euhydration during exercise in both body
positions (Table 1).
|
Serum glucose and blood lactate concentrations. No statistical differences in serum glucose concentration were observed during exercise in either body position or hydration status (Table 1). The low glucose concentration values in all conditions (2.8-3.2 mM) were asymptomatic responses to the preexercise ingestion of the carbohydrate-electrolyte solution, which elevated resting glucose concentration to 7-8 mM. Blood lactate concentration was significantly higher during supine compared with upright exercise in either hydration status (P < 0.05; Table 1).
Body temperature during exercise.
With euhydration in either body position,
Tes increased to 37.8-38.0 ± 0.1°C during exercise. With dehydration,
Tes increased during both upright
and supine exercise to 38.7-38.8 ± 0.1°C, which was
significantly higher than that during euhydration
(P < 0.05; Fig.
2). The same pattern of response was
observed in rectal temperature (Table 2).
Dehydration did not affect mean skin temperature in either exercise
position. However, during supine exercise, mean skin temperature was
significantly higher than during upright exercise (35.2 vs. 34.2°C,
respectively; P < 0.05) because of
the higher back skin temperature (34.2 vs. 37.8°C; respectively;
P < 0.05). Forearm skin temperature
was similar in all conditions during each 30-min bout of exercise (33.8-34.2°C; Table 2).
|
|
Influence of dehydration and hyperthermia on hemodynamics, skin
circulation, and plasma catecholamines during exercise.
The effects of dehydration and hyperthermia during the first 120 min of
upright exercise in these subjects have been reported in detail
previously (9) and in general were similar to the responses during the
subsequent 30 min of upright exercise presently reported. In the
30-min bouts, cardiovascular responses were measured during the
20- to 30-min period of exercise when the differences in body
temperature between the dehydration and euhydration conditions were the
largest (~0.8°C; Fig. 2). Specifically, comparing dehydration with euhydration during upright exercise, SV was 30 ± 6 ml lower and heart rate was 14 ± 2 beats/min higher during dehydration (P < 0.05; Fig.
3). In addition, cardiac
output and MAP were 3.0 ± 0.7 l/min and 6 ± 2 mmHg lower,
respectively, whereas systemic vascular resistance was 0.5 ± 0.2 mmHg · l1 · min
higher during dehydration (all P < 0.05) compared with euhydration values.
|
1 · min
higher during dehydration (P < 0.05)
compared with euhydration values (Fig. 3).
Comparing dehydration with euhydration during upright exercise, forearm
blood flow and FVC were 27 ± 6 and 22 ± 3% lower, respectively, during dehydration (both
P < 0.05; Fig.
4). In contrast, with dehydration during
supine exercise, forearm blood flow and FVC did not decline
significantly (Fig. 4).
|
|
Influence of body posture on hemodynamics, skin circulation, and plasma catecholamines during exercise. Compared with the effects of upright exercise in subjects with dehydration, supine exercise attenuated the increases in heart rate and the reductions in SV and cardiac output (7 ± 2 vs. 9 ± 1% higher heart rate, 13 ± 4 vs. 21 ± 3% lower SV, 8 ± 3 vs. 14 ± 3% lower cardiac output during supine vs. upright, respectively; all P < 0.05). Moreover, supine exercise prevented the significant reductions in MAP, forearm blood flow, and FVC as well as the significant increases in plasma catecholamines observed with dehydration during upright exercise.
