| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
Departments of Physiology and Internal Medicine, Wayne State University School of Medicine, and Veterans Affairs Medical Center, Detroit, Michigan 48201
 |
ABSTRACT |
|---|
Top
Abstract
Introduction
Methods
Results
Discussion
References
|
|---|
We investigated
the extent of functional parasympathetic and sympathetic activity to
the heart at rest and during mild to heavy dynamic exercise in
conscious dogs. The animals were chronically instrumented to monitor
mean arterial pressure (MAP), heart rate (HR), and terminal aortic
blood flow (TAQ) and trained to run on a motor-driven treadmill. MAP,
HR, and TAQ were monitored at rest and during steady-state dynamic
exercise ranging from mild [3.2 kilometers per hour (kph), 0%
grade] to heavy exercise (8 kph, 15% grade). Experiments were
performed before and after blocking the effects of either the
parasympathetic nerves (atropine 0.2 mg/kg iv) or sympathetic nerves
(atenolol 2.0 mg/kg iv) to the heart. In addition, blood samples were
taken at rest and at steady state during exercise, and plasma levels of
vasopressin and renin activity were assessed. At rest and during all
levels of exercise, muscarinic cholinergic receptor blockade caused a
marked increase in HR over control (saline treated) levels with little
effect on MAP or TAQ. 
-Adrenergic receptor blockade had no
significant effect on HR at rest and during mild exercise. At moderate
to heavy workloads, -receptor blockade significantly reduced MAP, HR, and TAQ and increased plasma vasopressin levels. We conclude that,
even during heavy dynamic exercise, significant functional parasympathetic tone to the heart exists. Thus, over a wide range of
exercise workloads, HR is under the tonic control of both sympathetic and parasympathetic nerves.
muscle blood flow; arterial blood pressure; sympathetic nervous system; parasympathetic nervous system; vasopressin; renin; oxygen consumption; autonomic nervous system
| |
INTRODUCTION |
|---|
|
Top
Abstract
Introduction
Methods
Results
Discussion
References
|
|---|
FROM REST to heavy dynamic exercise, heart rate (HR) in dogs increases from <100 to >250 beats/min (17, 21). HR at rest in dogs is under strong parasympathetic control with little if any tonic sympathetic activity, similar to that in aerobically conditioned humans (29, 31). The initial increase in HR with the transition from rest to mild exercise is thought to be due to rapid inhibition of the tonic parasympathetic tone, and as workload increases, sympathetic activity also rises to the heart and peripheral vasculature. Rowell and O'Leary (32) hypothesized that the ability to increase cardiac output via parasympathetic withdrawal during exercise may be of key importance in determining the level of sympathetic activity. For example, in sedentary animals such as laboratory rabbits or rats, the ability to increase cardiac output during even mild exercise via parasympathetic withdrawal may be limited. Recent studies by O'Hagan et al. (18) and DiCarlo et al. (4, 5) showed that sympathetic activity to the periphery increases even at the initiation of mild exercise in these species. In contrast, in species with greater cardiac performance and higher tonic parasympathetic tone (e.g., dogs, humans), Rowell (30, 31) and Rowell and O'Leary (32) suggested that sympathetic activity does not increase until all or nearly all parasympathetic restraint has been removed. However, recent investigations by O'Leary et al. (22, 23) and Sheriff et al. (34) indicate that, in dogs, sympathetic activity to the periphery is elevated at even relatively mild work rates in which substantial tonic parasympathetic tone to the heart probably still exists.
Thus the question remains whether sympathetic activity to the heart increases only when parasympathetic restraint is exhausted or whether during graded exercise sympathetic and parasympathetic activity progressively and concurrently waxes and wanes as workload increases. Therefore, in the present study, we examined the HR responses to graded exercise before and after blockade of the effects of parasympathetic or sympathetic nerves to the heart. Mean arterial pressure (MAP) and hindlimb blood flow were also measured, because changes in HR can also be elicited via changes in arterial pressure and muscle blood flow (20), both of which could be affected by cardiac autonomic blockade. We observed that the initial HR responses to mild exercise occur virtually solely via a reduction in parasympathetic tone to the heart. The effects of elevated sympathetic activity were observed at moderate-to-heavy work rates in which substantial parasympathetic tone to the heart still remains. A secondary aim of this study was to investigate the effects of workload on the release of renin and vasopressin, which, to our knowledge, have not been documented in this species over a wide range of workloads.
| |
METHODS |
|---|
|
Top
Abstract
Introduction
Methods
Results
Discussion
References
|
|---|
Experiments were performed on seven mongrel dogs of either sex (23-26 kg body wt) selected for their willingness to run on a motor-driven treadmill. All procedures were reviewed and approved by the Institutional Animal Investigation Committee and conformed to National Institutes of Health guidelines.
