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Department of Autonomic Neuroscience, Research Institute of Environmental Medicine, Nagoya University, Nagoya 464 - 8601, Japan
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ABSTRACT |
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 TOP
 ABSTRACT
 INTRODUCTION
SUBJECTS AND METHODS
RESULTS
DISCUSSION
REFERENCES
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To examine effects of static exercise on the arterial baroreflex control of vascular sympathetic nerve activity, 22 healthy male volunteers performed 2 min of static handgrip exercise at 30% of maximal voluntary force, followed by postexercise circulatory arrest (PE-CA). Microneurographic recording of muscle sympathetic nerve activity (MSNA) was made with simultaneous recording of arterial pressure (Portapres). The relationship between MSNA and diastolic arterial pressure was calculated for each condition and was defined as the arterial baroreflex function. There was a close relationship between MSNA and diastolic arterial pressure in each subject at rest and during static exercise and PE-CA. The slope of the relationship significantly increased by >300% during static exercise (P < 0.001), and the x-axis intercept (diastolic arterial pressure level) increased by 13 mmHg during exercise (P < 0.001). These alterations in the baroreflex relationship were completely maintained during PE-CA. It is concluded that static handgrip exercise is associated with a resetting of the operating range and an increase in the reflex gain of the arterial barorelex control of MSNA.
arterial pressure; microneurography; muscle sympathetic nerve activity; pressor response
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INTRODUCTION |
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TOP
ABSTRACT
INTRODUCTION
SUBJECTS AND METHODS
RESULTS
DISCUSSION
REFERENCES
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ARTERIAL BAROREFLEXES are important mechanisms for the overall regulation of circulation (1, 5, 27). Under resting conditions, an increase in arterial pressure stimulates arterial baroreceptors and decreases the heart rate and the peripheral vascular resistance in resting skeletal muscles. Handgrip exercise induces an increase in arterial pressure, and although the increase in pressure should stimulate the arterial baroreceptors, it is accompanied by increases in heart rate and peripheral vascular resistance in resting skeletal muscles. This phenomenon indicates that arterial baroreflex functions are modified during exercise and that this modification may include changes in the gain and/or operating range of the reflex (11, 12, 15, 18, 24, 25). There are a number of studies addressing changes in arterial baroreflex function during exercise. However, most of them have focused on the reflex control of heart rate (11, 12, 18, 21, 25) or arterial pressure (21, 25). In contrast, little is known about the effect of exercise on the arterial baroreflex control of vascular sympathetic nerve activity in humans.
A previous study (29) showed that partial pharmacological suppression of the exercise-induced increase in arterial pressure during static handgrip (nitroprusside infusion) augmented the exercise-induced increase in vascular sympathetic activity by >300%, while pharmacological accentuation of the exercise-induced increase in arterial pressure (phenylephrine infusion) attenuated the reflex increase in sympathetic activity by >50%. That study clearly indicated that the arterial baroreflex is effective in buffering the sympathetic activation induced by static muscle contraction. However, the detailed baroreflex relationship between vascular sympathetic activity and arterial pressure during static exercise remains unknown.
Accordingly, the purpose of this study was to examine the arterial baroreflex control of vascular sympathetic outflow during static handgrip exercise in humans. We performed microneurographic recording of vascular sympathetic nerve discharge to resting skeletal muscles (muscle sympathetic nerve activity; MSNA) in exercising volunteers and assessed the stimulus-response relation between diastolic arterial pressure and vascular sympathetic nerve activity during static exercise.
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SUBJECTS AND METHODS |
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TOP
ABSTRACT
INTRODUCTION
SUBJECTS AND METHODS
RESULTS
DISCUSSION
REFERENCES
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Subjects. After being informed of all procedures and risks, 22 healthy male volunteers with a mean age of 22 ± 2 (SE) yr, mean height of 171 ± 2 cm, and mean weight of 65 ± 2 kg gave written consent to serve as subjects for this investigation. All experimental procedures and protocols were approved by the Ethical Committee of the National Space Development Agency of Japan. All subjects were evaluated as being normally physically fit from a detailed medical history, physical examination, complete blood count, resting electrocardiogram, a panel of blood chemistry analyses, and a psychological test. No subjects were smokers, used recreational drugs, or had chronic medical problems. Each subject signed informed consent after a complete explanation of the testing procedures.