On the other hand, compared with upright exercise in euhydrated subjects, supine exercise restored two-thirds of the SV decline and prevented one-third of the increase in heart rate observed with upright exercise in dehydrated subjects (Fig. 3 and Table 1). During supine exercise in dehydrated and hyperthermic subjects, SV and cardiac output were not statistically different from those measured during upright exercise in euhydrated subjects [130 ± 11 vs. 141 ± 9 ml/beat SV and 20.9 ± 1.5 vs. 21.3 ± 1.1 l/min cardiac output, respectively; not significant (NS)]. Furthermore, MAP was significantly higher than that measured during upright exercise in euhydrated subjects (107 ± 2 vs. 93 ± 2 mmHg; P < 0.05; Fig. 3). The higher MAP during supine compared with upright exercise was accompanied by both higher systolic blood pressure (195 ± 7 vs. 172 ± 7 mmHg, respectively; P < 0.05) and diastolic blood pressure (62 ± 1 vs. 54 ± 3 mmHg, respectively; P < 0.05). In addition, during supine exercise in dehydrated subjects, forearm blood flow and FVC tended to be higher than during upright exercise in euhydrated subjects (18 and 7% higher, respectively; NS; Fig. 4, A and B), whereas plasma catecholamines were not different (Fig. 5). Furthermore, whether subjects were euhydrated or dehydrated, skin blood flow and CVC during supine exercise were significantly higher than during upright exercise (Table 2).Forearm blood flow, skin blood flow, FVC, and CVC during exercise in the follow-up study. During upright exercise, dehydration similarly reduced forearm blood flow and FVC as in the main study (i.e., 9-10%). Furthermore, with dehydration during upright exercise, laser Doppler skin blood flow and CVC were significantly (P < 0.05) lower compared with the same measurements with euhydration (Fig. 4, C and D). In contrast, dehydration did not significantly reduce forearm blood flow, skin blood flow, FVC, or CVC during supine exercise. Additionally, supine exercise resulted in higher laser Doppler skin blood flow and CVC than upright exercise in euhydrated subjects (Fig. 4, C and D). Nevertheless, dehydration compared with euhydration during supine exercise resulted in a delayed onset of vasodilatation (252 ± 21 vs. 203 ± 16 s, respectively; P < 0.05) and increased Tes threshold for vasodilatation (37.37 ± 0.11 vs. 37.05 ± 0.11°C, respectively; P < 0.05).
Sweating rate. No differences in total sweat volume during the 30 min of exercise were observed when subjects exercised in either state of hydration or either body position (mean range 0.8 ± 0.1-0.9 ± 0.1 l).
Rate of perceived exertion. With euhydration, the rate of perceived exertion was identical during exercise in both body positions (15 ± 1 units). With dehydration, the rate of perceived exertion tended to be higher than with euhydration during both upright (16 ± 1 vs. 15 ± 1 units; P = 0.08) and supine exercise (17 ± 1 vs. 15 ± 1 units; P = 0.06).
| |
DISCUSSION |
|---|
|
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
Our purpose was to determine whether the alterations in cardiovascular function caused by dehydration and hyperthermia during upright exercise were attenuated or prevented by augmenting central blood volume with exercise in the supine position. The exercise intensity, the amount of dehydration, and the increases in serum osmolality, serum sodium, and Tes during exercise in the upright position were identical to those in the supine position. The most important observations of the present study were that the reductions in MAP and CVC and the increase in plasma norepinephrine concentration that are characteristic of exercise in the upright position when subjects are dehydrated and hyperthermic were totally absent during supine exercise, despite equal dehydration and hyperthermia. Furthermore, supine exercise compared with upright exercise when subjects were dehydrated and hyperthermic restored two-thirds of the reduction in SV and prevented one-third of the increase in heart rate. These results suggest that a reduction in central blood volume and MAP are factors associated with reduced CVC and increased plasma norepinephrine with dehydration and hyperthermia during upright exercise.
The only previous study aimed at addressing whether supine exercise prevents or attenuates the effects of dehydration on SV and heart rate during exercise in the sitting position was performed by Saltin and Stenberg (30). They tested two subjects, first when euhydrated early in exercise and then again when dehydrated after a 195-min exercise period. They found an 18% decline in SV during exercise in both the supine and the sitting positions. However, Saltin and Stenberg (30) observed that cardiac output was maintained during prolonged upright exercise, in contrast to the present study, which elicited a more severe hyperthermic stress. Nevertheless, they observed MAP to be lower when subjects were dehydrated during prolonged upright exercise, as observed presently.