By use of aseptic procedures, an electromagnetic blood flow transducer was placed on the terminal aorta just proximal to the iliac arteries via a retroperitoneal approach in the left flank to monitor hindlimb blood flow. A catheter was inserted into the aorta above the flow probe via a side branch to monitor MAP. A vascular occluder was implanted just distal to the flow probe to ascertain the voltage output from the flow probe during complete vascular occlusion. In a second procedure performed 1 wk later, catheters were also placed in side branches of the femoral artery and vein and terminated in the abdominal aorta below the flow probe and in the abdominal vena cava, respectively. These catheters were used to collect arterial and venous blood samples and for drug infusion (venous). For all surgical procedures, as the animals recovered from the anesthetic, buprenorphine (0.015 mg/kg iv) and acepromazine (0.1 mg/kg im) were administered for analgesia and sedation, respectively. The animals were treated with cefazolin (500 mg iv) immediately pre- and postoperatively and with cephalexin (30 mg/kg po tid) for 1 wk postoperatively. The animals were allowed at least 1 wk for recovery.
Experimental protocol. All experiments were performed after the animals had completely recovered from the surgery and were afebrile, active, and of good appetite. The animal was brought to the laboratory and placed on the treadmill. The arterial catheter was connected to a pressure transducer (Spectromed 10 EZ) to monitor MAP, and the flow probe was connected to a blood flowmeter (Zepeda model 5SWF) to monitor terminal aortic blood flow (TAQ). Terminal aortic vascular conductance (TAC) was calculated as TAQ/MAP. HR was determined by a cardiotachometer triggered by the pulsatile output of the flowmeter. All variables were recorded on a Physiograph (Gould 3800), and beat-by-beat mean values were calculated by use of a laboratory computer and saved on hard disk for subsequent analysis.
Before each experiment (conducted on separate days), each animal was treated with saline as a vehicle control, the muscarinic cholinergic receptor antagonist atropine (0.2 mg/kg iv), or the-adrenergic
antagonist atenolol (2.0 mg/kg iv). The efficacy of the doses for each
drug was determined in preliminary experiments. Atropine at this dose
virtually completely blocked the nearly instantaneous bradycardia in
response to a rapid increase in MAP via bolus phenylephrine infusion
and atenolol at this dose markedly attenuated (~90%) the tachycardia
induced by isoproterenol infusion. Steady-state data were obtained at
rest and then at each of four workloads ranging from mild [3.2
kilometers per hour (kph), 0% grade]-to-heavy exercise (8.0 kph,
15% grade). The order of workloads was from mild to heavy exercise.
Each workload was maintained until all variables reached steady state
(3-5 min). At rest and during steady state at each workload,
arterial and venous blood samples were taken and analyzed for blood
gases (Radiometer ABL-3). Hindlimb oxygen consumption was calculated as
TAQ times (arterial 
venous) oxygen content. The arterial blood
samples were also analyzed for plasma vasopressin levels and renin
activity as described previously (23). Because our preliminary data
indicated that substantial parasympathetic activity exists even at the
highest workload, this was reinvestigated on a separate day. After a
brief warmup at low workloads, the highest workload was repeated, and once steady state had been achieved, atropine was infused acutely and
the changes in HR, MAP, TAQ, and TAC were observed.
Statistical analysis. The hemodynamic data were averaged for 1 min during steady state at rest and at each workload. Thus each animal served as its own control. Responses from each animal at rest and at each workload were averaged across animals to yield mean responses for the population studied. The values in each condition (workload × drug) were analyzed by analysis of variance (ANOVA) for repeated measures, and individual mean values were compared by test for simple effect using SYSTAT for Windows Software (version 5.02). The changes in HR, MAP, TAQ, and TAC in response to acute administration of atropine during heavy exercise were compared with the control values immediately before atropine infusion by paired t-tests. Statistical significance was assessed as P < 0.05. All data are reported as means ± SE.
