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Department of Integrative Physiology and Cardiovascular Research Institute, University of North Texas Health Science Center, Fort Worth, Texas 76107-2609
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ABSTRACT |
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 TOP
 ABSTRACT
 INTRODUCTION
METHODS AND PROCEDURES
RESULTS
DISCUSSION
REFERENCES
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The present investigation was designed to uncouple the hemodynamic physiological effects of thermoregulation from the effects of a progressively increasing central command activation during prolonged exercise. Subjects performed two 1-h bouts of leg cycling exercise with 1) no intervention and 2) continuous infusion of a dextran solution to maintain central venous pressure constant at the 10-min pressure. Volume infusion resulted in a significant reduction in the decrement in mean arterial pressure seen in the control exercise bout (6.7 ± 1.8 vs. 11.6± 1.3 mmHg, respectively). However, indexes of central command such as heart rate and ratings of perceived exertion rose to a similar extent during both exercise conditions. In addition, the carotid-cardiac baroreflex stimulus-response relationship, as measured by using the neck pressure-neck suction technique, was reset from rest to 10 min of exercise and was further reset from 10 to 50 min of exercise in both exercise conditions, with the operating point being shifted toward the reflex threshold. We conclude that the progressive resetting of the carotid baroreflex and the shift of the reflex operating point render the carotid-cardiac reflex ineffectual in counteracting the continued decrement in mean arterial pressure that occurs during the prolonged exercise.
threshold; saturation; operating point; central command
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INTRODUCTION |
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TOP
ABSTRACT
INTRODUCTION
METHODS AND PROCEDURES
RESULTS
DISCUSSION
REFERENCES
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ALTHOUGH THE HEMODYNAMIC responses associated with
prolonged exercise have been documented, the mechanisms involved in
blood pressure regulation during prolonged exercise have not been fully elucidated. After the initial response to the onset of dynamic exercise, prolonged exercise at a constant workload is characterized by
the redistribution of blood volume to the cutaneous circulation in
response to thermoregulatory demands (4, 17) resulting in a progressive
decrease in central blood volume (CBV), central venous pressure (CVP),
and total peripheral resistance (TPR). This redistribution consequently
results in a progressive decrease in stroke volume (SV) and mean
arterial pressure (MAP) and a concomitant increase in heart rate (HR),
a phenomenon which has been termed cardiovascular drift. The increase
in HR also occurs progressively, presumably as a compensatory response
to the decrease in central filling volume and SV, and results in the
maintenance of cardiac output (
c). However, despite
the use of whole body surface cooling or saline infusion during
prolonged exercise to return CBV to precardiovascular drift values, HR
continues to increase, and a slight downward drift in MAP remains (11,
18). These data raise the question as to whether there is a loss of
baroreflex regulation of arterial blood pressure during prolonged
dynamic exercise.
Potts et al. (16) have previously demonstrated that at the onset of
25% maximal oxygen uptake
(
O2 max) and 50%
O2 max exercise, the
carotid baroreflex (CBR) was classically reset in direct relation to
the intensity of exercise and that the operating point (i.e.,
prestimulus MAP) was relocated toward the threshold of the reflex.
Recently, we have demonstrated that the CBR continued to be reset
upward in relation to exercise intensity from 50 to 100%
O2 max (10) and
furthermore that the relocation of the operating point continued toward
threshold in direct relation to the increasing exercise intensity. It
has been proposed that the mechanism of resetting of the CBR at the
onset of dynamic exercise is a result of the activation of the
feed-forward mechanism or "central command" (16, 19). We submit
1) that with prolongation of
exercise at a constant workload, further increases in central command
with progressive motor fiber recruitment (5, 9) will be reflected by
increases in HR and ratings of perceived exertion (RPE) and will result
in a continual upward resetting of the CBR. In addition, we propose
2) that with exercise at a greater
intensity than the 50%
O2 max used by Potts et
al. (16), the operating point would be further shifted toward or below
the threshold pressure of the baroreflex. Therefore we hypothesize that, as prolonged steady-state exercise continues and cardiovascular drift becomes manifest, MAP would fall below the operating range of the
progressively reset CBR, which would then become ineffectual in
correcting the downward drift in MAP. Hence the objective of the
present investigation was to demonstrate that the apparent loss of
arterial blood pressure regulation seen during prolonged, constant-load
dynamic exercise can be attributed to a progressive resetting of the
CBR in relation to increases in central command. Furthermore, we
suggest that the resetting is independent of the CBV displacement that
occurs in response to the thermoregulatory stress incurred during
prolonged moderate- to high-intensity dynamic exercise.