Measurements. MSNA was recorded by microneurography from the tibial nerve of the leg. An electrocardiogram was monitored from chest lead II, and respiration was measured with a thermistor. Finger arterial pressure was measured using a volume-clamp method (Portapres, TNO Institute of Applied Physics Biomedical Instrumentation) (35). Arterial pressure values were confirmed every minute by an automated upper arm sphygmomanometer (BP203MII, Nippon Colin, Komaki, Japan). The finger cuff of the Portapres was attached to two digits of the left hand at the height of the heart level and inflated alternately to prevent pain due to continuous air pressure load.
Microneurography.
A tungsten microelectrode with a shaft diameter of 120 µm and an
electrode impedance of 2-5 M
(model 26-05-1,
Frederick Haer, Bowdoinham, ME) was inserted percutaneously into the
muscle nerve fascicles of the tibial nerve at the popliteal fossa
without anesthesia. Nerve signals were fed into a high-input impedance
preamplifier (Kohno Instruments, Nagoya, Japan; input impedance 100 M; gain 40,000) with two active band pass filters set between 500 and 5,000 Hz and monitored with a loudspeaker. MSNA was identified according to the following discharge characteristics: 1)
pulse synchronous spontaneous efferent discharges, 2)
afferent activity evoked by tapping of the soleus muscle but not in
response to a gentle skin touch, and 3) enhancement during
phase II of Valsalva's maneuver.
Experimental protocol. The subjects lay in the supine position. Each subject performed two brief (<5 s) maximal contractions using a handgrip dynamometer (Digital Grip Dynamometer, Takei Kiki Kogyo, Japan), and the average of these two contractions was determined as the maximal voluntary contraction (MVC). After this MVC determination, the subjects were permitted to rest quietly in the supine position for over 30 min. At least 10 min after a satisfactory recording site for MSNA was obtained, preexercise baseline recordings of MSNA, finger arterial pressure, upper arm arterial pressure, and heart rate were performed for 2 min. Static handgrip exercise was performed at 30% of MVC with the dominant arm for 2 min. Subjects were breathing spontaneously throughout experimental periods, but they were required not to breathe deeply, hold their breath, or do Valsalva maneuvers. Furthermore, subjects were prohibited from contracting other limbs. The absolute force output from a handgrip dynamometer was displayed to the subjects on an oscilloscope with the target force.
Next, postexercise circulatory arrest (PE-CA) was done to estimate the effect of muscle metaboreflex (14, 26, 34). PE-CA was performed for 2 min as follows: 5 s before the release of isometric handgrip, the upper arm cuff was inflated to suprasystolic arterial pressure (>230 mmHg), and the subjects then released their grip. After PE-CA, the upper arm cuff was deflated, and 2 min of recovery recording was done. MSNA, electrocardiogram, and finger arterial pressure were continuously recorded during preexercise rest, handgrip, PE-CA, and recovery and stored on a DAT recorder (PC-216Ax, Sony Magnescale, Japan).Data analysis. MSNA was full-wave rectified and fed through a resistance-capacitance integrating circuit with a time constant of 0.1 s to obtain the mean voltage neurogram, which was displayed along with the electrocardiograms, arterial pressure, and respiration on a pen recorder (RECTI-HORIZ, NEC San-Ei, Tokyo, Japan). MSNA was expressed as 1) MSNA burst rate, i.e., the mean number of sympathetic bursts per minute; 2) MSNA burst amplitude; and 3) total MSNA, i.e., the sum of the MSNA burst amplitudes of all bursts for each analyzed period per minute. To calculate the MSNA burst amplitude in the mean voltage neurogram, all burst amplitudes were measured using a paper sheet. The mean MSNA burst amplitude during 2 min of preexercise rest was given the arbitrary value of 100 (arbitrary units), and all other MSNA burst amplitudes during handgrip, PE-CA, and recovery were expressed in relation to this value. The beat-to-beat data for R-R interval and systolic and diastolic arterial pressure were obtained by detecting R-wave peaks and identifying peaks and troughs on the arterial pressure wave, respectively. The analyzed periods included preexercise rest (2 min) and the last minute of each exercise, PE-CA, and recovery.