The present study was designed to test subjects who were trained in
both modes of cycling exercise while measurements were made at the same
O2 and in a counterbalanced
order to control for the effect of exercise per se on
O2 and heart rate drifts. In
addition, subjects experienced an identical rise in core temperature with dehydration (Tes ~0.8°C
higher than with euhydration) when exercising in the supine and upright
positions, allowing the identification of the independent effect of
increased central blood volume and venous return. Supine exercise was
performed with the legs above the heart level and the trunk lying on a
table in the horizontal position. Our main assumption is that this
manipulation did indeed cause a significantly higher venous return,
central blood volume, and left ventricular end-diastolic volume
compared with those measured during upright exercise. Previous reports
of SV, central blood volume, central venous pressure, and left
ventricular end-diastolic volume during supine versus upright exercise
support the present assumption (1, 5, 26). More specifically, the
presently observed 10- to 20-ml higher SV during supine versus upright
cycling in euhydrated and dehydrated subjects was probably the result of a higher left ventricular end-diastolic volume, because end-systolic volume is already very low during moderately intense exercise (<30 ml
end-systolic volume; see Ref. 26).
We have recently shown that the lowering of SV with dehydration during upright exercise is related to the combined influences of hypovolemia, concomitant to dehydration-induced plasma volume losses, and hyperthermia (10). This is based on the observation that, when dehydration-induced hypovolemia and hyperthermia are fully prevented by an intravenous infusion of a plasma volume expander and exercise is performed in the cold, no reductions in SV, cardiac output, or MAP are observed despite the 3- to 4-l extravascular dehydration (10). In addition, these variables are unaltered during prolonged exercise when euhydration is maintained and Tes is stabilized at ~38°C (8, 9). Separately, dehydration-induced hypovolemia and hyperthermia (+1°C higher core temperature) exert similar effects because both reduce SV 7-8% and increase heart rate 5% without significantly affecting cardiac output or MAP (10). It is when they are combined during upright exercise, as in the present study, that cardiac output declines because of the synergistic 19-27% reduction in SV (8-11, 21-23, 29, 31).
Our important observation that supine exercise, even in dehydrated and hyperthermic subjects, restored FVC and CVC and lowered plasma norepinephrine to levels observed during exercise in euhydrated subjects emphasizes the important effect of central blood volume on baroreflex control of skin circulation and the sympathetic nervous system. It therefore appears that the reductions in CVC and increase in norepinephrine concentration observed during upright exercise in dehydrated and hyperthermic subjects are caused by reductions in central blood volume. It is known that central blood volume greatly influences the circulation to skin from the observations that elevations in central blood volume with water immersion or supine exercise offset the plateauing of skin blood flow at high core temperatures that are normally seen during exercise in the upright position in euhydrated subjects (24, 25). MAP was also maintained at euhydration levels in the present study during supine exercise in dehydrated subjects but declined significantly during upright exercise in dehydrated subjects. Therefore, the reduced MAP with dehydration during upright exercise was also associated with significant increases in plasma norepinephrine and epinephrine (50-95%) and reductions in forearm skin blood flow and FVC (27 ± 6 and 22 ± 8%, respectively; Fig. 4, A and B). Apparently, the present effect of dehydration (i.e., 3,300 ml) on reducing skin blood flow during upright exercise is not caused only by the concomitant 200- to 300-ml reduction in plasma volume. In this light, Montain and Coyle (21) have previously shown that plasma volume expansion during upright cycling in similarly dehydrated subjects failed to restore forearm blood flow or reduced core temperature, possibly because it did not sufficiently raise central blood volume.
During upright exercise, a lowered central blood volume and a reduced MAP with dehydration and hyperthermia would likely result in the unloading of both low- and high-pressure baroreceptors (19, 28). There are three possibilities by which low- and high-pressure mechanoreflexes (baroreceptors) could mediate the significant reductions in CVC and FVC with dehydration and hyperthermia during upright exercise. High- and low-pressure mechanoreflexes could be inhibiting active vasodilator outflow, superimposing sympathetic vasoconstriction on the cutaneous blood flow response, or influencing both processes (14-18, 22). The elevation of plasma norepinephrine by dehydration during upright exercise and the restoration of plasma norepinephrine by supine exercise despite dehydration support the notion that cutaneous vasoconstriction is involved in dehydration-induced vasoconstriction of the skin (22). However, this does not lessen or exclude the possibility that withdrawal of active vasodilation is also involved. Taken together, these results indicate that factors such as hypernatremia, hyperosmolality, and hyperthermia, which were identical during upright and supine exercise with dehydration, are not the primary signals mediating the reduced CVC and FVC with dehydration during upright exercise. These factors, however, might influence the time and Tes at the onset of vasodilation and potentiate the action of other mechanisms (6, 18, 23). A more plausible possibility is that dehydration during upright exercise is sensed through reductions in central blood volume and MAP and that this reduces CVC by sympathetic vasoconstriction of the cutaneous circulation and possibly by withdrawal of active vasodilation.