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METHODS AND PROCEDURES |
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TOP
ABSTRACT
INTRODUCTION
METHODS AND PROCEDURES
RESULTS
DISCUSSION
REFERENCES
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To uncouple the effects of increases in central command from the global
hemodynamic responses to prolonged exercise, volunteer subjects
performed 1 h of dynamic leg cycling exercise at 65% O2 max with
1) no intervention and
2) maintenance of cardiac filling
volume via the continuous infusion of a solution of 6% dextran in
saline. At 10 and 50 min of exercise, CBR stimulus-response curves were
generated by using a variable-pressure neck collar, as previously
demonstrated in our laboratory (16). We anticipated that maintenance of
cardiac filling volume would oppose the compensatory component of the
increase in HR (compensating for the fall in SV) during the exercise
bout; however, the central-command-related increases in HR would
remain. In addition, although the infusion of dextran in saline
counteracts the fall in SV by maintaining central filling volume, the
decrease in TPR due to cutaneous vasodilation during the exercise would
remain. Therefore we anticipated that some degree of diminution of MAP
would occur and would proceed uncorrected due to the relocation of the
operating arterial pressure in relation to the progressively reset CBR.
Subjects
Eight healthy subjects (aged 27.9 ± 1.6 yr) gave written informed consent for participation in this investigation, which was approved by the Institutional Review Board of the University of North Texas Health Science Center at Fort Worth. All subjects were free of known cardiovascular and pulmonary disorders and were not taking any prescribed medications. Subject data are summarized in Table 1.
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Protocol
At least 2 days before participating in the experimental protocol, each subject performed a graded exercise test for the determination ofO2 max during
semirecumbent leg cycling exercise. On the experimental day, each
subject performed two 1-h bouts of constant-load dynamic leg cycling
exercise at ~65%
O2 max in the
semirecumbent position. The exercise consisted either of constant-load
leg cycling exercise with no intervention or of constant-load leg
cycling with continuous intravenous infusion of a solution of 6%
dextran in saline. The infusion rate of the dextran solution was varied so that CVP did not fall below the pressure value recorded at 10 min of
exercise. The exercise bouts were performed in an environment at
24°C with 40-60% relative humidity and were separated by a rest period of sufficient length (at least 3 h) to return HR and MAP to
approximate baseline values. CBR stimulus-response curves were
constructed at rest, after attainment of steady-state exercise (after
~10 min of constant-load exercise), and during the last 10-12
min of each experimental exercise bout, by using a modification of the
neck pressure-neck suction (NP-NS) protocol previously developed by
Potts et al. (16). For the experimental bouts with infusion of dextran
in saline, the infusions were begun after the first exercise NP-NS
protocol (i.e., at 20 min of exercise) and were maintained throughout
the exercise bout at an infusion rate that would maintain CVP at the
level no lower than that attained immediately before the execution of
the first exercise NP-NS protocol. During each exercise bout, HR,
O2 uptake
(O2), MAP, and
CVP were continuously monitored and recorded. In addition, at 10-min intervals, temperature at the auditory canal, c,
and RPE were assessed. Venous blood samples were also drawn
periodically for the measurement of venous hemoglobin, hematocrit,
O2 content, O2 saturation, and concentrations
of lactate and catecholamines (norepinephrine and epinephrine). The
concentration of atrial natriuretic peptide (ANP) was also assessed in
the blood samples to discern the effects of the infusion of the dextran
solution on the cardiac stretch receptors.
Measurements
Maximal exercise stress test and
O2 measures.
Subjects who were determined to be acceptable by means of physical
examination performed a graded exercise test for the determination of
O2 max. The subjects
exercised in the 70° semi-recumbent back-supported posture at
progressively increasing workloads on a constant-load cycle ergometer
until they reached volitional fatigue. During the test, measurements
included the rate of O2 (using breath-by-breath open-circuit spirometry) and continuous electrocardiogram monitoring (using a 12-lead monitoring system). Subjects returned to the laboratory no less than 2 days after maximal
exercise testing for the performance of the experimental exercise bouts.