Arterial baroreflex control of MSNA. As described in previous reports (6-8, 16, 32), the baroreflex relationship between MSNA and diastolic arterial pressure was determined from spontaneous changes in diastolic arterial pressure to changes in MSNA for each subject. Beat-by-beat values for MSNA burst amplitudes (arbitrary units) were averaged over 2-mmHg diastolic arterial pressure ranges, and a weighted linear regression between MSNA burst amplitude and diastolic pressure was performed. The relationship was defined as the arterial baroreflex contol of MSNA.
Statistical analysis. A one-way repeated-measures analysis of variance (preexercise rest, exercise, PE-CA, and recovery) was performed. Tests for simple effects were done with Scheffé's F procedure when the main effect was found to be significant. The baroreflex relation between sympathetic activity and diastolic arterial pressure was determined by least-squares linear regression analysis with repeated measures. To determine baroreflex regressions, the statistical criteria for a significant correlation were that the correlation coefficient r was >0.70 with P < 0.05 by Fisher's r to z (P value). Data are expressed as means ± SE. A P < 0.05 level of difference was considered significant.
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RESULTS |
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TOP
ABSTRACT
INTRODUCTION
SUBJECTS AND METHODS
RESULTS
DISCUSSION
REFERENCES
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Static handgrip and PE-CA.
Figure 1 shows representative data from
one subject during static handgrip exercise and PE-CA. Table
1 shows sympathetic and cardiovascular
responses from all subjects. MSNA gradually and progressively increased
during static handgrip exercise (P < 0.0001) and
remained elevated above baseline during PE-CA (P < 0.0001). Heart rate increased during exercise and returned to the
baseline during PE-CA. Systolic and diastolic arterial pressure increased during exercise and remained at higher levels above baseline
during PE-CA. Breathing frequency did not change during exercise and
PE-CA.
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Arterial baroreflex control of MSNA.
The relationship between MSNA and diastolic arterial pressure derived
from the data in Fig. 1 is shown in Fig.
2. A significant negative correlation was
observed between them in each condition, and this relationship was used
to assess the arterial baroreflex control of MSNA. Similarly to the
subject represented in Figs. 1 and 2, a significantly negative
correlation between MSNA and diastolic arterial pressure was observed
in each subject. The mean r (correlation coefficient) of
individual regressions was 0.82 ± 0.02 at rest, 0.89 ± 0.03 during handgrip exercise, 0.91 ± 0.02 during PE-CA, and 0.87 ± 0.02 during recovery. The mean slope of the relationship from all
subjects was 3.2 ± 0.5 arbitrary units/mmHg at rest, and this
significantly increased by >300% during static handgrip exercise
(12.1 ± 2.1 arbitrary units/mmHg, P < 0.001)
(Fig. 3). Moreover, the mean slope
remained elevated during PE-CA (12.9 ± 2.7 arbitrary units/mmHg,
P < 0.001) and then returned to baseline during
recovery (Fig. 3). The mean x-axis intercept (threshold
diastolic pressure) of the relationship from all subjects was 77.1 ± 1.4 mmHg at rest, and this significantly increased by 13 mmHg during
static exercise (89.6 ± 1.9 mmHg, P < 0.001)
(Fig. 3). The increase in the mean intercept was maintained during
PE-CA (89.6 ± 2.4 mmHg, P < 0.001), and the
intercept returned to baseline during recovery (Fig. 3).
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DISCUSSION |
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TOP
ABSTRACT
INTRODUCTION
SUBJECTS AND METHODS
RESULTS
DISCUSSION
REFERENCES
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Sympathetic vascular contraction plays an important role in regulating the circulation during exercise (5, 27), but little is known about the arterial baroreflex control of vascular sympathetic outflow during static exercise in humans. The present study for the first time examined the arterial baroreceptor-MSNA stimulus-response relationship during static exercise in humans and showed that the operating range of the arterial baroreflex shifted to a higher pressure (resetting) and that the gain was markedly increased during static exercise.