| |
RESULTS |
|---|
|
Top
Abstract
Introduction
Methods
Results
Discussion
References
|
|---|
Figure 1 shows the effects of selective
cardiac autonomic blockade on the hemodynamic responses to graded
exercise. Muscarinic cholinergic receptor blockade (MX) increased HR at
rest and at each level of exercise over the values obtained in the
control experiments. In addition, although in the control experiments and after -adrenergic blockade (X) HR significantly increased with the transition from rest to mild exercise and with each successive workload (P < 0.05), after MX, HR
did not increase with the transition from rest to mild exercise (3.2 kph, 0% grade, P > 0.05). At 6.4 kph, 0% grade, HR after MX was significantly higher vs. that at the
lowest workload within this group (P < 0.05). X caused only a small, nonsignificant decrease in HR at
rest and during mild exercise. However, as exercise intensity increased
to moderate levels, X caused a significant reduction in HR compared
with control. X also significantly reduced MAP at higher workloads vs. control. Both TAQ and TAC were significantly reduced at all workloads vs. control after X, whereas MX had no effect on either TAQ or TAC during exercise.
|
Figure 2 shows the effects of selective
cardiac autonomic blockade on plasma vasopressin levels, renin
activity, and hindlimb oxygen consumption at rest and during graded
exercise. X caused a large, significant increase in plasma
vasopressin levels at the highest workload vs. control. MX had little
effect on vasopressin release vs. control except for a modest increase
during mild exercise. Plasma renin activity significantly increased
with exercise workload (P < 0.05, ANOVA workload effect). The increases in renin activity tended to be
larger after MX but these differences did not reach statistical
significance (P > 0.05). As
expected, X attenuated the increases in plasma renin activity vs.
control as workload increased. At the highest workload, X caused a
small but significant reduction in hindlimb oxygen consumption vs.
control, whereas MX had no effect.
|
Figure 3 shows the responses in HR, MAP, and TAQ before and after the administration of atropine during heavy exercise from one experiment. Atropine caused a large increase in HR, indicating that significant, functional parasympathetic tone still exists at this exercise intensity. For all experiments, atropine caused a large, significant increase in HR from 216 ± 8 to 252 ± 7 beats/min. MAP also increased slightly but significantly from 130 ± 5 to 136 ± 5 mmHg, and no significant change in either TAQ or TAC occurred.
|
| |
DISCUSSION |
|---|
|
Top
Abstract
Introduction
Methods
Results
Discussion
References
|
|---|
The main new finding in this study is that, in conscious dogs during dynamic exercise, tonic parasympathetic activity to the heart remains during even heavy exercise workloads. The effects of sympathetic activation to the heart do not become apparent until moderate workloads are attained. Thus, over a wide range of exercise workloads, both functional parasympathetic and sympathetic activity to the heart exists.
Autonomic control of HR at rest and during exercise.
Across species the amount of tonic parasympathetic and sympathetic
activity to the heart at rest varies widely. For example, in rats, both
muscarinic cholinergic and X affect HR almost equally at rest
indicating significant tonic activity of both arms of the autonomic
nervous system in this species (25). In contrast, in resting humans, MX
markedly increases HR, and X has a much smaller chronotropic effect
(37). In the present study using dogs, X had only a slight,
nonsignificant (P = 0.31) effect on HR
at rest and MX caused a substantial increase in HR (see Fig. 1). Thus
the autonomic control of HR at rest in dogs more closely resembles that
in humans than in rats.
X, the
tachycardic response was not different from that observed in the
saline-treated control experiments. These data indicate that, in dogs,
the initial rapid tachycardic response to mild exercise occurs solely
via inhibition of parasympathetic activity. However, in other species
with less tonic parasympathetic tone at rest (e.g., rats), the initial
tachycardia with mild exercise occurs via both parasympathetic
withdrawal and sympathetic activation (25).