Cardiovascular variables.
HR and O2 were continuously
monitored via electrocardiogram and a customized breath-by-breath
mouthpiece apparatus, respectively. c was measured
at 10-min intervals by using the acetylene rebreathing method (21),
with SV being calculated from the division of c by
HR. Arterial blood pressure and CVP were measured directly via
catheters inserted by a consulting physician into the radial artery and
brachial vein, respectively, of each subject. Placement of the dual
lumen CVP catheter at the fourth intercostal space was confirmed with
the use of fluoroscopy. Both pressures were monitored by using
disposable pressure transducers (Cobe) interfaced with pressure
monitors (Hewlett-Packard 78342A). The pressure transducers were
calibrated and established at zero reference pressure at the
midaxillary and third intercostal space before and after the
experiment, and catheters were appropriately connected to a pressurized
saline bag for saline flush. Mean, systolic, and diastolic blood
pressure, along with CVP and HR, were recorded beat-by-beat on-line by
using a personal computer (Gateway 2000, sampling rate 100/s) and
customized software. O2 was
similarly recorded breath-by-breath by using a personal computer (Dell
Optiplex Gxi, sampling rate 250/s) and customized software. In
addition, at 10-min intervals, venous blood samples were taken from the second port of the dual lumen CVP catheter and RPE (Borg scale) were
supplied by the subject (1). At the same time periods, body temperature
was measured by using a Thermoscan Instant Thermometer, which utilizes
a sealed auditory canal position to measure the infrared heat radiation
from the tympanic membrane and provides a calculated temperature
reading that is adjusted to an oral measurement.
Venous blood samples. Venous blood samples were drawn from the second port of the dual lumen CVP catheter at rest, at 10, 20, 50, and 60 min of exercise and after 10 min of recovery from the exercise. These samples were subjected to hematocrit analysis (microcentrifuge), and the hemoglobin concentration (g/dl), O2 saturation (%), and O2 content (ml/dl) of each sample were measured and recorded (IL 282 CO-Oximeter). Also, the concentration of lactate in each venous blood sample was recorded (YSI 2300 Stat). In addition, the catacholamines, epinephrine and norepinephrine, were separated in each of these samples via isocratic high-pressure liquid chromatography, and the plasma concentrations (pmol/ml) of epinephrine and norepinephrine were quantified electrochemically at 650 mV. Finally, the plasma concentration (pmol/ml) of ANP was measured using a radioimmunoassay kit (Penninsula Laboratories).
CBR.
CBR function during exercise was analyzed via a slight modification of
the NP-NS method previously reported by Potts et al. (16), in which
brief (5-s) pressure and suction stimuli are applied to the carotid
sinus region of the subject's neck and the peak HR and MAP responses
to the individual stimuli are recorded. To accommodate the high
workloads used in the present experiments, the modifications were
designed to enable the subjects to breathe freely during the 5-s
carotid sinus stimuli, in contrast to the end-expiratory breath hold
maneuver previously used at rest and during lighter exercise workloads
(16). On the basis of data from Eckberg et al. (3), who demonstrated
that, at a breathing frequency of 24 breaths/min, no difference existed
between the responses to neck collar stimuli during inspiration and
expiration, we predicted that, by choosing the peak HR and MAP response
to each stimulus, CBR stimulus-response curves could be modeled, with
appropriate repeatability, at high exercise workloads. In addition, the
time required to construct a stimulus-response curve during exercise
was reduced to a maximum of 10-12 min to minimize the confounding
effects of cardiovascular drift on CBR function. Before the present
investigation was conducted, the repeatability of the modified NP-NS
technique was established. The HR responses (carotid-cardiac
baroreflex) to several levels of carotid sinus stimulation were
recorded after 10 min of dynamic leg cycling exercise at 68%
O2 max in one subject
during four separate bouts of exercise. The gain, threshold, and
saturation values for each of the four individual CBR stimulus-response
curves, as well as the means, SE, coefficients of variation, and 95%
confidence intervals of these values are listed in Table
2.