The results from this study are in general agreement with previous studies that showed resetting of the arterial baroreflex during exercise in animals (3, 24, 33) and humans (12, 25). Walgenbach and Donald (33) first reported that when a sensory input from carotid baroreceptor (carotid sinus pressure) was held constant, exercise-induced increases in heart rate and arterial blood pressure were augmented compared with when carotid sinus pressure was allowed to follow the changes in arterial blood pressure in dogs. This finding was thought to show that the arterial baroreflex was reset to a higher operating pressure range during exercise. This concept was supported by a study from DiCarlo and Bishop (3) showing that partial suppression of exercise-induced increase in blood pressure augmented the reflex increases in renal sympathetic nerve activity and heart rate in rabbits. Recently, Potts et al. (25) and Iellamo et al. (11, 12) assessed the stimulus-response relationship of the carotid baroreflex during exercise in humans and reported that the baroreflex relationship is reset to a higher operating pressure range when reflex responses are determined by heart rate and mean arterial pressure. Moreover, Martinez-Nieves et al. (15) found a similar exercise-induced resetting of the baroreflex control of hindlimb vascular conductance in hypertensive rats. The present study confirms these previous findings and adds new information to our understanding of the neural mechanism during exercise: static exercise causes resetting of the arterial baroreflex control of vascular sympathetic outflow in humans.
The data from this study clearly demonstrate that the gain in the
arterial baroreflex control of vascular sympathetic outflow was greatly
increased by >300% during static exercise. The increase in the gain
is consistent with a previous report by Scherrer et al.
(29). They showed that the sympathetic excitation caused by static handgrip during infusion of nitroprusside was more than two
times greater than the simple algebraic sum of the excitation caused by
handgrip alone or that caused by infusion of nitroprusside alone. Their
finding may in part be explained by the baroreflex relationship with a
steeper slope during exercise observed in this study, because a reflex
increase in MSNA caused by a certain magnitude of hypotension will be
more on a regression line during exercise compared with at rest (Fig.
2). The increased gain of the arterial baroreflex control of vascular
sympathetic outflow, however, stands in contrast to previous reports in
humans that showed no change (25), or a decrease
(21), in the gain of the carotid baroreceptor-systemic
arterial pressure relationship during exercise. Moreover, a recent
study in rats showed that a spontaneous baroreflex gain in hindlimb
vascular conductance was unchanged, or partially attenuated, during
exercise (15). This discrepancy may be due to a difference
in the experimental approaches that determined the reflex outflow in
this (vascular sympathetic nerve activity) and previous studies
(systemic arterial pressure and vascular conductance). Because several
studies have demonstrated that 
-adrenergic receptor-mediated
vasoconstrictor responsiveness is attenuated during exercise (2,
4, 9, 10), the decreased constrictor response of vessels can
mask the augmented ability of a reflex sympathetic response, resulting in no change or an attenuation, rather than an increase, in the total
baroreflex gain involving vascular responses.
The mechanism responsible for the modification of arterial baroreflex control of vascular sympathetic nerve activity during static handgrip exercise was not completely understood in this study. However, the muscle metaboreflex (28) may contribute to the altered baroreflex response. This is based on the finding that during PE-CA, in which chemosensitive muscle afferents are stimulated and the muscle metaboreflex is activated while the muscle mechanoreflex and central command are inoperative (14, 26, 34), exercise-induced modification (including a resetting and an increase in the gain) of the arterial baroreflex was entirely maintained. This finding confirms the concept of a reflex interaction between the muscle reflex and the arterial baroreflex (11, 23). This concept is supported by neurophysiological and electrophysiological evidence showing that afferent fibers from arterial baroreceptor and skeletal muscle receptor synapse in discrete regions of the medulla that are related to cardiovascular regulation, including the nucleus tractus solitarii (13, 17, 20, 22). Therefore, we suggest that some of the modification of the arterial baroreflex during static exercise was caused by the muscle metaboreflex.
There are lots of studies addressing the exercise-induced alteration in arterial baroreflex function, but most (3, 12, 21, 23-25, 33) involved isotonic or isokinetic exercise (e.g., dynamic) rather than isometric (e.g., static) exercise. In contrast, we examined the effect of static exercise on baroreflex function in the present study. It is possible that different mechanisms are involved in altering baroreflex control of vascular sympathetic nerve activity during static vs. dynamic exercise. Further investigations are necessary to clarify this point.
Limitation. We used a nonperturbational spontaneous method to assess the arterial baroreflex function. Compared with perturbational methods, the nonperturbational spontaneous method has several limitations. The nonperturbational spontaneous method assesses a limited range of pressure for the stimulus-response barorelex relationship, while the perturbational methods allow the examination of a prevailing range of pressure. Furthermore, the nonperturbational baroreflex determination might be more affected by spontaneous changes in central venous pressure and respiratory gating compared with perturbational methods.