An unresolved question regards the mechanisms responsible for the 11 ml/beat (8%) lower SV with dehydration and hyperthermia during supine
exercise compared with that in subjects euhydrated with a lower core
temperature. This still-reduced SV was associated with the persistent
dehydration-induced hypovolemia, hyperthermia, and elevated heart rate.
Indeed recent results support the notion that increases in heart rate,
paralleling the rise in core temperature from 36 to 40°C
(r2 = 0.98;
P = 0.001), contributes to reductions in SV with heat stress, particularly at core temperatures >38°C when cutaneous blood flow reaches a plateau level (11). Providing a more direct support of this hypothesis, Fritzsche et al. (7) have recently demonstrated that blunting the progressive rise in heart rate during 60 min of exercise with 
-blockade totally prevents the decline in SV
from occurring after 15 min of cycling exercise in a thermoneutral environment.
In summary, these results suggest that the decline in cutaneous vascular conductance and the increased plasma norepinephrine concentration with dehydration during upright exercise, independent of hyperthermia, are associated with a reduction in central blood volume and a lower arterial blood pressure. Furthermore, increased central blood volume derived from exercise in the supine position reversed most of the reduction in SV experienced with dehydration, whereas the persistent reduction in SV was associated with an elevated heart rate and hyperthermia.
| |
ACKNOWLEDGEMENTS |
|---|
We give special thanks to the volunteer subjects for enthusiasm. The expertise and interest of James D. Fluckey, who performed the catecholamine analysis, and Dr. Peter A. Farrell, in whose laboratory (Pennsylvania State University) the analysis was performed, are greatly appreciated.
| |
FOOTNOTES |
|---|
J. González-Alonso and R. Mora-Rodríguez were supported by scholarships from the Ministry of Education and Science of Spain. This study was partially supported by the Spanish Ministry of Education and Science. The catecholamine analysis was supported by a grant from the Gatorade Sports Science Institute.
Present address of J. González-Alonso: The Copenhagen Muscle Research Center, Rigshospitalet, section 7652, Tagensvej 20, DK-2200 Copenhagen N, Denmark.
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. §1734 solely to indicate this fact.
Address for reprint requests and other correspondence: E. F. Coyle, University of Texas, Human Performance Laboratory, Bellmont Hall, Rm. 222, Austin, TX 78712 (E-mail: coyle{at}mail.utexas.edu).
Received 7 October 1998; accepted in final form 29 March 1999.
| |
REFERENCES |
|---|
|
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
1.
Bevegård, S.,
A. Holmgren,
and
B. Johnson.
Circulatory studies in well-trained athletes at rest and during exercise, with special reference to stroke volume and the influence of body position.
Acta Physiol. Scand.
57:
26-50,
1963[Medline].
2.
Borg, G.
Simple rating methods for estimation of perceived exercise.
In: Physical Work and Effort, edited by G. Borg. New York: Pergamon, 1975, p. 39-46.
3.
Collier, C. R.
Determination of mixed venous CO2 tensions by rebreathing.
J. Appl. Physiol.
9:
25-29,
1956
4.
Dill, D. B.,
and
D. L. Costill.
Calculations of percentage changes in volumes of blood, plasma, and red blood cells with dehydration.
J. Appl. Physiol.
37:
247-248,
1974
5.
Ekelund, L. G.
Circulatory and respiratory adaptations during prolonged exercise.
Acta Physiol. Scand. Suppl.
292:
1-38,
1967.