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RESULTS |
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TOP
ABSTRACT
INTRODUCTION
METHODS AND PROCEDURES
RESULTS
DISCUSSION
REFERENCES
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Cardiovascular variables.
The maintenance of a consistent thermal stress between the two exercise
conditions was of primary importance to our investigation. Accordingly,
the increases in body temperature during the hour of exercise
(~2°C) were not significantly different between the two exercise
conditions at any time of measurement. The alterations in several
cardiovascular variables recorded during the exercise bouts are
reported below as percent change from the measurement taken at 10 min
of exercise. The absolute measurement values for each of these
variables recorded at 10 min of exercise are listed in Table
3.
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c was maintained
over this period, i.e., no significant differences were found in
c from 10 to 60 min of exercise. There were no significant differences in CVP at rest or during the first 20 min of
exercise between the two exercise bouts. However, when infusion of a
dextran solution was begun at 20 min of exercise and maintained
throughout the exercise period (mean infusion volume, 419 ± 45 ml),
CVP rose continuously (50.4 ± 10.3% during the 40 min of
infusion), such that CVP was significantly greater at 40, 50, and 60 min of exercise with volume infusion than at the same periods of
control exercise. Volume infusion resulted in the maintenance of SV
during the exercise bout, i.e., no significant differences were found
in SV from 10 to 60 min of exercise. However, TPR continued to fall to
a statistically similar extent as during the control condition (Fig.
1). As a result, a significant decrement was seen in MAP with exercise
time. However, by minute 50, this
decrement was significantly less than in the control condition (total
MAP decrease of 6.7 ± 1.8%) (Fig. 1). In addition, HR rose to the same extent as in the control condition as a function of exercise time
(12.3 ± 2.0%) and c also increased
significantly over the hour of exercise (9.4 ± 2.2%) due to the
maintenance of SV, see Fig. 1. Figure 1 also illustrates a significant
increase in the arteriovenous O2
difference [(a-v)O2]
from 10 to 60 min of the control exercise bout (12.1 ± 2.7%) which
was absent during exercise with volume infusion. The disparity between
the (a-v)O2 of the control vs. the
infusion-exercise bouts, which was statistically significant at 60 min
of exercise, was presumed to be due to the effect of the increase in
flow
(c)
on O2 extraction. However, despite
a significant difference in
O2-carrying capacity at 60 min
(control: 20.41 ± 0.96 vs. infusion: 18.54 ± 0.92 ml/dl,
P = 0.012), the resultant difference
in percent O2 extraction was not
significant (0.96 ± 0.052 vs. 0.92 ± 0.069%,
P = 0.65).
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Indexes of Central Command
The indexes of central command measured in the current investigation were statistically similar between the two exercise bouts, as clearly illustrated in Fig. 2. HR rose 12.5 ± 2.2% in the control condition and 12.3 ± 2.0% in the volume-infusion experiment. RPEs also rose significantly with exercise time in the control and volume-infusion bouts (34.9 ± 4.4 and 32 ± 4.7%, respectively).
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O2
O2 was observed
to drift upward similarly during both exercise bouts. Percent change in
this measurement was calculated from 20 min rather than from 10 min due
to an increase in O2 at the
10-min value, presumably due to anticipation of the impending NP-NS
protocol, which was administered between 10 and 20 min of exercise
(Fig. 2).
Blood Measurements
Venous blood samples were drawn during the resting period before each exercise bout; at 10, 20, 50, and 60 min of exercise; and after 10 min of recovery from the exercise. The infusion of an average of 419 ± 45 ml of dextran solution significantly reduced the measured hematocrit at 50 and 60 min of exercise, as well as during recovery, compared with the control condition. Accordingly, hemoglobin content (g/dl) was also significantly less in these blood samples. The infusion did not significantly affect the O2 saturation nor the O2 content of the venous blood, although a nonsignificant trend existed for an increased venous O2 saturation during exercise with volume infusion. This trend corresponded to a nonsignificant trend for a decreased (a-v)O2 during volume infusion, asc was higher during this condition compared with control. In addition, the plasma concentrations of epinephrine and
norepinephrine were similar during the two exercise conditions, as was
the concentration of ANP; this indicates that the cardiac stretch
receptors were not affected by this degree of volume infusion. Figure
3 illustrates the measurements of
hematocrit, hemoglobin, epinephrine, norepinephrine, and lactate in the
venous blood samples.