Conversely, the perturbational methods also have several limitations. Pharmacological agents and extensive surgical procedures may have indirect effects on, and somewhat modify, experimental results. Moreover, perturbational methods in which arterial pressure is greatly changed may produce nonphysiological artifacts. Therefore, there is no perfect methodology for evaluating the arterial barorelex function (15). We examined a limited range of arterial pressure-to-baroreflex relationships. However, this is a physiological range of pressure. Under physiological conditions, the arterial baroreflex functions within this narrow range, and the baroreceptor-MSNA stimulus-response relationship is linear (32). In addition, although we cannot exclude a possible influence of the cardiopulmonary baroreflex on the sympathetic response, it is thought that the cardiopulmonary baroreflex has little role in the control of MSNA during static handgrip exercise in humans (30, 31). Furthermore, the breathing frequency was held constant during exercise and PE-CA in this study, suggesting that respiration exerted less influence on the alteration of the baroreflex function. In conclusion, the arterial baroreflex control of vascular sympathetic nerve activity was greatly modified during static handgrip exercise in humans: the baroreceptor-vascular sympathetic response relationship was rightward shifted to a higher pressure, and the gain in the reflex was markedly increased. In addition, the muscle metaboreflex appears to be involved in this modification.Perspectives
Potts and Li (23) recently suggested the concept that modification of the baroreflex during exercise plays two functional roles: 1) to buffer the degree of sympathoexcitation evoked by the exercise pressor reflex, and 2) to increase sympathoexcitation at the onset of exercise to minimize the fall in arterial blood pressure. The baroreceptor-MSNA stimulus-response relationship during static handgrip exercise observed in this study confirms and partially explains this concept because 1) the negative relationship between MSNA and arterial pressure was entirely preserved with a steeper slope during static exercise, and 2) across all diastolic arterial pressures the MSNA was higher during static exercise. Therefore, it is likely that the modification of the arterial baroreflex is a powerful modulator of sympathoexcitation during exercise (23), having both buffering and excitatory effects on the sympathetic neural activity. The buffering effect is consistent with the results from Scherrer et al. (30) and DiCarlo et al. (3), showing that partial pharmacological suppression/elevation of the exercise-induced rise in arterial pressure augmented/attenuated the reflex sympathetic activation, respectively. The buffering effect may in part be related to data from Potts and Li (23), showing that when carotid sinus pressure was higher, the reflex increase in systemic arterial pressure during muscle contraction was lower, and vice versa. Furthermore, the excitatory effect may be in agreement with the study from Melcher and Donald (19), showing that when no baroreceptor systems were able to participate in the regulation of circulation, the systemic arterial pressure greatly dropped during exercise in dogs.| |
ACKNOWLEDGEMENTS |
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This study was carried out as a part of "Ground Research Announcement for Space Utilization" promoted by the Japan Space Forum. It was supported partly by Grant-in-Aid for Scientific Research 11470017 from the Ministry of Education, Science, Sport, and Culture of Japan and by Research Grant for Cardiovascular Diseases 9C-1 from the Ministry of Health and Welfare of Japan.
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FOOTNOTES |
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Address for reprint requests and other correspondence: A. Kamiya, Dept. of Autonomic Neuroscience, Research Institute of Environmental Medicine, Nagoya Univ., Furo-cho, Chikusa-ku, Nagoya 464-8601, Japan (E-mail: akamiya{at}riem.nagoya-u.ac.jp).
The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
Received 8 February 2001; accepted in final form 4 June 2001.
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REFERENCES |
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TOP
ABSTRACT
INTRODUCTION
SUBJECTS AND METHODS
RESULTS
DISCUSSION
REFERENCES
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1.
Bevergard, BS,
and
Shepherd JT.
Circulatory effects of stimulating the carotid arterial stretch receptors in man at rest and during exercise.
J Clin Invest
45:
132-142,
1966.
2.
Buckwalter, JB,
Mueller PJ,
and
Clifford PS.
1-Adrenergic-receptor responsiveness in skeletal muscle during dynamic exercise.
J Appl Physiol
85:
2277-2283,
1998
3.
DiCarlo, SE,
and
Bishop VS.
Onset of exercise shifts operating point of arterial baroreflex to higher pressures.
Am J Physiol Heart Circ Physiol
262:
H302-H307,
1992.
4.
