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1 Department of Integrative Physiology and Cardiovascular Research Institute, University of North Texas Health Science Center, Fort Worth, Texas 76107-2609; and 2 Copenhagen Muscle Research Center, Rigshospitalet, DK-2200 Copenhagen, Denmark
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ABSTRACT |
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 TOP
 ABSTRACT
 INTRODUCTION
METHODS AND PROCEDURES
RESULTS
DISCUSSION
REFERENCES
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Recent
investigations have demonstrated that at the onset of
low-to-moderate-intensity leg cycling exercise (L) the carotid baroreflex (CBR) was classically reset in direct relation to the intensity of exercise. On the basis of these data, we proposed that the
CBR would also be classically reset at the onset of moderate- to
maximal-intensity L exercise. Therefore, CBR stimulus-response relationships were compared in seven male volunteers by using the neck
pressure-neck suction technique during dynamic exercise that ranged in
intensity from 50 to 100% of maximal oxygen uptake (
O2 max). L
exercise alone was performed at 50 and 75%
O2 max, and L
exercise combined with arm (A) exercise (L + A) was performed at 75 and 100%
O2 max.
O2 consumption and heart rate (HR)
increased in direct relation with the increases in exercise intensity.
The threshold and saturation pressures of the carotid-cardiac reflex at
100% O2 max were
>75% O2 max, which
were in turn >50%
O2 max (P < 0.05), without a change in the
maximal reflex gain (Gmax). In
addition, the HR response value at threshold and saturation at 75%
O2 max was >50%
O2 max
(P < 0.05) and 100%
O2 max was
>75%
O2 max
(P < 0.07). Similar changes were
observed for the carotid-vasomotor reflex. In addition, as exercise
intensity increased, the operating point (the prestimulus blood
pressure) of the CBR was significantly relocated further from the
centering point (Gmax) of the
stimulus-response curve and was at threshold during 100%
O2 max. These
findings identify the continuous classic rightward and upward resetting
of the CBR, without a change in Gmax, during increases in dynamic
exercise intensity to maximal effort.
threshold; saturation; operating point; central command; exercise pressor reflex
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INTRODUCTION |
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TOP
ABSTRACT
INTRODUCTION
METHODS AND PROCEDURES
RESULTS
DISCUSSION
REFERENCES
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RECENT INVESTIGATIONS (12, 17) have demonstrated in humans that at the onset of low- to moderate-intensity leg cycling exercise the carotid baroreflex (CBR) was classically reset, i.e., the open-loop stimulus-response relationship was shifted to operate around the prevailing arterial blood pressure of the exercise, without an alteration in the maximal gain or sensitivity of the reflex. The resetting of the reflex occurred in direct relation to the intensity of exercise (12, 17), and modeling (7) of the reflex stimulus-response relationship indicated that the operating point (the prestimulus arterial pressure) was relocated away from the centering point and toward the reflex threshold (17). However, this modeling procedure has not been used in experiments designed to examine baroreflex function during high-intensity or maximal exercise. Therefore we proposed that the CBR would be classically reset in relation to exercise intensity at the onset of moderate- to maximal-intensity leg cycling exercise, with a concomitant relocation of the reflex operating point toward the reflex threshold, as has been demonstrated previously at lower intensities of exercise (12, 17).
Potential causal mechanisms for the resetting of the CBR include the
feed-forward, centrally originated signals that activate in parallel
the cardiovascular and somatomotor responses to exercise, i.e., central
command, (4, 5, 9, 19) and the feedback reflexes which originate in the
active skeletal musculature due to chemical and mechanical error
signals, i.e., the exercise-pressor reflex (9, 19). It has been
proposed that the immediate resetting of the CBR at the onset of
dynamic exercise is primarily the result of the activation of central
command (17, 19), a phenomenon that is directly related to the
intensity of exercise or, more specifically, the activation of an
appropriate number of motor fibers to execute the exercise (4, 5, 20).