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Finally, measures of lactic acid (in mmol/l) indicated that the concentration of this metabolite was significantly higher at 10 and 20 min of control exercise compared with the exercise with volume infusion (Fig. 3). As infusion of the dextran in saline solution had not begun at this time, we submit that this discrepancy may be an effect of order because the volume infusion exercise bouts were consistently performed after several hours of recovery from the control exercise bouts. This order was necessary to prevent the confounding effects of increased blood volume on the hemodynamic responses to exercise in the control condition because the experiment was designed to be undertaken in one experimental day to minimize the invasive procedures experienced by the volunteer subjects.
Carotid-Cardiac Baroreflex
Modeling of the carotid-cardiac baroreflex stimulus-response relationship demonstrated that the reflex was significantly shifted rightward on the carotid sinus pressure axis from rest to 10 min of exercise and also from 10 to 50 min of exercise in both exercise conditions. Figure 4, A-C, illustrates each shift in the carotid-cardiac baroreflex threshold, centering point, and saturation. Figure 4D shows that no reflex shift was accompanied by a significant decrement in reflex gain, and Fig. 4E shows the operating point pressure at rest and at 10 and 50 min of exercise. The operating point of the carotid-cardiac baroreflex was significantly relocated from rest, at which time there was no significant difference between the operating point and centering point pressures, to 10 min of exercise and further from 10 to 50 min of exercise. These shifts occurred away from the reflex centering point and toward the threshold of the reflex such that there was no significant difference between the operating point and threshold pressures at 50 min of exercise (Fig. 4F).
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Carotid-Vasomotor Baroreflex
We were unable to obtain threshold, saturation, and gain values for the individual carotid-vasomotor stimulus-response relationships elicited by the NP-NS protocol due to the inability to attain convergence in the modeling procedure. However, Fig. 5 illustrates the mean responses of the eight subjects to each level of carotid sinus perturbation at rest as well as at 10 and 50 min of exercise in both exercise conditions. The mean stimulus-response relationships constructed at rest for both conditions followed the usual sigmoidal shape. Therefore, the model of Kent et al. (8) was used to calculate threshold, saturation, and gain values for these curves. These values were similar during rest before the two exercise bouts [81.7, 120.9, and
0.30, respectively, in the control
condition, and 72.1, 109.1, and 0.33, respectively, in the
volume-infusion condition (the resting measurement was before
infusion)]. However, we were unable to adequately model the mean
or individual responses at 10 and 50 min of exercise to the logistic
equation of Kent et al. (8). Interestingly, the shape of those
carotid-vasomotor curves no longer fit the typical sigmoidal shape but
appeared to become progressively steeper on the left- hand, or pressure stimulus, portion of the curve and in the volume-infusion condition flatter on the right-hand, or suction stimulus, portion of the curve.
To quantify this observation, the individual curves were divided into
left- and right-hand portions, constituting the three lowest and four
highest carotid sinus pressures, respectively. Table
4 describes the slope of the entire
carotid-vasomotor baroreflex stimulus-response relationship for each
condition at 10 and 50 min of exercise. In addition, Table 4 describes
the slope for the left- and right-hand portions of the curves
individually.
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DISCUSSION |
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TOP
ABSTRACT
INTRODUCTION
METHODS AND PROCEDURES
RESULTS
DISCUSSION
REFERENCES
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Prolonged Exercise and Cardiovascular Drift
In the present investigation, 1 h of leg cycling exercise at 65%O2 max elicited
the cardiovascular and hemodynamic responses that have been previously
documented for prolonged moderate- to high-intensity dynamic exercise
(4, 20) (Fig. 1). The progressive decrease in MAP seen during prolonged
exercise, after the initial increase at exercise onset, has been
attributed to a redistribution of circulating blood volume to the
cutaneous circulation in response to thermoregulatory demands (18).
Accordingly, our data illustrate that CVP decreased significantly from
10 to 60 min of exercise, presumably due to a greater percentage of
c being distributed to the cutaneous circulation.