DiCarlo, SE,
Collins HL,
Howard MG,
Chen CY,
Scislo TJ,
and
Patil RD.
Postexertional hypotension: a brief review.
Sports Med
5:
17-27,
1994.
5.
Eckberg, DL,
and
Sleight P.
Human Baroreflexes in Health and Disease. New York: Oxford Univ Press, 1992, p. 3-299.
6.
Fagius, J,
and
Berne C.
Rapid resetting of human baroreflex working range: insights from sympathetic recordings during acute hypoglycaemia.
J Physiol (Lond)
442:
91-101,
1991
7.
Kamiya, A,
Iwase S,
Kitazawa H,
Mano T,
Vinogradova OL,
and
Kharchenko IB.
Baroreflex control of muscle sympathetic nerve activity after 120 days of 6° head-down bed rest.
Am J Physiol Regulatory Integrative Comp Physiol
278:
R445-R452,
2000
8.
Halliwill, JR,
Taylor JA,
and
Eckberg DL.
Impaired sympathetic vascular regulation in humans after acute dynamic exercise.
J Physiol (Lond)
495:
279-288,
1996
9.
Howard, MG,
and
DiCarlo SE.
Reduced vascular responsiveness after a single bout of dynamic exercise in the conscious rabbit.
J Appl Physiol
73:
2662-2667,
1992
10.
Howard, MG,
DiCarlo SE,
and
Stallone JN.
Acute exercise attenuates phenylephrine-induced contraction of rabbit isolated aortic rings.
Med Sci Sports Exerc
24:
1102-1107,
1992[Web of Science][Medline].
11.
Iellamo, F,
Hughson RL,
Castrucci F,
Legramante JM,
Raimondi G,
Peruzzi G,
and
Tallarida G.
Evaluation of spontaneous baroreflex modulation of sinus node during isometric exercise in healthy humans.
Am J Physiol Heart Circ Physiol
267:
H994-H1101,
1994
12.
Iellamo, F,
Legramante JM,
Raimondi G,
and
Peruzzi G.
Baroreflex control of sinus node during dynamic exercise in humans: effects of central command and muscle reflexes.
Am J Physiol Heart Circ Physiol
272:
H1157-H1164,
1997
13.
Kalia, M,
Mei SS,
and
Kao FF.
Central projections from ergoreceptors (C fibers) in muscle involved in cardiopulmonary responses to static exercise.
Circ Res
48, Suppl I:
I-48-I-62,
1981.
14.
Mark, AL,
Victor RG,
Nerhed C,
and
Wallin BG.
Microneurographic studies of the mechanisms of sympathetic nerve responses to static exercise in humans.
Circ Res
57:
461-469,
1985
15.
Martinez-Nieves, B,
Collins HL,
and
DiCarlo SE.
Arterial baroreflex regulation of regional vascular conductance at rest and during exercise.
Am J Physiol Regulatory Integrative Comp Physiol
278:
R1634-R1642,
2000
16.
Matsukawa, T,
Sugiyama Y,
Watanabe T,
Kobayashi F,
and
Mano T.
Baroreflex control of muscle sympathetic nerve activity is attenuated in the elderly.
J Auton Nerv Syst
73:
182-185,
1998[Web of Science][Medline].
17.
McMahon, SE,
McWilliam PN,
Robertson J,
and
Kaye JC.
Inhibition of carotid sinus baroreceptor neurons in the nucleus tractus solitarius of the anaesthetized cat by electrical stimulation of hindlimb afferent fibers (Abstract).
J Physiol (Lond)
452:
224P,
1992.
18.
McWilliam, PN,
Yang T,
and
Chen LX.
Changes in the baroreceptor reflex at the start of muscle contraction in the decerebrate cat.
J Physiol (Lond)
436:
549-558,
1991
19.
Melcher, A,
and
Donald DE.
Maintained ability of carotid baroreflex to regulate arterial pressure during exercise.
Am J Physiol Heart Circ Physiol
241:
H838-H849,
1981
20.
Nyberg, G,
and
Bromqvist A.
The central projection of muscle afferent fibers to the lower medulla and upper spinal cord: an anatomical study in the cat with the transganglionic transport method.
J Comp Neurol
230:
99-109,
1984[Web of Science][Medline].
21.
Papelier, Y,
Escourrou P,
Gauthier JP,
and
Rowell LB.