As workload increases to moderate and heavy levels, sympathetic
activity increases and parasympathetic activity decreases. These
changes in autonomic tone have been ascribed to changes in central
command, resetting of the arterial baroreflex and/or activation
of muscle afferents. The relative roles of these systems are not
completely understood. Clearly, central command has strong control over
parasympathetic activity (37). However, the role of central command in
the control of sympathetic tone is unclear. Previous studies in humans
have concluded that central command increases (37), causes little
change in (7), or even decreases sympathetic activity (13). Several
recent studies strongly support the concept that the arterial
baroreflex is reset to a higher operating pressure in proportion to the
exercise workload (4, 16, 24, 26, 27, 38). The arterial baroreflex
exerts powerful control over both parasympathetic and sympathetic tone. However, the relative roles of each arm of the autonomic nervous system
in arterial baroreflex control of HR may change from rest to exercise
as the baseline level of autonomic activity is altered (24). Muscle
afferents also may exert strong control over sympathetic activity
(14, 15, 19). Control of parasympathetic tone by muscle afferents
is less apparent; activation of muscle metaboreceptors causes little
effect on HR after sympathetic blockade (19).
Recently Rowell (30) and Rowell and O'Leary (32) suggested that,
during graded exercise, sympathetic activity does not increase until
parasympathetic restraint is exhausted. In support of this concept,
several studies have shown that, in humans, muscle sympathetic nerve
activity and vascular resistance in inactive areas do not increase
until HR approaches ~100 beats/min, the approximate HR obtained with
removal of parasympathetic activity. In addition, Overton (25) observed
in rats that, even during mild exercise (and beyond), the absolute
levels of HR after MX were not different from control (saline treated)
and that X reduced HR by nearly 100 beats/min, indicating
parasympathetic restraint was virtually abolished even at mild work
rates in rats. In this setting, further reflex increases in HR can only
occur via increases in sympathetic activity. However, other studies,
including the present investigation, do not totally support this
concept. In the present investigation, during moderate-to-heavy
exercise, HR was significantly higher after MX and significantly lower
after X. Indeed, the absolute level of HR during heavy exercise (at ~80% of HR reserve) was nearly equidistant between that observed after MX or X. In addition, when atropine was administered acutely during heavy exercise, a significant tachycardia occurred. This tachycardia was accompanied by no significant change in TAQ or TAC and
a small increase in MAP. Inasmuch as MAP slightly increased and no
change in TAQ occurred with atropine infusion, it is unlikely that the
rapid tachycardic response to atropine infusion was due to any change
in sympathetic activity arising from the arterial baroreflex or the
muscle metaboreflex. Similar HR results were reported by Billman and
Dujardin (1), who estimated the extent of parasympathetic activity at
rest and during mild-to-moderate exercise in dogs via time series
analysis of respiratory sinus arrhythmia. They also concluded that
substantial parasympathetic tone exists in these settings. The present
study expands these observations to higher workloads. These data
indicate that, even during heavy exercise in which sympathetic activity
is substantially elevated, marked tonic functional parasympathetic tone
still exists. Close examination of the data from Robinson et al. (28)
also shows that some parasympathetic tone remains in humans during workloads which elicit increases in sympathetic activity.
The retention of tonic parasympathetic tone during exercise may be
advantageous in terms of the ability to rapidly respond to changes in
blood pressure. Warner and Cox (39) showed that the time constants of
the chronotropic responses to changes in sympathetic vs.
parasympathetic tone are markedly different. Steady-state responses to
changes in sympathetic tone may require up to a full minute or more to
occur, whereas the time course of the chronotropic responses to changes
in parasympathetic activity are nearly two orders of magnitude shorter.
Thus, during heavy exercise, the tonic parasympathetic tone may allow
for a rapid tachycardia in responses to sudden decreases in arterial
blood pressure.
Cardiac vs. peripheral sympathetic activity.
After X, HR was not different from the saline-treated control levels
at rest and during mild-to-moderate exercise. These data could be
interpreted as indicating that no functionally significant sympathetic
activity to the heart was present in these settings. However, recent
studies from our laboratory (22, 23) and from Sheriff et al. (34)
indicate that sympathetic tone to the hindlimbs in dogs exists at rest
and increases with even mild exercise. We (23) observed that ganglionic
blockade significantly increased hindlimb vascular conductance at rest
and during mild exercise. In addition, intra-arterial infusion of the
-adrenergic antagonist prazosin increased hindlimb vascular
conductance in proportion to the workload; e.g., in response to
prazosin infusion larger vasodilations in the active skeletal muscle
occurred with increasing levels of dynamic exercise up to and including
heavy workloads (22). Sheriff et al. (34) also observed that, after
ganglionic blockade, both hindlimb and total vascular conductance
progressively increased during the early stages of dynamic exercise so
that, during relatively mild exercise, vascular conductance increased to levels in excess of those normally observed at higher work rates.