Central command has been proposed to interact with the CBR at the level
of the neuron pool that receives the baroreflex afferents, thus
producing a lateral shift in the CBR stimulus-response relationship,
such that the reflex operates around the exercise-induced increase in
blood pressure (19). Therefore, increases in exercise intensity to
maximal effort would result in increases in indexes of central command,
such as heart rate (HR), along with the increase in
O2 uptake
(O2), and may be reflected by
a continued rightward resetting of the CBR (9). However, modulation of
the CBR can also occur by activation of the exercise-pressor reflex
(13), which has been proposed to produce an upward vertical shift in
the CBR stimulus-response relationship due to increased sympathetic
activation (19). Therefore we proposed to analyze the vertical and
horizontal components of the resetting of the CBR stimulus-response
relationship during dynamic exercise ranging in intensity from moderate
to maximal 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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Subjects
Seven healthy men (aged 25.4 ± 0.75 yr) gave written informed consent for this investigation, which was approved by the Ethics Committee of the Fredriksberg Municipalities. 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
Each subject performed two graded exercise tests at least 2 days before participation in the experiment. The primary test was a maximal exercise test for the determination of maximal O2 uptake (O2 max) during
upright, seated, back-supported leg cycling exercise. The second test
involved the measurement of
O2 during arm ergometry
performed at several graded exercise workloads to determine the arm
exercise workload which would elicit a
O2 of ~25% of the leg
cycling
O2 max. On
the experimental day, each subject performed four bouts (10-15 min
each) of constant-load dynamic exercise in a 20°C, 40-60%
relative humidity environment, in the same body position that was used
during the preliminary exercise tests. Each exercise bout was separated
by a rest period of sufficient length of time to return HR and mean
arterial pressure (MAP) to baseline values. Exercise
bout 1 consisted of leg cycling exercise at 50% of the predetermined leg cycling
O2 max (50% L).
Exercise bout 2 consisted of leg
cycling at the same workload, with the addition of arm-cranking
exercise at a workload that elicited 25% of the leg cycling
O2 max, such that the
whole body O2 was ~75%
of leg O2 max
(75% L + A). Exercise bout 3 (75% L)
consisted of leg cycling alone at a workload eliciting the same
O2 as was attained during
the bout 2 combined exercise. Finally,
exercise bout 4 consisted of leg
cycling at the same workload as in bout
3, with the addition of arm-cranking exercise at a
workload that elicited 25% of the leg cycling
O2 max such that the
whole body O2 approximated
leg O2 max (Max L + A). Presentation of exercise bouts
1-4 to each subject was randomized on the
experimental day. Table 2 lists the
absolute O2 measures and
wattage achieved for each level of exercise. During each exercise bout,
HR, O2, and MAP were
continuously monitored and recorded. At rest and after attainment of
steady-state exercise in each experimental exercise bout, CBR
stimulus-response curves were constructed by using a modification of
the neck pressure-neck suction (NP-NS) protocol previously developed by
Potts et al. (17).
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Measurements
Maximal exercise test and
O2 measures.
Subjects who were determined acceptable by physical examination
performed two graded exercise tests for the determination of
O2. The test for leg
O2 max was performed
in the upright posture on a constant-load cycle ergometer. The arm
ergometry exercise test was performed in the seated position, with a
constant-load cycle ergometer that was modified for arm ergometry.
During each maximal exercise test, the subject exercised to volitional
fatigue, and measurements included the rate of
O2 [using
breath-by-breath open-circuit spirometry (Medgraphics CPX/D,
MN)] and continuous electrocardiogram monitoring by
using a 12-lead monitoring system. Subjects returned to the laboratory
no less than 2 days after maximal-exercise testing for performance of
the experimental exercise bouts.
HR and arterial blood pressure. During each experimental test, HR was continuously monitored via electrocardiogram. Arterial blood pressure was measured directly via a catheter placed into the right femoral artery. The pressure was monitored by using disposable pressure transducers (Baxter) that were interfaced with a pressure monitor (Danika Elektronik, Dialogue 2000). 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 HR, were recorded beat-by-beat on-line by using a personal computer (Zitech Pro, Pentium 90) and customized software (sampling rate, 250/s).
CBR function.
CBR function during exercise was analyzed via a slight modification of
the NP-NS method previously reported by Potts et al. (17). To
accommodate the high workloads used in the present experiments, the
modification was 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 (17). On the basis of data from Eckberg et al. (3)
which 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 at high exercise workloads with appropriate repeatability. Furthermore, operating-point pressures were established for each stimulus and defined as the prevailing MAP before neck pressure or neck
suction was applied. The carotid sinus pressure that resulted from the
applied stimuli was estimated by adding the recorded neck chamber
pressure or suction to the prestimulus MAP attained two beats before
the beginning of the maneuver. In addition, the time required to
construct a stimulus-response curve during the 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 have been reported previously
(10).