Carotid baroreflex control of blood pressure and heart rate in men during dynamic exercise.
J Appl Physiol
77:
502-506,
1994
22.
Person, RJ.
Somatic and vagal afferent convergence on solitary tract neurons in cat: electrophysiological characteristics.
Neuroscience
30:
283-295,
1989[Web of Science][Medline].
23.
Potts, JT,
and
Li J.
Interaction between carotid baroreflex and exercise pressor reflex depends on baroreflex afferent input.
Am J Physiol Heart Circ Physiol
274:
H1841-H1847,
1998
24.
Potts, JT,
and
Mitchell JH.
Rapid resetting of carotid baroreceptor reflex by afferent input from skeletal muscle receptors.
Am J Physiol Heart Circ Physiol
275:
H2000-H2008,
1998
25.
Potts, JT,
Shi XR,
and
Raven PB.
Carotid baroreflex responsiveness during dynamic exercise in humans.
Am J Physiol Heart Circ Physiol
265:
H1928-H1938,
1993
26.
Ray, CA,
Secher NH,
and
Mark AL.
Modulation of sympathetic nerve activity during posthandgrip muscle ischemia in humans.
Am J Physiol Heart Circ Physiol
266:
H79-H83,
1994
27.
Rowell, LB.
Human Cardiovascular Control. New York: Oxford Univ Press, 1993, p. 302-479.
28.
Rowell, LB,
and
O'Leary DS.
Reflex control of circulation during exercise: chemoreflexes and mechanoreflexes.
J Appl Physiol
69:
407-418,
1990
29.
Scherrer, U,
Pryor SL,
Bertocci LA,
and
Victor RG.
Arterial baroreflex buffering of sympathetic activation during exercise-induced elevation in arterial pressure.
J Clin Invest
86:
1855-1861,
1990.
30.
Scherrer, U,
Vissing SF,
and
Victor RG.
Effects of lower-body negative pressure on sympathetic responses to static exercise in humans. Microneurographic evidence against cardiac baroreflex modulation of the exercise pressor reflex.
Circulation
78:
49-59,
1988
31.
Seals, DR.
Cardiopulmonary baroreflexes do not modulate exercise-induced sympathoexcitation.
J Appl Physiol
64:
2197-2203,
1988
32.
Sundlöf, G,
and
Wallin BG.
Human muscle nerve sympathetic activity at rest. Relationship to blood pressure and age.
J Physiol (Lond)
274:
621-637,
1978
33.
Walgenbach, SC,
and
Donald DE.
Inhibition by carotid baroreflex of exercise-induced increases in arterial pressure.
Circ Res
52:
253-262,
1983
34.
Wallin, BG,
Victor RG,
and
Mark AL.
Sympathetic outflow to resting muscles during static handgrip and postcontraction muscle ischemia.
Am J Physiol Heart Circ Physiol
256:
H105-H110,
1989
35.
Wesseling, KH,
Jansen JRC,
Settels JJ,
and
Schreuder JJ.
Computation of aortic flow from pressure in humans using a nonlinear, three-element model.