This fall in CBV resulted in a decreased cardiac filling volume, which
was reflected by a concomitant reduction in SV and a compensatory
increase in HR. When CVP, and thus SV, were maintained via a continuous
infusion of a solution of 6% dextran in saline during the prolonged
exercise protocol, a progressive decrement in MAP remained (6.71 ± 1.83%), albeit to a lesser degree than in the control condition,
presumably due to the fall in TPR (11.59 ± 1.30%), corresponding
to cutaneous vasodilation. As previously reported (11), no significant
difference existed in the rise in HR between the two exercise
conditions. c was relatively constant throughout the
control exercise condition; however, due to the maintenance of CBV and
SV, c increased appreciably during the
volume-infusion condition (9.4 ± 2.2%) in relation to the increase
in HR (Fig. 1). The fact that TPR and MAP continued to decrease
throughout the exercise with infusion, despite a maintained or
increased CBV, SV, and c, taken in conjunction with
the data of previous investigations (6, 11, 18), indicates that thermoregulatory blood-volume redistribution was an important component
of the cardiovascular drift. However, these data also raise the
question as to whether baroreflex control of blood pressure was
diminished or fatigued during the prolonged exercise, particularly in
the light of a maintained increase in HR despite the countermeasures used in the present and previous investigations (6, 11).
Carotid Arterial Baroreflex
In the present investigation, the construction of carotid-cardiac baroreflex stimulus-response curves during the control exercise bouts indicated that the baroreflex was indeed classically reset from the resting condition to the onset of the exercise, as well as being further reset by the prolongation of the bout to 1 h (Fig. 4). The shifts seen in the carotid-cardiac baroreflex reflex due to prolongation of exercise time were similar to those seen by Potts et al. (16), Papelier et al. (13), and Norton et al. (10) in response to increases in exercise intensity. In addition, the modeling of the baroreflex stimulus-response curves illustrated that prolongation of exercise, much like increases in exercise intensity (10, 16), results in a relocation of the reflex operating point (i.e., prestimulus MAP) toward threshold and away from the centering point of the reflex. The rightward shift of the carotid-cardiac baroreflex threshold and saturation values were in direct relation to the increases seen in the indexes of central command (i.e., HR, RPE). In fact, the increase in HR and the rightward shift in reflex threshold both approximated a change of 12.5% from 10 to 60 min of exercise under the control condition. In the dextran-infusion experiments, in which CVP was maintained and even increased during the hour of exercise, the threshold and saturation pressures of the carotid-cardiac baroreflex relationships were similarly reset (Fig. 4). Again, the data indicate that there was no significant difference in reflex gain during this protocol. Importantly, the maintenance of CVP, and thus SV, had no significant effect on the upward drift in HR during the exercise bout. In addition, RPE drifted upward to an equal extent as during the control condition. Taken together, these data indicate that central command activation was similar in the two exercise conditions. Accordingly, the rightward shifts in the reflex threshold and saturation values were also directly related to the rise in HR, RPE, and alsoO2 during the
infusion experiments. In evidence, HR and the reflex threshold
increased ~12.3 and 12.5%, respectively, during the hour of exercise
with volume infusion.
The individual carotid-vasomotor baroreflex stimulus-response relationships could not be modeled in this investigation; however, the data summarized in Fig. 5 show that the reflex appears to be reset rightward and upward, similar to the carotid-cardiac baroreflex. In addition, although the stimulus-response curves generated at rest during both conditions conformed to the typical sigmoid shape, the curves at 10 and 50 min of exercise appeared to become progressively steeper in response to positive pressure stimuli and in the volume-infusion condition flatter in response to negative (suction) stimuli (Table 4). A similar alteration in the carotid-vasomotor baroreflex (and not the carotid-cardiac baroreflex) was found by Papelier et al. (14) during postexercise leg muscle ischemia induced by thigh cuff inflation and was attributed by the authors to an activation of the muscle chemoreflex. This reflex is thought to have a modulatory effect, predominantly on the efferent, or response arm of the vasomotor component of the CBR, via the activation of the sympathetic nervous system (12, 14, 19). The change in shape of the carotid-vasomotor baroreflex curves in the present investigation may also be attributable to chemoreflex activation. Conceivably, the steeper slope of the lefthand portion of the curve, that indicates an increased gain of response to hypotensive stimuli, may be an effort to increase blood pressure and alleviate a chemical error signal in the exercising muscles. However, the increased gain of the left side of the relationship did not result in a correction of the downward drift in MAP seen in the present investigation. Therefore, we must speculate that the assumed activation of the muscle reflex was not sufficient to counteract the effect of the rightward resetting of the stimulus-response relationship that may occur in response to a progressively increasing central command. This change in shape was the primary cause of the inability to model the carotid-vasomotor baroreflex relationship by using the logistic equation developed by Kent et al. (8). However, movement artifacts that primarily affect the directly measured arterial pressure may have compounded the within-subject variability of the blood pressure measurement.