6.
Fortney, S. M.,
C. B. Wenger,
J. R. Bove,
and
E. R. Nadel.
Effect of hyperosmolality on control of blood flow and sweating.
J. Appl. Physiol.
57:
1688-1695,
1984
7.
Fritzsche, R. G.,
T. W. Switzer,
B. J. Hodgkinson,
and
E. F. Coyle.
Stroke volume decline during prolonged exercise is influenced by the increase in heart rate.
J. Appl. Physiol.
86:
799-805,
1999
8.
González-Alonso, J.,
J. A. L. Calbet,
and
B. Nielsen.
Muscle blood flow is reduced with dehydration during prolonged exercise in humans.
J. Physiol. (Lond.)
513:
895-905,
1998
9.
González-Alonso, J.,
R. Mora-Rodríguez,
P. R. Below,
and
E. F. Coyle.
Dehydration reduces cardiac output and increases systemic and cutaneous vascular resistance during exercise.
J. Appl. Physiol.
79:
1487-1496,
1995
10.
González-Alonso, J.,
R. Mora-Rodríguez,
P. R. Below,
and
E. F. Coyle.
Dehydration markedly impairs cardiovascular function in hyperthermic endurance athletes during exercise.
J. Appl. Physiol.
82:
1229-1236,
1997
11.
González-Alonso, J.,
C. Teller,
S. L. Andersen,
F. B. Jensen,
T. Hyldig,
and
B. Nielsen.
Influence of body temperature on the development of fatigue during prolonged exercise in the heat.
J. Appl. Physiol.
86:
1032-1039,
1999
12.
Hardy, J. D.,
and
E. F. DuBois.
The technique of measuring radiation and convection.
J. Nutr.
15:
461-475,
1938.
13.
Hjemdahl, P.
Catecholamine measurements by high-performance liquid chromatography.
Am. J. Physiol.
247 (Endocrinol. Metab. 10):
E13-E20,
1984
14.
Johnson, J. M.,
and
L. B. Rowell.
Forearm skin and muscle vascular responses to prolonged leg exercise in man.
J. Appl. Physiol.
39:
920-924,
1975
15.
Johnson, J. M.,
L. B. Rowell,
and
G. L. Brengelmann.
Modification of the skin blood flow-body temperature relationship by upright exercise.
J. Appl. Physiol.
37:
880-886,
1974
16.
Kellogg, D. L.,
J. M. Johnson,
W. L. Kenney,
P. E. Pérgola,
and
W. A. Kosiba.
Mechanisms of control of skin blood flow during prolonged exercise in humans.
Am. J. Physiol.
265 (Heart Circ. Physiol. 34):
H562-H568,
1993
17.
Kellogg, D. L.,
J. M. Johnson,
and
W. A. Kosiba.
Baroreflex control of the cutaneous active vasodilator system in humans.
Circ. Res.
66:
1420-1426,
1990
18.
Kenney, W. L.,
and
J. M. Johnson.
Control of skin blood flow during exercise.
Med. Sci. Sports Exerc.
24:
303-312,
1992[Medline].
19.
Mack, G. W.,
C. A. Thompson,
D. F. Doerr,
E. F. Doerr,
E. R. Nadel,
and
V. A. Convertino.
Diminished baroreflex control of forearm vascular resistance following training.
Med. Sci. Sports Exerc.
23:
1367-1374,
1991[Medline].
20.
McHardy, G. L. R.
The relationship between the differences in pressure and content in carbon dioxide in arterial and venous blood.
Clin. Sci.
32:
299-309,
1967[Medline].
21.
Montain, S. J.,
and
E. F. Coyle.
Fluid ingestion during exercise increases skin blood flow independent of blood volume.
J. Appl. Physiol.
73:
903-910,
1992
22.
Mora-Rodríguez, R.,
J. González-Alonso,
P. R. Below,
and
E. F. Coyle.
Plasma catecholamines and hyperglycemia influence thermoregulation during prolonged exercise in the heat.
J. Physiol. (Lond.)
491:
529-540,
1996[Medline].
23.
