| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
Department of Physiology, Kyoto Prefectural University of Medicine, Kamigyo-ku, Kyoto 602-0841, Japan
 |
ABSTRACT |
|---|
Top
Abstract
Introduction
Methods
Results
Discussion
References
|
|---|
To elucidate the role of increased plasma
osmolality (Posmol), which occurs during exercise in the
regulation of cutaneous vasodilation (CVD) during exercise, we
determined the relationship between the change in esophageal
temperature (
Tes) required to elicit CVD (Tes threshold for
CVD) and Posmol during light and moderate exercise (30 and
55% of peak oxygen consumption, respectively) and passive body
heating. Then we compared the relationship with the data obtained in
our previous study [A. Takamata, K. Nagashima, H. Nose, and T. Morimoto. Am. J. Physiol. 273 (Regulatory Integrative Comp. Physiol.
42): R197-R204, 1997], in which we determined the relationships during passive body heating following isotonic (0.9% NaCl) or hypertonic (2 or 3% NaCl) saline infusions in the same subjects. Posmol values at 5 min after the onset of
exercise were 287.5 ± 0.9 mosmol/kgH2O during light exercise
and 293.0 ± 1.2 mosmol/kgH2O
during moderate exercise. Posmol just before passive body
heating was 289.9 ± 1.4 mosmol/kgH2O. The
Tes threshold for CVD was 0.09 ± 0.05°C during light exercise, 0.31 ± 0.09°C during
moderate exercise, and 0.10 ± 0.05°C during passive body heating. The relationship between the
Tes threshold for CVD and Posmol was shown to be on the same regression line both
during exercise and during passive body heating with or without
infusions [A. Takamata, K. Nagashima, H. Nose, and T. Morimoto.
Am. J. Physiol. 273 (Regulatory Integrative Comp. Physiol.
42): R197-R204, 1997]. Our data suggest that the elevated
body core temperature threshold for CVD during exercise could be the
result of increased Posmol induced by exercise and is not
due to reduced plasma volume or the intensity of the exercise itself.
body temperature threshold; thermoregulation; exercise intensity
| |
INTRODUCTION |
|---|
|
Top
Abstract
Introduction
Methods
Results
Discussion
References
|
|---|
CUTANEOUS CIRCULATION is primarily controlled by thermal drive or body temperature, and a couple of nonthermal factors are known to modify this thermoregulatory response (6). Exercise has been known to modify thermoregulatory cutaneous vasodilation (CVD) by elevating the body core temperature threshold for CVD (6, 8). Several studies have reported that the effect of exercise is intensity dependent; low-intensity exercise does not alter thermoregulatory CVD, whereas high-intensity exercise shifts the body core temperature threshold for CVD (10, 15, 18). Kellogg et al. (7) reported that the shifted esophageal temperature (Tes) threshold for CVD was not abolished with sympathetic adrenergic blockade by bretylium tosylate and concluded that the shifted body temperature threshold for CVD is not due to increased vasoconstrictor tone but rather to reduced active vasodilator outflow. However, the stimulus that induces an exercise-induced shift in the body temperature threshold for CVD remains unknown (6, 8).
Dehydration is another factor that modifies thermoregulatory CVD (1, 6,
11). Recently, we have shown that an increase in plasma osmolality
(Posmol) linearly elevates the change in Tes
(Tes) threshold for CVD (17).
In addition, an increase in Posmol in response to exercise
intensity occurs in a fashion similar to the increase in
Tes threshold for CVD (2, 13). From these facts, we hypothesized that the exercise-induced shift in
the threshold for CVD is due to an exercise-induced increase in
Posmol.