Collectively, these data indicate that sympathetic tone to skeletal
muscle exists at rest and increases progressively with exercise
intensity.
X on HR at rest and during mild exercise may not
accurately reflect the level of cardiac efferent sympathetic activity
due to the concept of accentuated antagonism (36). When marked
parasympathetic tone exists, the effect of changes in sympathetic
activity may be obscured. Levy and Zieske (12) showed, in anesthetized
dogs, that the tachycardic effects of direct electrical stimulation of
the sympathetic nerves to the heart are dependent on the prevailing
level of parasympathetic activity. At high parasympathetic nerve
activity, sympathetic stimulation has negligible effects on HR.
Similarly, we observed in conscious dogs (19) that, during postexercise
circulatory occlusion of the previously active skeletal muscle, no
tachycardia was evident unless the effects of parasympathetic nerves
are removed (via MX), indicating that elevated parasympathetic activity
during the recovery from exercise can overwhelm the reflex increases in
sympathetic tone caused by sustained activation of skeletal muscle
metabosensitive afferents. Thus, during mild-to-moderate exercise,
sympathetic activity to the heart may be elevated. However, the
remaining functional tonic parasympathetic tone may obscure the
chronotropic effects. In support of this concept, Huang and Feigl (9)
reported that, during graded exercise in dogs, sympathetic vasoconstriction of the ventricular myocardium occurs during even mild
exercise (HR ~120 beats/min), a workload well within the range of
tonic parasympathetic activity (see Fig. 1). If it is assumed the
sympathetic tone to the sinoatrial node increases as does sympathetic
tone to the ventricular myocardium, these data indicate that the lack
of a significant effect of X on HR during mild exercise may not
accurately reflect changes in sympathetic activity to the heart.
Indeed, although no significant effect of X was observed until
workload increased to 6.4 kph, 10% grade, after MX, HR significantly
increased at a lower workload (6.4 kph, 0% grade). We attempted to
observe the HR responses to graded exercise with combined MX and X.
However, several of the animals would not perform more than moderate
workloads. No aversive stimuli were used to force the animals to run
(e.g., electrical shock or other negative reinforcement stimuli).
Although this is a limitation in the experimental design, using
"volitional" exercise has the distinct advantages including
lessening any adverse emotional consequences involved in acclimatizing
the animals to the laboratory and performing the exercise. Another
caveat is that the intrinsic HR can also increase with increases in
body temperature. Jose et al. (10) concluded that, in humans, HR
increases ~7
beats · min
1 · °C1
increase in internal temperature. If the same relationship exists in
dogs, given that Musch et al. (17) showed that these workloads increased internal temperature in dogs ~1-1.5°C, a small
portion of the tachycardia (~7-11 beats/min) could be due to the
direct effects of increased internal temperature on intrinsic HR.
Plasma renin and vasopressin responses to dynamic exercise in dogs.
A secondary objective of this study was to document the changes in
arterial plasma renin activity and vasopressin concentration during
graded dynamic exercise in dogs. Although these measurements have been
made in other species (2, 6, 8, 35), to our knowledge, this is the
first study to measure these hormonal responses to a wide range of
dynamic exercise in dogs. Both plasma renin activity and vasopressin
concentration increased with increasing workloads (significant ANOVA
workload effect). MX tended to increase both variables over control
levels. As expected, X virtually abolished the changes in renin
release with graded exercise. X also increased the release of
vasopressin at the highest workload attained. This increased release of
vasopressin may be a consequence of the lower arterial pressure or
lower hindlimb blood flow, inasmuch as both the arterial baroreflex and
the muscle metaboreflex are capable of eliciting substantial increases
in vasopressin release (23, 40). The levels of plasma vasopressin
achieved during heavy exercise after X approach vasoactive levels
(3) and therefore may have contributed to the lower hindlimb blood flow and vascular conductance observed in this setting (see Fig. 1).
| |
ACKNOWLEDGEMENTS |
|---|
The authors thank S. Harris and R. Augustyniak for technical assistance.
| |
FOOTNOTES |
|---|
This study was supported by National Heart, Lung, and Blood Institute Grants HL-55473, HL-45038, and HL-02844 and Merit Award of the Dept. of Veterans Affairs.
Address for reprint requests: D. S. O'Leary, Dept. of Physiology, Wayne State Univ. School of Medicine, 540 E. Canfield Ave, Detroit, MI 48201.