J Appl Physiol
74:
2566-2573,
1993
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S. Ogoh, J. P. Fisher, P. B. Raven, and P. J. Fadel Arterial baroreflex control of muscle sympathetic nerve activity in the transition from rest to steady-state dynamic exercise in humans Am J Physiol Heart Circ Physiol, October 1, 2007; 293(4): H2202 - H2209. [Abstract] [Full Text] [PDF]
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M. Ichinose, S. Koga, N. Fujii, N. Kondo, and T. Nishiyasu Modulation of the spontaneous beat-to-beat fluctuations in peripheral vascular resistance during activation of muscle metaboreflex Am J Physiol Heart Circ Physiol, July 1, 2007; 293(1): H416 - H424. [Abstract] [Full Text] [PDF]
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 J. R. Padley, N. N. Kumar, Q. Li, T. B.V. Nguyen, P. M. Pilowsky, and A. K. Goodchild Central Command Regulation of Circulatory Function Mediated by Descending Pontine Cholinergic Inputs to Sympathoexcitatory Rostral Ventrolateral Medulla Neurons Circ. Res., February 2, 2007; 100(2): 284 - 291. [Abstract] [Full Text] [PDF]
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A. Houssiere, B. Najem, N. Cuylits, S. Cuypers, R. Naeije, and P. van de Borne Hyperoxia enhances metaboreflex sensitivity during static exercise in humans Am J Physiol Heart Circ Physiol, July 1, 2006; 291(1): H210 - H215. [Abstract] [Full Text] [PDF]
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M. Ichinose, M. Saito, N. Kondo, and T. Nishiyasu Time-dependent modulation of arterial baroreflex control of muscle sympathetic nerve activity during isometric exercise in humans Am J Physiol Heart Circ Physiol, April 1, 2006; 290(4): H1419 - H1426. [Abstract] [Full Text] [PDF]
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A. Kamiya, T. Kawada, K. Yamamoto, D. Michikami, H. Ariumi, T. Miyamoto, S. Shimizu, K. Uemura, T. Aiba, K. Sunagawa, et al. Dynamic and static baroreflex control of muscle sympathetic nerve activity (SNA) parallels that of renal and cardiac SNA during physiological change in pressure Am J Physiol Heart Circ Physiol, December 1, 2005; 289(6): H2641 - H2648. [Abstract] [Full Text] [PDF]
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M. Ichinose and T. Nishiyasu Muscle metaboreflex modulates the arterial baroreflex dynamic effects on peripheral vascular conductance in humans Am J Physiol Heart Circ Physiol, April 1, 2005; 288(4): H1532 - H1538. [Abstract] [Full Text] [PDF]
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M. Ichinose, M. Saito, T. Ogawa, K. Hayashi, N. Kondo, and T. Nishiyasu Modulation of control of muscle sympathetic nerve activity during orthostatic stress in humans Am J Physiol Heart Circ Physiol, November 1, 2004; 287(5): H2147 - H2153. [Abstract] [Full Text] [PDF]
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S. Nagura, T. Sakagami, A. Kakiichi, M. Yoshimoto, and K. Miki Acute shifts in baroreflex control of renal sympathetic nerve activity induced by REM sleep and grooming in rats J. Physiol., August 1, 2004; 558(3): 975 - 983. [Abstract] [Full Text] [PDF]
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K. Yamamoto, T. Kawada, A. Kamiya, H. Takaki, T. Miyamoto, M. Sugimachi, and K. Sunagawa Muscle mechanoreflex induces the pressor response by resetting the arterial baroreflex neural arc Am J Physiol Heart Circ Physiol, April 1, 2004; 286(4): H1382 - H1388. [Abstract] [Full Text] [PDF]
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M. Ichinose, M. Saito, H. Wada, A. Kitano, N. Kondo, and T. Nishiyasu Modulation of arterial baroreflex control of muscle sympathetic nerve activity by muscle metaboreflex in humans Am J Physiol Heart Circ Physiol, February 1, 2004; 286(2): H701 - H707. [Abstract] [Full Text] [PDF]
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 H. M. Stauss Heart rate variability Am J Physiol Regulatory Integrative Comp Physiol, November 1, 2003; 285(5): R927 - R931. [Full Text] [PDF]
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K. Miki, M. Yoshimoto, and M. Tanimizu Acute shifts of baroreflex control of renal sympathetic nerve activity induced by treadmill exercise in rats J. Physiol., April 1, 2003; 548(1): 313 - 322. [Abstract] [Full Text] [PDF]
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D. N. Mayorov and G. A. Head Glutamate receptors in RVLM modulate sympathetic baroreflex in conscious rabbits Am J Physiol Regulatory Integrative Comp Physiol, February 1, 2003; 284(2): R511 - R519. [Abstract] [Full Text] [PDF]
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H. M. Stauss Baroreceptor reflex function Am J Physiol Regulatory Integrative Comp Physiol, August 1, 2002; 283(2): R284 - R286. [Full Text] [PDF]
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J. Schnermann Exercise Am J Physiol Regulatory Integrative Comp Physiol, July 1, 2002; 283(1): R2 - R6. [Full Text] [PDF]
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V F Gladwell and J H Coote Heart rate at the onset of muscle contraction and during passive muscle stretch in humans: a role for mechanoreceptors J. Physiol., May 1, 2002; 540(3): 1095 - 1102. [Abstract] [Full Text] [PDF]
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5.3x + 380.1 (r = 0.98) at rest (solid line in A).
This equation at rest is shown as a broken line for handgrip exercise
(B), PE-CA (C), and recovery (D). The
linear equation was y = 