The purpose of the present study was to elucidate the role of the
exercise-induced increase in Posmol in the regulation of CVD during exercise. We determined the relationship between the change
in Tes required to elicit CVD
(Tes threshold for CVD) and
Posmol during light (~30% of peak oxygen consumption;
O2 peak)- and moderate
(~55%
O2 peak)-intensity
exercise and passive body heating. Then we compared these relationships
with those found during passive body heating following isotonic or
hypertonic saline infusions obtained in our previous study in the same
subjects (17) to account for the role of the intensity of exercise
itself and the exercise-induced reduction in plasma volume (PV).
| |
METHODS |
|---|
|
Top
Abstract
Introduction
Methods
Results
Discussion
References
|
|---|
Subjects
This study was approved by the Review Board on Human Experiments, Kyoto Prefectural University of Medicine. Six healthy male subjects gave their written informed consent before participating in the study. The subjects who participated in this study were the same as in our previous study (17). The experiments were conducted 1 mo after our previous study, and the subjects did not participate in any exercise training program during this period. Thus we assumed that any changes in the state of their training and acclimation from the previous study were minimal. Their age was 26 ± 3 yr (mean ± SE); body weight, 67.9 ± 6.9 kg; and peak aerobic power (O2 peak) measured
with a cycle ergometer in a recumbent position before the experiments,
47.6 ± 4.4 ml · min
1 · kg
body wt1.
Protocol
Control period. Subjects reported to the laboratory at 1000. They had refrained from heavy exercise for 24 h and from salty food, alcohol, and caffeine for 17 h before arriving at the laboratory. They were allowed to eat breakfast and drink water if they desired. On reporting to the laboratory they were provided with 200 ml of water to avoid dehydration. Then the subjects sat on a chair for 1 h during the control period. At the end of the control period, a blood sample was taken.Exercise/passive body heating. In the
exercise protocol, subjects were asked to exercise with a cycle
ergometer in a semirecumbent position at intensities of ~30%
O2 peak (light
exercise) or at ~55%
O2 peak (moderate
exercise) for 40 min after a 10-min resting period at a room
temperature of 28°C. In the passive heating protocol, the subjects
immersed their lower legs in water at 42°C with a room temperature
of 28°C for 40 min following a 10-min preheating control period.
Blood samples were taken just before (0 min) and at 5, 20, and 40 min
after the onset of exercise and just before and at 20 and 40 min after
the onset of passive body heating.
Measurements
Tes was measured with a copper-constantan thermocouple placed in polyethylene tubing (PE-90). The tip of the probe was advanced at a distance of one-fourth of the subject's standing height from the external nares. Skin blood flow was measured with a laser Doppler flowmeter on the chest, with the assumption that the chest skin response represents the whole body skin response (Advance ALF 21). The site of the probe placement on the chest skin was always the same for each subject. These data were collected by a computer through an analog-to-digital converter every 1 s, and mean values of every 30 s were used for further analyses. Heart rate (HR) was continuously monitored from electrocardiograph recording, and blood pressure was measured every 1 min with an R-wave gated automated sphygmomanometer (Colin STBP-780). Mean arterial pressure (MAP) was calculated as
(SBP 
DBP) + DBP, where SBP is systolic blood pressure and DBP is diastolic blood pressure. Cutaneous vascular conductance (CVC) was calculated as the
laser-Doppler flowmeter voltage output divided by MAP and shown as a
percentage of the mean value of pre-exercise or preheating control
(CVC).
Blood samples were drawn without stasis, and an aliquot for measurement
of Posmol was immediately transferred into the tube containing heparin and centrifuged. The separated plasma was stored in
the freezer at 20°C until measurement. Blood for the
determination of hematocrit and hemoglobin concentration was processed
immediately. Posmol was measured by the freezing-point
depression (Fiske one-ten osmometer), hematocrit by microhematocrit
tube centrifugation, and hemoglobin concentrations by the
cyanomethemoglobin method (Sigma hemoglobin kit).