Received 7 March 1997; accepted in final form 16 June 1997.
| |
REFERENCES |
|---|
|
Top
Abstract
Introduction
Methods
Results
Discussion
References
|
|---|
1.
Billman, G. E.,
and
J.-P. Dujardin.
Dynamic changes in cardiac vagal tone as measured by time-series analysis.
Am. J. Physiol.
258 (Heart Circ. Physiol. 27):
H896-H902,
1990
2.
Cooley, J. L.,
K. W. Hinchcliff,
K. H. McKeever,
D. R. Lamb,
and
W. W. Muir III.
Effect of furosemide on plasma atrial natriuretic peptide and aldosterone concentrations and renin activity in running horses.
Am. J. Vet. Res.
55:
273-277,
1994[Medline].
3.
Cowley, A. W.
Vasopressin and Cardiovascular Regulation (26th ed.). Baltimore, MD: University Park, 1982.
4.
DiCarlo, S. E.,
and
V. S. Bishop.
Onset of exercise shifts operating point of arterial baroreflex to higher pressures.
Am. J. Physiol.
262 (Heart Circ. Physiol. 31):
H303-H307,
1992
5.
DiCarlo, S. E.,
C.-Y. Chen,
and
H. L. Collins.
Onset of exercise increases lumbar sympathetic nerve activity in rats.
Med. Sci. Sports Exercise
28:
677-684,
1996[Medline].
6.
Freund, B. J.,
E. M. Shizuru,
G. M. Hashiro,
and
J. R. Claybaugh.
Hormonal, electrolyte, and renal responses to exercise are intensity dependent.
J. Appl. Physiol.
70:
900-906,
1991
7.
Friedman, D. B.,
J. M. Johnson,
J. H. Mitchell,
and
N. H. Secher.
Neural control of the forearm cutaneous vasoconstrictor response to dynamic exercise.
J. Appl. Physiol.
71:
1892-1896,
1991
8.
Ghaemmaghami, F.,
A. M. Allevard,
J. Fareh,
G. Geelen,
and
C. Gharib.
Effects of acute exercise and prolonged exercise training on blood pressure, vasopressin and plasma renin activity in spontaneously hypertensive rats.
Eur. J. Appl. Physiol.
62:
198-203,
1991.
9.
Huang, A. H.,
and
E. O. Feigl.
Adrenergic coronary vasoconstriction helps maintain uniform transmural blood flow distribution during exercise.
Circ. Res.
62:
286-298,
1988
10.
Jose, A. D.,
F. Stitt,
and
D. Collison.
The effects of exercise and changes in body temperature on the intrinsic heart rate in man.
Am. Heart J.
79:
488-498,
1970[Medline].
11.
Kozelka, J. W.,
and
R. D. Wurster.
Ascending pathways mediating somatoautonomic reflexes in exercising dogs.
J. Appl. Physiol.
62:
1186-1191,
1987
12.
Levy, M. N.,
and
H. Zieske.
Autonomic control of cardiac pacemaker activity and atrioventricular transmission.
J. Appl. Physiol.
27:
465-470,
1969
13.
Mark, A. L.,
R. G. Victor,
C. Nerhed,
and
B. G. Wallin.
Microneurographic studies of the mechanisms of sympathetic nerve responses to static exercise in humans.
Circ. Res.
57:
461-469,
1985
14.
Matsukawa, K.,
P. T. Wall,
L. B. Wilson,
and
J. H. Mitchell.
Reflex stimulation of cardiac sympathetic nerve activity during static muscle contraction in cats.
Am. J. Physiol.
267 (Heart Circ. Physiol. 36):
H821-H827,
1994
15.
Matsukawa, K.,
P. T. Wall,
L. B. Wilson,
and
J. H. Mitchell.
Neurally mediated renal vasoconstriction during isometric muscle contraction in cats.
Am. J. Physiol.
262 (Heart Circ. Physiol. 31):
H833-H838,
1992
16.
Melcher, A.,
and
D. E. Donald.
Maintained ability of carotid baroreflex to regulate arterial pressure during exercise.
Am. J. Physiol.
241 (Heart Circ. Physiol. 10):
H838-H849,
1981
17.
Musch, T. I.,
D. B. Friedman,
G. C. Haidet,
J. Stray-Gundersen,
T. G. Waldrop,
and
G. A. Ordway.
Arterial blood gases and acid-base status of dogs during graded dynamic exercise.