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RESULTS |
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TOP
ABSTRACT
INTRODUCTION
METHODS AND PROCEDURES
RESULTS
DISCUSSION
REFERENCES
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Carotid-Cardiac Baroreflex Response to Dynamic Exercise
No significant differences were seen in the carotid-cardiac baroreflex maximal gain, or sensitivity, between any exercise bout. However, significant lateral shifts were seen in the threshold and saturation pressures of the reflex in relation to increases in exercise intensity (Fig. 1). These shifts occurred regardless of the type of exercise being performed, i.e., L or combined L + A exercise, with the exception of the comparison between the threshold pressures obtained during the 75% L + A and Max L + A exercise bouts. Failure to attain statistically significant differences between these bouts may be attributable to the large SE of the mean for threshold pressure in both bouts or to an achievement of the maximal saturation of the reflex. However, as the shift between these two bouts of exercise approached significance at P < 0.07, the results of this investigation indicate that the carotid-cardiac baroreflex was classically reset (i.e., a shift in reflex threshold and saturation without a concomitant change in reflex maximal gain) from rest toO2 max. The examination of vertical shifts in threshold and saturation (i.e., the
y-axis coordinate or HR response to
the corresponding threshold or saturation pressure value) between all
exercise bouts yielded similar results. Neither the values for
threshold or saturation nor the values for the corresponding HR
response were significantly different between the 75% L
and 75% L + A. Table 3 quantifies the
lateral (threshold and saturation pressure values) and vertical
(corresponding HR response values) shifts of the carotid-cardiac
stimulus-response relationship during the various exercise protocols
used in this investigation. These data also demonstrate the lack of a
significant difference in reflex maximal gain throughout the exercise
bouts.
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The position of the operating point of the carotid-cardiac baroreflex
during the resting condition was 90.9 ± 7.6 mmHg. During the four
exercise bouts (50% L, 75% L + A, 75% L, and maximal exercise) the
operating points were 102.4 ± 6.4, 112.7 ± 5.8, 115.9 ± 6.7, and 118.6 ± 7.7 mmHg, respectively. In addition, the operating points were significantly shifted away from the centering
point and toward the threshold of the carotid-cardiac stimulus-response
relationship in relation to exercise intensity (Table 3). No
significant difference was found between the position of the operating
points relative to the centering points of the L only and combined L + A exercise bouts at 75%
O2 max.
Carotid-Vasomotor Baroreflex Response to Dynamic Exercise
The carotid-vasomotor baroreflex stimulus-response relationships of only four subjects were statistically analyzed because of an inability to model the baroreflex-function curves for each exercise bout performed by the other three subjects. Although rhythmic variation in MAP recordings, due to the effect of the movement of the exercising leg on the intravascular catheter, can hinder modeling of carotid-vasomotor stimulus-response curves, a primary difficulty in the present investigation lay in obtaining reliable threshold values for these curves. This would imply that stronger or more prolonged neck pressure stimuli may have been required to achieve maximal reflex vasomotor responses during these exercise types and intensities. However, Papelier et al. (13) also demonstrated a steepening of the lefthand portion of the carotid-vasomotor baroreflex (and not the carotid-cardiac baroreflex) during postexercise leg muscle ischemia induced by thigh cuff inflation. This alteration was attributed by the authors to an activation of the muscle chemoreflex, which 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 (11, 13, 19). Therefore, the inability to model the baroreflex stimulus-response relationship during certain bouts of exercise may also be attributable to chemoreflex activation.No significant differences were seen in the carotid-vasomotor
baroreflex maximal gain, or sensitivity, at any exercise intensity. However, significant lateral and vertical shifts (i.e., the
y-axis coordinate or MAP response to
the corresponding threshold or saturation pressure value) were seen in
the location of the threshold and saturation of the carotid-vasomotor
baroreflex with increases in exercise intensity, with the exception of
vertical shifts from rest to 50% L exercise (Table
4). These shifts occurred regardless of the
type of exercise being performed, i.e., L or combined L + A exercise.