Data Analyses
We defined the body core temperature threshold for CVD as theTes required to elicit a rapid
increase in CVC (Tes
threshold for CVD), characterized by an increase in CVC over three
consecutive measurements. We employed the
Tes threshold for CVD instead
of absolute Tes value because the
day-to-day variability in baseline Tes among the 6 conditions
employed, including our previous infusion study (17), was 0.10 ± 0.03°C, which was larger than the
Tes threshold for CVD during
passive body heating and light exercise, although the mean baseline
Tes between conditions were not
statistically different. We assumed that day-to-day variation
"reset" the onset of thermoregulatory responses (10, 17). This
assumption is derived from the fact that circadian variation or
menstrual variation in female subjects shifted the
Tes thresholds for the sweating and CVD, but the Tes required
to elicit these responses are not influenced by these shifts (5, 16).
Thus to examine the effect of exercise and plasma osmolality and to
eliminate day-to-day variation, we determined the
Tes required for CVD instead of absolute Tes thresholds.
Percent change in PV was calculated from hematocrit and hemoglobin concentration using the following equation
|
![× {[1 − (Hct<SUB>A</SUB>/100)]/[1 − (Hct<SUB>B</SUB>/100)]} − 100](/content/vol275/issue1/fulltext/R286/img003.gif)
|
PV is percent change in PV, Hb is hemoglobin concentration, and Hct
is hematocrit. Subscript B indicates before (control) and A, after
(experiment).
The values were shown as mean and SE of six subjects. The effects of exercise intensity or time were determined by ANOVA with repeated measures. The differences between data of specific interest were determined by Fisher's least-significant difference test. A P value < 0.05 was considered to indicate statistical significance. Regression analysis was performed using standard least-squares test.
| |
RESULTS |
|---|
|
Top
Abstract
Introduction
Methods
Results
Discussion
References
|
|---|
Table 1 shows Posmol and PV
during the experiment. Posmol just before passive body
heating was 289.9 ± 1.4 mosmol/kgH2O. Posmol
values at 5 min after the onset of light and moderate exercise were 287.5 ± 0.9 and 293.0 ± 1.2 mosmol/kgH2O, respectively. PV at 5 min after the onset of light and moderate exercise were 1.7 ± 1.5 and 4.9 ± 0.9%, respectively.
|
Figure 1 shows the relationship between
CVC and Tes. The
relationship shifted rightward during moderate exercise compared with
during passive body heating or light exercise. We determined the
threshold for CVD in each condition in each subject.
Tes threshold for CVD was 0.10 ± 0.05°C during passive body heating, 0.09 ± 0.05°C
during light exercise, and 0.31 ± 0.09°C during moderate
exercise. The Tes threshold for
CVD during moderate exercise was higher than that during passive body
heating, but the Tes threshold
for CVD during light exercise was not different from that found during
passive body heating.
|
In Fig. 2, we compared the relationship
between the Tes threshold for
CVD and Posmol during exercise and passive body heating with those during passive body heating following hypertonic (2 or 3%
NaCl) or isotonic (0.9% NaCl) saline infusion that were obtained in
our previous study (17). Posmol values of exercise experiments were those at 5 min after the onset of exercise.
Posmol values of passive body heating experiments (with or
without infusion) were those just before the onset of passive body
heating (17). The data both during exercise and passive body heating
with or without infusions were shown to be on the same regression line (Fig. 2). The regression equation determined in the present study (y = 0.40x 11.39), including the data during exercise and passive body
heating with and without infusions, was not different from that
determined during passive body heating with and without infusions in
our previous study (y = 0.44x 12.69).
|
| |
DISCUSSION |
|---|
|
Top
Abstract
Introduction
Methods
Results
Discussion
References
|
|---|
Exercise increases body temperature threshold for CVD in an exercise
intensity-dependent manner (6). Moderate to heavy exercise elevates the
Tes threshold for CVD, whereas
light exercise does not influence the
Tes threshold for CVD (10, 18).