J. Appl. Physiol.
61:
1914-1919,
1986
18.
O'Hagan, K.,
L. B. Bell,
S. W. Mittelstadt,
and
P. S. Clifford.
Effect of dynamic exercise on renal sympathetic nerve activity in conscious rabbits.
J. Appl. Physiol.
74:
2099-2104,
1993
19.
O'Leary, D. S.
Autonomic mechanisms of muscle metaboreflex control of heart rate.
J. Appl. Physiol.
74:
1748-1754,
1993
20.
O'Leary, D. S.
Heart rate control during exercise by baroreceptors and skeletal muscle afferents.
Med. Sci. Sports Exercise
28:
210-217,
1996[Medline].
21.
O'Leary, D. S.,
R. C. Dunlap,
and
K. W. Glover.
Role of endothelium-derived relaxing factor in hindlimb reactive and active hyperemia in conscious dogs.
Am. J. Physiol.
266 (Regulatory Integrative Comp. Physiol. 35):
R1213-R1219,
1994
22.
O'Leary, D. S.,
E. D. Robinson,
and
J. L. Butler.
Is active skeletal muscle functionally vasoconstricted during dynamic exercise in conscious dogs?
Am. J. Physiol.
272 (Regulatory Integrative Comp. Physiol. 41):
R386-R391,
1997
23.
O'Leary, D. S.,
N. F. Rossi,
and
P. C. Churchill.
Muscle metaboreflex control of vasopressin and renin release.
Am. J. Physiol.
264 (Heart Circ. Physiol. 33):
H1422-H1427,
1993
24.
O'Leary, D. S.,
and
D. P. Seamans.
Effect of exercise on autonomic mechanisms of baroreflex control of heart rate.
J. Appl. Physiol.
75:
2251-2257,
1993
25.
Overton, J. M.
Influence of autonomic blockade on cardiovascular responses to exercise in rats.
J. Appl. Physiol.
75:
155-161,
1993
26.
Papelier, Y.,
P. Escourrou,
J. P. Gauthier,
and
L. B. Rowell.
Carotid baroreflex control of blood pressure and heart rate in men during dynamic exercise.
J. Appl. Physiol.
77:
502-506,
1994
27.
Potts, J. T.,
X. R. Shi,
and
P. B. Raven.
Carotid baroreflex responsiveness during dynamic exercise in humans.
Am. J. Physiol.
265 (Heart Circ. Physiol. 34):
H1928-H1938,
1993
28.
Robinson, B. F.,
S. E. Epstein,
G. D. Beiser,
and
E. Braunwald.
Control of heart rate by the autonomic nervous system.
Circ. Res.
19:
400-411,
1966
29.
Rowell, L. B.
Human Circulation Regulation During Physical Stress. New York: Oxford Univ. Press, 1986.
30.
Rowell, L. B.
Control of regional circulations during exercise.
In: Reflex Control of the Circulation, edited by I. H. Zucker,
and J. P. Gilmore. Boca Raton, FL: CRC, 1991, vol. 27, p. 795-828.
31.
Rowell, L. B.
Human Cardiovascular Control. New York: Oxford Univ. Press, 1993.
32.
Rowell, L. B.,
and
D. S. O'Leary.
Reflex control of the circulation during exercise: chemoreflexes and mechanoreflexes.
J. Appl. Physiol.
69:
407-418,
1990
33.
Rowell, L. B.,
D. S. O'Leary,
and
D. L. Kellogg, Jr.
Integration of cardiovascular control systems in dynamic exercise.
In: Handbook of Physiology. Exercise: Regulation and Integration of Multiple Systems. Bethesda, MD: Am. Physiol. Soc., 1996, sect. 12, chapt. 17, p. 770-838.
34.
Sheriff, D. D.,
L. B. Rowell,
and
A. M. Scher.
Is rapid rise in vascular conductance at onset of dynamic exercise due to muscle pump?
Am. J. Physiol.
265 (Heart Circ. Physiol. 34):
H1227-H1234,
1993
35.
Stebbins, C. L.,
J. D. Symons,
M. D. McKirnan,
and
F. F. Y. Hwang.
Factors associated with vasopressin release in exercising swine.
Am. J. Physiol.
266 (Regulatory Integrative Comp. Physiol. 35):
R118-R124,
1994
36.