Interestingly, the threshold, saturation, and corresponding y-axis response values for 75% L + A
were observed to be greater than the values for 75% L for each
subject. However, due to the small numbers of subjects and measurement
variance, this observation did not result in any statistically
significant differences.
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The position of the operating point of the carotid-vasomotor baroreflex
during the resting condition was 79.9 ± 7.8 mmHg, and during the
four exercise bouts (50% L, 75% L + A, 75% L, and maximal exercise),
the positions were 90.1 ± 5.2, 104.5 ± 5.0, 107.5 ± 4.9, and 111.3 ± 3.2 mmHg, respectively. In addition, the operating
point of the carotid-vasomotor baroreflex was significantly shifted
away from the centering point and toward the threshold of the reflex
with progressive increases in exercise workload in a manner similar to
that reported for the carotid-cardiac baroreflex (Tables 3 and 4). No
significant difference was found between the position of the operating
points relative to the centering points of the L only and combined L + A exercise bouts at 75% O2 max.
Because the data from only four subjects of the total seven subjects were analyzed so that a one-way repeated-measures ANOVA could be used across all conditions for each subject, the attainment of statistical significance indicated the strength of the data of this investigation.
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DISCUSSION |
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TOP
ABSTRACT
INTRODUCTION
METHODS AND PROCEDURES
RESULTS
DISCUSSION
REFERENCES
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The findings of the present investigation support our hypothesis that
the CBR stimulus-response relationship was classically reset upward and
rightward in relation to increases in work intensity. This conclusion
supports the investigations of Melcher and Donald (8) in the dog model,
as well as those of Potts et al. (17) and Papelier et al. (12) in the
exercising human. Each of those investigations also demonstrated a
reset, but functional and equally sensitive, baroreflex during exercise
compared with during the resting condition. However, the present
investigation further demonstrates that this phenomenon occurs over a
wide range of exercise intensities, up through exercise at
O2 max [vs. the submaximal exercise workloads of 50%
O2 max and ~75%
O2 max utilized in the
investigations of Potts et al. (17) and Papelier et al. (12),
respectively]. In addition, the data of the present investigation
extend the findings of Potts et al. (17), in that the relocation of
the operating point (the prestimulus MAP) away from the
centering point (point of maximal gain) and toward the threshold of the
reflex occurred, in relation to exercise intensity, through
exercise intensities up to
O2 max.
Physiologically, the relocation of the operating point toward
threshold provides a greater range of response to hypertensive events
stimulated by the activation of the exercise pressor reflex, as
suggested by the work of Sheriff et al. (23).
From recent investigations, the concept has arisen of a complex
interaction between central command and the reflexes initiated by the
stimulation of chemically and mechanically sensitive receptors in the
exercising muscles. Iellamo et al. (6) have identified the unique
effects of the stimulation of each of these muscle receptors on
baroreflex control of HR. Additionally, Potts and Li (16) have
demonstrated that, in anesthetized dogs, the effect of the stimulation
of fibers that carry afferent signals from skeletal muscle may depend
on the basal level of baroreceptor activity. However, the relative
effects of central command and the exercise-pressor reflex on CBR
resetting during dynamic exercise remain unclear. Rowell and O'Leary
(20) have postulated that central command activation produces a
rightward lateral shift in the CBR stimulus-response relationship
through an interaction at the level of the neuron pool that receives
the baroreflex afferents, such that the reflex operates around the
exercise-induced increase in blood pressure. In addition, they proposed
that activation of the exercise-pressor reflex would produce an upward
vertical shift in the CBR stimulus-response relationship due to
increased sympathetic activation (20). However, although A exercise is known to elicit higher lactate accumulations (14), HR (14, 15), and
ratings of perceived exertion (15) than L exercise at the same absolute
O2, the potential for a
disproportionate activation of the muscle metaboreflex in conjunction
with a heightened central command activation did not result in
significant differences in the resetting of the CBR during L and
combined L + A exercise.