However, the stimulus that induces the shift in body temperature
threshold for CVD still remains unknown (6, 8). Because
Posmol increases during exercise and the pattern of the
increase in Posmol and body temperature threshold for CVD
in response to exercise intensity are similar (2, 10, 13), we examined
the involvement of increased Posmol in the elevated body
temperature threshold for CVD. To account for the role of
exercise-induced reduction in PV and exercise intensity itself, we
compared the relationship between the
Tes threshold for CVD and
Posmol during exercise of different intensities with those
found during passive body heating and during passive body heating with
isotonic or hypertonic saline infusion (17).
The Tes threshold for CVD
increased during moderate exercise compared with passive body heating,
with an increased Posmol and a reduced PV (Fig. 1, Table
1). Neither the Tes threshold for CVD, Posmol, or PV were changed by light exercise
(Fig. 1, Table 1). The increase in Posmol and the shift in
Tes threshold for CVD were
comparable with the results obtained in other studies (2, 10, 13). The
relationship between Tes
threshold for CVD and Posmol during exercise was similar to
that obtained in passively heated subjects with infusions (17), and the
data both during exercise and passive body heating with or without infusions were shown to be on the same regression line (Fig. 2). The
Tes threshold for CVD
correlated linearly with Posmol regardless of exercise
intensity or PV level (Fig. 2). PV just before the onset of passive
body heating in infusion studies increased by ~10% (17). Thus the
present data are consistent with our hypothesis that the primary factor
responsible for the shift of the body temperature threshold for CVD
during exercise is increased Posmol and not reduced PV or
the intensity of the exercise itself.
Mack et al. (9) reported that baroreceptor unloading with a lower body
negative pressure of 40 mmHg increased the body temperature
threshold for CVD during exercise. Thus baroreceptor unloading has an
impact on body temperature threshold for CVD. Nose et al. (12) reported
that the right atrial pressure increased at the onset of exercise in a
semirecumbent position. Reeves et al. (14) reported that pulmonary
wedge pressure and right atrial pressure increased during upright cycle
exercise. Arterial pressure increased immediately after the onset of
exercise, and PV expansion by infusion did not influence the
relationship between Tes
threshold for CVD and Posmol (Fig. 2). In addition, the
effect of exercise intensity on the
Tes threshold for CVD in supine
position was similar to that in our study (10). Taken together, the
involvement of baroreceptor unloading itself could be excluded.
Although it is unknown whether the resetting of baroreflex plays a
role, exercise did not shift the relationship between
Tes threshold for CVD and
Posmol, suggesting that exercise-induced resetting of
baroreflex is probably not involved in the exercise-induced shift in
body temperature threshold for CVD.
We determined the relationship between the
Tes threshold for CVD against
the Posmol obtained 5 min after the onset of exercise in
the exercise experiments. The increase in Posmol in
response to exercise intensity was similar to those found in other
studies (2). In addition, a blood sample was taken before CVD occurred in our present study and Posmol was assumed to have reached
a plateau by this time (4) and remained constant throughout the exercise period thereafter (Table 1). Thus our analysis is reasonable for a determination of the relationship between
Tes threshold for CVD and
Posmol during exercise. The Posmol before
passive body heating was higher than at 5 min after the onset of light exercise. This may reflect the difference of hydration status between
the experiments. However, because we analyzed the relationship between
Tes threshold for CVD and
Posmol, this difference did not influence our analysis.
Posmol gradually increased during passive body heating and
became similar to that during moderate exercise at the end of
experiment (Table 1), but the relationship between CVC and
Tes during the passive body
heating did not shift rightward during the experiment with the increase
in Posmol (Fig. 1). Fortney et al. (3) reported that
hypertonic saline infusion during exercise did not alter forearm blood
flow response. This result was different from their previous study (4),
in which they found hypertonic saline infusion before exercise shifted
the Tes threshold for forearm
blood flow. In addition, they failed to increase forearm blood flow by
infusion of hypotonic saline during exercise (3). Taken together, we postulate that increased Posmol has an effect on the onset
of CVD but that it does not influence the relationship between CVC and
body core temperature once CVD has occurred. Because the increase in
forearm blood flow had already occurred when they started infusions in
the later study by Fortney et al. (3), the contradictory results could
be explained by our hypothesis, although further study is required.