Stramba-Badiale, M.,
E. Vanoli,
G. M. De Ferrari,
D. Cerati,
R. D. Foreman,
and
P. J. Schwartz.
Sympathetic-parasympathetic interaction and accentuated antagonism in conscious dogs.
Am. J. Physiol.
260 (Heart Circ. Physiol. 29):
H335-H340,
1991
37.
Victor, R. G.,
S. L. Pryor,
N. H. Secher,
and
J. H. Mitchell.
Effects of partial neuromuscular blockade on sympathetic nerve responses to static exercise in humans.
Circ. Res.
65:
468-476,
1989
38.
Walgenbach, S. C.,
and
D. E. Donald.
Inhibition by carotid baroreflex of exercise-induced increases in arterial pressure.
Circ. Res.
52:
253-262,
1983
39.
Warner, H. R.,
and
A. Cox.
A mathematical model of heart rate control by sympathetic and vagus efferent information.
J. Appl. Physiol.
17:
349-355,
1962
40.
Yamashita, H., H. Kannan, K. Inenaga, and K. Koizumi. The
role of cardiovascular and muscle afferent systems in control of body
water balance. J. Auton. Nerv. Syst.
1992.
This article has been cited by other articles:
|
|
 |
|
  D. J. Duncker and R. J. Bache Regulation of Coronary Blood Flow During Exercise Physiol Rev, July 1, 2008; 88(3): 1009 - 1086. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 F. Iellamo, J. A. Sala-Mercado, M. Ichinose, R. L. Hammond, M. Pallante, T. Ichinose, L. W. Stephenson, and D. S. O'Leary Spontaneous baroreflex control of heart rate during exercise and muscle metaboreflex activation in heart failure Am J Physiol Heart Circ Physiol, September 1, 2007; 293(3): H1929 - H1936. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. A. Sala-Mercado, M. Ichinose, R. L. Hammond, T. Ichinose, M. Pallante, L. W. Stephenson, D. S. O'Leary, and F. Iellamo Muscle metaboreflex attenuates spontaneous heart rate baroreflex sensitivity during dynamic exercise Am J Physiol Heart Circ Physiol, June 1, 2007; 292(6): H2867 - H2873. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Kukielka, D. R. Seals, and G. E. Billman Cardiac vagal modulation of heart rate during prolonged submaximal exercise in animals with healed myocardial infarctions: effects of training Am J Physiol Heart Circ Physiol, April 1, 2006; 290(4): H1680 - H1685. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. A. Sala-Mercado, R. L. Hammond, J.-K. Kim, N. F. Rossi, L. W. Stephenson, and D. S. O'Leary Muscle metaboreflex control of ventricular contractility during dynamic exercise Am J Physiol Heart Circ Physiol, February 1, 2006; 290(2): H751 - H757. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J.-K. Kim, J. A. Sala-Mercado, R. L. Hammond, J. Rodriguez, T. J. Scislo, and D. S. O'Leary Attenuated arterial baroreflex buffering of muscle metaboreflex in heart failure Am J Physiol Heart Circ Physiol, December 1, 2005; 289(6): H2416 - H2423. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. L. Hammond, R. A. Augustyniak, N. F. Rossi, K. Lapanowski, J. C. Dunbar, and D. S. O'Leary Alteration of humoral and peripheral vascular responses during graded exercise in heart failure J Appl Physiol, January 1, 2001; 90(1): 55 - 61. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. L. Hammond, R. A. Augustyniak, N. F. Rossi, P. C. Churchill, K. Lapanowski, and D. S. O'Leary Heart failure alters the strength and mechanisms of the muscle metaboreflex Am J Physiol Heart Circ Physiol, March 1, 2000; 278(3): H818 - H828. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H. R. Burger, M. P. Chandler, D. W. Rodenbaugh, and S. E. DiCarlo Dynamic exercise shifts the operating point and reduces the gain of the arterial baroreflex in rats Am J Physiol Regulatory Integrative Comp Physiol, December 1, 1998; 275(6): R2043 - R2048. [Abstract] [Full Text] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Visit Other APS Journals Online |
, Control (saline treated); 
, atropine; 
, atenolol.
* P < 0.05 vs. control; for
other specific comparisons within groups see text. bpm, Beats per
minute; kph, kilometers per hour.
O2) at rest and
during graded exercise. 