Nadel, E. R.,
S. M. Fortney,
and
C. B. Wenger.
Effect of hydration state on circulatory and thermal regulations.
J. Appl. Physiol.
49:
715-721,
1980
24.
Nielsen, B.,
L. B. Rowell,
and
F. Bonde-Petersen.
Cardiovascular responses to heat stress and blood volume displacements during exercise in man.
Eur. J. Appl. Physiol.
52:
370-374,
1984.
25.
Nose, H.,
G. W. Mack,
X. Shi,
T. Morimoto,
and
E. R. Nadel.
Effect of saline infusion during exercise on thermal and circulatory regulations.
J. Appl. Physiol.
69:
609-616,
1990
26.
Poliner, L. R.,
G. J. Dehmer,
S. E. Lewis,
R. W. Parkey,
C. G. Blomqvist,
and
J. T. Willerson.
Left ventricular performance in normal subjects: a comparison of the responses to exercise in the upright and supine positions.
Circulation
62:
528-534,
1980
27.
Pugh, L. G. C.,
J. I. Corbett,
and
R. H. Johnson.
Rectal temperatures, weight losses, and sweating rate in marathon running.
J. Appl. Physiol.
23:
347-352,
1957.
28.
Renlund, D. G.,
G. Gerstenblith,
J. L. Fleg,
L. C. Becker,
and
E. D. Lakatta.
Interaction between left ventricular end-diastolic volume and end-systolic volumes in normal humans.
Am. J. Physiol.
258 (Heart Circ. Physiol. 27):
H437-H481,
1990.
29.
Rowell, L. B.,
H. J. Marx,
R. A. Bruce,
R. D. Conn,
and
F. Kusumi.
Reductions in cardiac output, central blood volume, and stroke volume with thermal stress in normal men during exercise.
J. Clin. Invest.
45:
1801-1816,
1966.
30.
Saltin, B.,
and
J. Stenberg.
Circulatory response to prolonged severe exercise.
J. Appl. Physiol.
19:
833-838,
1964
31.
Sawka, M. N.,
R. G. Knowlton,
and
J. B. Critz.
Thermal and circulatory responses to repeated bouts of prolonged exercise.
J. Appl. Physiol.
19:
833-838,
1979.
32.
Vissing, S. F.,
U. Scherrer,
and
R. G. Victor.
Increase of sympathetic discharge to skeletal muscle but not to the skin during lower negative pressure in humans.
J. Physiol. (Lond.)
381:
233-241,
1994.
33.
Whitney, R. J.
The measurement of volume changes in human limbs.
J. Physiol.
121:
1-27,
1953.
This article has been cited by other articles:
|
|
 |
|
  L. Nybo Hyperthermia and fatigue J Appl Physiol, March 1, 2008; 104(3): 871 - 878. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. Gonzalez-Alonso, C. G. Crandall, and J. M. Johnson The cardiovascular challenge of exercising in the heat J. Physiol., January 1, 2008; 586(1): 45 - 53. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C. D. Bradford, J. D. Cotter, M. S. Thorburn, R. J. Walker, and D. F. Gerrard Exercise can be pyrogenic in humans Am J Physiol Regulatory Integrative Comp Physiol, January 1, 2007; 292(1): R143 - R149. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. N. Cheuvront, R. Carter III, J. W. Castellani, and M. N. Sawka Hypohydration impairs endurance exercise performance in temperate but not cold air J Appl Physiol, November 1, 2005; 99(5): 1972 - 1976. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. E. Wilson, R. Carter III, M. J. Cutler, J. Cui, M. L. Smith, and C. G. Crandall Active recovery attenuates the fall in sweat rate but not cutaneous vascular conductance after supine exercise J Appl Physiol, February 1, 2004; 96(2): 668 - 673. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. Gonzalez-Alonso, R. Mora-Rodriguez, and E. F. Coyle Stroke volume during exercise: interaction of environment and hydration Am J Physiol Heart Circ Physiol, February 1, 2000; 278(2): H321 - H330. [Abstract] [Full Text] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Visit Other APS Journals Online |
Significantly higher than euhydrated, supine value
(P < 0.05).