It still remains unknown whether osmotic inhibition of CVD is the
result of reduced active vasodilator outflow or increased vasoconstrictor tone (6). Kellogg et al. (7) reported that the shifted
esophageal temperature threshold for CVD during exercise was not
abolished with sympathetic adrenergic blockade by bretylium tosylate
and concluded that the shifted body temperature threshold for CVD is
not due to increased vasoconstrictor tone but rather reduced active
vasodilator outflow. Thus, if the exercise-induced shift in the
Tes threshold for CVD is
mediated by increased Posmol caused by exercise, the
efferent pathway that shifts the
Tes threshold for CVD, found in
our previous study, can be attributed to the reduced active vasodilator
outflow. An experiment to examine the efferent mechanism of osmotic
inhibition of CVD is expected to be performed.
In summary, we confirmed that exercise inhibits thermoregulatory CVD in an exercise intensity-dependent fashion by elevating the body temperature threshold. Our results were consistent with our hypothesis that the increased body temperature threshold for CVD during exercise is due to the increased Posmol that occurs during exercise. In addition, this inhibitory effect seems to be acting on the onset of CVD specifically.
| |
ACKNOWLEDGEMENTS |
|---|
This study was supported in part by the Ministry of Education, Science, Culture, and Sports of Japan and the Ono Sports Science Foundation.
| |
FOOTNOTES |
|---|
Present address of H. Nose: Dept. of Sports Medicine, Research Institute for Aging and Adaptation, Shinshu University School of Medicine, Matsumoto 390, Japan.
Address for reprint requests: A. Takamata, Dept. of Physiology, Kyoto Prefectural Univ. of Medicine, Kawaramachi Hirokoji, Kamigyo-ku, Kyoto 602-0841, Japan (E-mail: akira{at}phys.kpu-m.ac.jp).
Received 22 December 1997; accepted in final form 31 March 1998.
| |
REFERENCES |
|---|
|
Top
Abstract
Introduction
Methods
Results
Discussion
References
|
|---|
1.
Baker, M. A.
Thermoregulation in dehydrated vertebrates.
In: Milestones in Environmental Physiology: Progress in Biometeorology. The Hague, The Netherlands: SPB Academic, 1989, vol. 7, p. 101-107.
2.
Convertino, V. A.,
L. C. Keil,
E. M. Bernauer,
and
J. E. Greenleaf.
Plasma volume, osmolality, vasopressin, and renin activity during graded exercise in man.
J. Appl. Physiol.
50:
123-128,
1981
3.
Fortney, S. M.,
N. B. Vroman,
W. S. Backett,
S. Permutt,
and
N. D. LaFrance.
Effect of exercise hemoconcentration and hyperosmolality on exercise responses.
J. Appl. Physiol.
65:
519-524,
1988
4.
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
5.
Hessemer, V.,
and
K. Brück.
Influence of menstrual cycle on shivering, skin blood flow, and sweating responses measured at night.
J. Appl. Physiol.
59:
1902-1910,
1985
6.
Johnson, J. M.,
and
D. W. Proppe.
Cardiovascular adjustments to heat stress.
In: Handbook of Physiology. Environmental Physiology. Bethesda, MD: Am. Physiol. Soc., 1996, sect. 4, vol. I, chapt. 11, p. 215-243.
7.
Kellogg, D. L., Jr.,
J. M. Johnson,
and
W. A. Kosiba.
Control of internal temperature threshold for active cutaneous vasodilation by dynamic exercise.
J. Appl. Physiol.
71:
2476-2482,
1991
8.
Kenney, W. L.,
and
J. M. Johnson.
Control of skin blood flow during exercise.
Med. Sci. Sports Exerc.
24:
303-312,
1992[Medline].