Exercise Intensity
DiCarlo and Bishop (1) have examined the time course of the resetting of the arterial baroreflex in exercising rabbits. These researchers have demonstrated an immediate resetting of the reflex, at the onset of exercise, which persists when the exercise pressure response is attenuated by intravenous infusion of nitroglycerin. These data suggest that central command may mediate resetting of the operating point of the arterial baroreflex toward higher pressures, thus contributing to the characteristic sympathoexcitatory response elicited at the onset of exercise. Their investigation also demonstrated that an intact arterial baroreflex was required for the sympathoexcitatory response to exercise to be expressed, because it was absent in sinoaortic-denervated rabbits (1). Additionally, Ebert (2) has shown that the anticipation of static exercise in humans results in an alteration in carotid-cardiac and carotid-vasomotor responses to neck pressure and neck suction stimuli. These findings support the role of a quicker acting, feed-forward type of mechanism, such as "central command," as the primary mechanism responsible for the resetting of the CBR during dynamic exercise. In the present investigation, as in the investigations of Potts et al. (17), Papelier et al. (12), and Melcher and Donald (8), baroreflex resetting occurred in direct relation to increases in exercise intensity, which in turn is related to increases in central command activation, with the recruitment of greater numbers of motor fiber units to perform the higher intensity of exercise.A + L Exercise
In the present investigation, the addition of A exercise to L exercise presented a complex physiological picture. Not only does arm work elicit different chemical, thermal, and perceptive responses to exercise than does leg work (14, 15), the additional muscle mass must receive an adequate proportion of cardiac output to sustain the exercise (21). The question of how cardiac output is distributed to exercising muscle during high-intensity dynamic exercise was raised by Secher et al. in 1977 (22). These investigators found that the addition of arm-cranking exercise to leg-cycling exercise resulted in an increase in HR andO2
without a concomitant increase in MAP or pulse pressure. However, leg
vascular conductance was decreased during the addition of arm exercise.
Therefore, for a maintenance of a relatively similar MAP between the
two exercise bouts, arm vasodilation and leg vasoconstriction must have
been balanced, in conjunction with the observed modest rise in cardiac
output. The question of the origin of the signal that elicited the
increased leg vascular resistance in the face of the increased exercise
workload can possibly be explained by our reflex-resetting model. An
augmented central command activation with increased active muscle mass
(addition of arm-cranking exercise to leg-cycling exercise, i.e.,
increased numbers of active muscle fibers) will result in an upward and
rightward shift in the CBR stimulus-response curve. If, after a
transient rise, MAP returned to a value similar to that observed during
leg exercise alone, as in the investigation of Secher et al. (22), the
MAP would then lie nearer to the threshold of the reset baroreflex
function curve, which would be perceived as a hypotensive stimuli and
would result in an activation of the efferent sympathetic limb of the autonomic nervous system and produce a reduced vascular conductance in
the leg musculature.
Potential Limitations
In the present investigation, we used brief, external carotid sinus stimuli to construct open-loop, stimulus-response relationships for the CBR during moderate to maximal intensities of exercise. These 5-s stimuli produced rapid reflex HR and MAP responses. Although these responses may not represent the full expression of baroreflex responsiveness to a longer stimuli, the maximal HR and MAP response to each stimulus were used to construct repeatable (10) reflex stimulus-response relationships which were then modeled by using the logistic function, described by Kent et al. (7), that we have used in our laboratory in previous investigations (17). The brevity of the carotid-sinus stimuli facilitated the minimalization of the influence of the extracarotid baroreceptors, such that the reflex responses recorded during and immediately after the stimuli were attributed to the noninvasively isolated carotid arterial baroreflex. In addition, the reflex responses in HR in relation to the carotid sinus stimuli have been termed the carotid-cardiac baroreflex, whereas the reflex responses in MAP in relation to these stimuli have been termed the carotid-vasomotor baroreflex. We have used this terminology because, due to the brevity of the carotid sinus stimuli, we have assumed that the reflex alterations in blood pressure would be primarily caused by reflex-induced changes in peripheral vascular resistance. Raven et al. (18) have demonstrated that, during the 5-s stimuli, the resultant change in HR affects cardiac output, and thus MAP, in the face of a constant stroke volume. However, after the stimulus, the MAP response persists, despite a return of HR to baseline. This indicates that peripheral vascular resistance, not cardiac output, primarily affected the peak MAP response that occurs after the termination of the stimuli. This interpretation reflects the latency of response of the sympathetic nervous system, which achieves 50-80% of complete sympathetic effector response within 5 s (26).The results of this investigation are similar to those of Potts et al.