In the present investigation, the carotid-cardiac baroreflex was
progressively reset rightward and upward during the prolonged exercise
bout. In addition, the operating point of the carotid-cardiac baroreflex was relocated away from the centering point and toward the
threshold of the baroreflex in direct relation to exercise time and,
thus, central command activation. Therefore, we propose that, as the
thermoregulatory stress related to the prolonged steady-state exercise
developed in the control condition and cardiovascular drift became
manifest, MAP fell below the operating range of the reset CBR,
rendering it ineffectual in correcting the downward drift in MAP. The
same resetting occurred in the volume-infusion exercise bouts,
presumably resulting in the same scenario of drift in MAP, albeit to a
lesser degree than in the control condition because of the maintenance
of CVP and SV. The resetting of the carotid-cardiac baroreflex during
the prolonged exercise was shown to occur in direct relation to
increases in the indexes of central command and
O2 due to the need for
progressive motor fiber recruitment (7, 20). These data, along with
those of other investigations such as Potts et al. (16), Norton et al.
(10), and DiCarlo and Bishop (2), support the role of central command
in CBR resetting during dynamic exercise. Also, the increasing
O2 in relation to motor fiber
recruitment may play a role in the resetting via an increased muscle
afferent input to the cardiovascular center (15, 19). In addition, the
alterations in the shape of the carotid-vasomotor baroreflex support an
additional role for the exercise pressor reflex in modulating
baroreflex control of blood pressure under certain exercise conditions
(14) and may reflect the occlusive interaction between the exercise
pressor reflex and the carotid-vasomotor reflex recently identified by
Potts et al. (15).
In summary, the present investigation was successful in uncoupling the global hemodynamic responses to the thermal stress associated with prolonged exercise from the effects of baroreflex resetting. This resetting results in an increased range of response of the carotid-cardiac reflex to hypertension. However, it renders the reflex ineffectual in counteracting a fall in arterial pressure, such as occurs during prolonged exercise with the manifestation of cardiovascular drift.
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ACKNOWLEDGEMENTS |
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We thank the subjects for their interest and cooperation. In addition, we thank Guari Patankar for enthusiastic aid in data reduction and Lisa Marquez for secretarial support in preparation of the manuscript.
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FOOTNOTES |
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This study was supported in part by the Life Sciences Division of the National Aeronautics and Space Administration (NASA) of the United States of America under NASA Grant No. NGT-70409, NASA Specialized Center of Research and Training Grant NAGW-3582, NASA Grant NAG 5-4668, and the American College of Sports Medicine-NASA Space Physiology Student Research Award.
This work was part of K. H. Norton's dissertation as submitted to the University of North Texas Health Science Center for the fulfillment of the requirements for the degree of Doctor of Philosophy.
Present address of K. H. Norton: Laboratory for Cardiovascular Science, Gerontology Research Center, NIA/NIH, 5600 Nathan Shock Blvd., Baltimore, MD 21224.
Address for reprint requests and other correspondence: P. B. Raven, University of North Texas Health Science Center, Department of Integrative Physiology, 3500 Camp Bowie Blvd., Fort Worth, TX 76107-2699.
Received 19 September 1997; accepted in final form 9 March 1999.
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REFERENCES |
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TOP
ABSTRACT
INTRODUCTION
METHODS AND PROCEDURES
RESULTS
DISCUSSION
REFERENCES
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