9.
Mack, G. W.,
T. Nishiyasu,
and
X. Shi.
Baroreceptor modulation of cutaneous vasodilator and sudomotor responses to thermal stress in humans.
J. Physiol. (Lond.)
483:
537-547,
1995[Medline].
10.
Mack, G. W.,
H. Nose,
A. Takamata,
T. Okuno,
and
T. Morimoto.
Influence of exercise intensity and plasma volume on active cutaneous vasodilation in humans.
Med. Sci. Sports Exerc.
26:
209-216,
1994[Medline].
11.
Morimoto, T.
Thermoregulation and body fluids: role of blood volume and central venous pressure.
Jpn. J. Physiol.
40:
165-179,
1990[Medline].
12.
Nose, H.,
A. Takamata,
G. W. Mack,
Y. Oda,
T. Kawabata,
S. Hashimoto,
M. Hirose,
E. Chihara,
and
T. Morimoto.
Right atrial pressure and forearm blood flow during prolonged exercise in a hot environment.
Pflügers Arch.
426:
177-182,
1994[Medline].
13.
Nose, H.,
A. Takamata,
G. W. Mack,
Y. Oda,
T. Okuno,
D.-H. Kang,
and
T. Morimoto.
Water and electrolyte balance in the vascular space during graded exercise in humans.
J. Appl. Physiol.
70:
2757-2762,
1991
14.
Reeves, J. T.,
B. M. Groves,
A. Cymerman,
J. R. Sutton,
P. D. Wagner,
D. Turkevich,
and
C. S. Houston.
Operation Everest II: cardiac filling pressures during cycle exercise at sea level.
Respir. Physiol.
80:
147-154,
1990[Medline].
15.
Smolander, J.,
J. Saalo,
and
O. Korhonen.
Effect of work load on cutaneous vascular response to exercise.
J. Appl. Physiol.
71:
1614-1619,
1991
16.
Stephenson, L. A.,
C. B. Wenger,
B. H. O'Donovan,
and
E. R. Nadel.
Circadian rhythm in sweating and cutaneous blood flow.
Am. J. Physiol.
246 (Regulatory Integrative Comp. Physiol. 15):
R321-R324,
1984
17.
Takamata, A.,
K. Nagashima,
H. Nose,
and
T. Morimoto.
Osmoregulatory inhibition of thermally induced cutaneous vasodilation in passively heated humans.
Am. J. Physiol.
273 (Regulatory Integrative Comp. Physiol. 42):
R197-R204,
1997
18.
Taylor, W. F.,
J. M. Johnson,
W. A. Kosiba,
and
C. M. Kwan.
Graded cutaneous vascular responses to dynamic leg exercise.
J. Appl. Physiol.
64:
1803-1809,
1988
This article has been cited by other articles:
|
|
 |
|
  H. Mitono, H. Endoh, K. Okazaki, T. Ichinose, S. Masuki, A. Takamata, and H. Nose Acute hypoosmolality attenuates the suppression of cutaneous vasodilation with increased exercise intensity J Appl Physiol, September 1, 2005; 99(3): 902 - 908. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. Ichinose, K. Okazaki, S. Masuki, H. Mitono, M. Chen, H. Endoh, and H. Nose Ten-day endurance training attenuates the hyperosmotic suppression of cutaneous vasodilation during exercise but not sweating J Appl Physiol, July 1, 2005; 99(1): 237 - 243. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 Y. Nakajima, T. Mizobe, A. Takamata, and Y. Tanaka Baroreflex modulation of peripheral vasoconstriction during progressive hypothermia in anesthetized humans Am J Physiol Regulatory Integrative Comp Physiol, October 1, 2000; 279(4): R1430 - R1436. [Abstract] [Full Text] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Visit Other APS Journals Online |
) and moderate exercise (
) and passive body heating (
)
and passive body heating following isotonic or hypertonic saline
infusion (
) in the same subjects (