(17) and Papelier et al. (12) in that the baroreflex was reset at the
onset of exercise in relation to exercise intensity. However, the
present investigation extends these findings to maximal exercise. In
addition, a disparity exists between the results of Papelier et al. and
those of the present investigation. This disparity may be related to
the experimental techniques used in each study. Papelier et al. used
longer carotid sinus perturbations (20 s) to elicit reflex
stimulus-response relationships in humans during exercise at
intensities up to ~75%
O2 max. They found no
alteration in the relationship of the operating point to the reflex
responses to positive and negative pressure stimuli. Also, Papelier et
al. used a NP-NS protocol wherein the operating pressure was fixed at
zero neck pressure and the carotid sinus stimuli were equally
distributed around the operating point pressure. In addition, because
no modeling of the stimulus-response relationship was utilized, it is
not possible to calculate whether the operating point had moved in
relation to the reflex centering point or threshold, regardless of its
location relative to the reflex responses to the carotid sinus stimuli.
In other words, although the operating point may have remained at the
same location relative to a stimulus response, the response value
itself may have been closer to or at the threshold of the reflex as
exercise intensity increased, thus resulting in the operating point
being relocated in relation to the threshold as well.
In contrast, we plotted the operating pressure within the modeled curves and clearly demonstrate its relocation within the reset baroreflex-function curve. We suggest that our random-order presentation of short carotid sinus stimuli allowed us to model the baroreflex function curves and thereby demonstrate the relocation of the operating point toward the threshold of the reset baroreflex. The data of the present study clearly indicate that the operating point progressively relocates toward the threshold pressure and away from the centering point of the reflex-function curve in direct relation to the intensity of exercise (Tables 3 and 4). We propose that, as parasympathetic activity gradually decreases with increasing workload, further tachycardia via this mechanism becomes limited as the workload increases toward maximum (17). The identification of the shift in the operating point toward threshold with increasing vagal withdrawal suggests that this may be mediated by increasing central command. It should be noted that a discrepancy existed between the operating point pressures established for the carotid-cardiac and carotid-vasomotor baroreflexes at rest and during each exercise intensity. These differences are attributable to a limitation in the technique employed, wherein different stimulus-response sets may have been used to quantify HR from those utilized to establish MAP, because each stimulus does not always produce a valid HR and MAP response. Due to the moment-to-moment alterations in arterial blood pressure inherent in the pulsatile nature of the system, it is likely that the discrepancy arose because the prestimulus pressure was established at different time points. Regardless of the limitations in the methodology used, it is clear that the operating point relocated progressively closer to the threshold and farther from the centering point as the intensity of the exercise increased.
In conclusion, the results of this investigation support the concept of continued regulation of arterial blood pressure by the CBR during exercise. The carotid-cardiac and carotid-vasomotor reflexes were reset upward and rightward in direct relation to the intensity of exercise, with a concomitant shift of the reflex operating point away from the centering point and toward the threshold of the reflex (Tables 3 and 4). This resetting positions the reflex to respond to changes in systemic arterial pressure from the prevailing pressure of the steady-state dynamic exercise, with a particular augmentation in the range of response to hypertension.
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ACKNOWLEDGEMENTS |
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The authors thank the subjects for their interest and cooperation. In addition, we thank Inge Holm for coordination of K. Norton's stay in Copenhagen 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 NGT-70409, NASA Specialized Center of Research and Training Grant NAGW-3582, and NASA Grant NAG5-4668; by the American College of Sports Medicine NASA Space Physiology Student Research Award; by the Danish National Research Scholarship; and by National Heart, Lung, and Blood Institute Grant HL-45547.
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 of Cardiovascular Science, Gerontology Research Center, NIA/NIH, 4940 Eastern Ave., Baltimore, MD 21224.
Address for reprint requests and other correspondence: P. B. Raven, University of North Texas Health Science Center, Dept. of Integrative Physiology, 3500 Camp Bowie Blvd. Fort Worth, TX 76107-2699.
Received 19 September 1997; accepted in final form 23 February 1999.
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REFERENCES |
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TOP
ABSTRACT
INTRODUCTION
METHODS AND PROCEDURES
RESULTS
DISCUSSION
REFERENCES
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