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Am J Physiol Heart Circ Physiol 273: H2613-H2619, 1997;
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Vol. 273, Issue 6, H2613-H2619, December 1997

Daily exercise attenuates the sympathetic component of the arterial baroreflex control of heart rate

Heidi L. Collins and Stephen E. Dicarlo

Department of Physiology, Northeastern Ohio Universities College of Medicine, Rootstown, Ohio 44272

    ABSTRACT
Top
Abstract
Introduction
Methods
Results
Discussion
References

The influence of daily spontaneous running (DSR) on the sympathetic (SC) and parasympathetic components of the arterial baroreflex control of heart rate (HR) was examined in 16 female Long Evans rats [8 sedentary (SED) and 8 DSR]. After 8-9 wk of SED control or DSR, animals were chronically instrumented with arterial and venous catheters. DSR resulted in an increased heart weight-to-body weight ratio (2.71 ± 0.11 vs. 3.09 ± 0.09 g/kg) and a resting bradycardia (378 ± 6 vs. 330 ± 5 beats/min). Arterial baroreflex function was examined during ramp infusions of phenylephrine and sodium nitroprusside under the following three experimental conditions: 1) control, 2) after beta 1-adrenergic receptor blockade (beta 1-X), and 3) after muscarinic-cholinergic receptor blockade (M-X). Arterial baroreflex function parameters were compared between SED and DSR rats. In the control condition, DSR attenuated the range (182 ± 15 vs. 124 ± 18 beats/min), maximum HR (464 ± 9 vs. 394 ± 15 beats/min), and maximal gain (Gmax; 5.57 ± 0.42 vs. 3.2 ± 0.45 beats · min-1 · mmHg-1). Similarly, after M-X, DSR attenuated the range (84 ± 5 vs. 62 ± 8 beats/min), maximum HR (449 ± 11 vs. 412 ± 11 beats/min), and Gmax (2.73 ± 0.37 vs. 1.57 ± 0.32 beats · min-1 · mmHg-1). In contrast, after beta 1-X, DSR did not alter the range (61 ± 13 vs. 70 ± 7 beats/min), maximum HR (326 ± 9 vs. 313 ± 7 beats/min), or Gmax (3.04 ± 0.54 vs. 3.75 ± 0.52 beats · min-1 · mmHg-1). Results demonstrate that DSR attenuated the arterial baroreflex control of HR by reducing the SC.

autonomic nervous system

    INTRODUCTION
Top
Abstract
Introduction
Methods
Results
Discussion
References

IT IS WELL KNOWN that endurance exercise training attenuates the arterial baroreflex regulation of heart rate (HR). Exercise training reduced the maximum HR response, range, and/or maximal gain (Gmax) of the arterial baroreflex regulation of HR in the rat (6, 8), rabbit (10), dog (14), and human (18). The reduced baroreflex function may be due to alterations in the reflex control of the sympathetic and/or parasympathetic components of the arterial baroreflex control of HR. Evidence suggests that endurance exercise training results in an apparent increase in resting parasympathetic and a decrease in resting sympathetic efferent activity (7). Furthermore, previous studies have reported that the arterial baroreflex control of directly measured sympathetic nerve activity to the kidney (10, 11, 21) and hindlimb (6) is attenuated after exercise training. However, the effect of exercise training on the parasympathetic and sympathetic components of the arterial baroreflex control of HR has not been determined. The regulation of sympathetic activity to the heart and periphery may be different, since it is well known that sympathetic nerve activity is differentially regulated to a variety of sites (29).

Arterial baroreflex-mediated reflex changes in HR have been used to identify individuals and animals at risk for sudden cardiac death (1-3, 27). An enhanced reflex increase in the parasympathetic and/or an attenuated reflex increase in the sympathetic component of the arterial baroreflex is associated with a reduced risk for ventricular fibrillation (VF) and sudden cardiac death (2, 3, 15, 25, 26). Thus interventions that reduce the reflex activation of cardiac sympathetic or increase the reflex activation of cardiac parasympathetic components may prevent sudden cardiac death due to VF. In this context, exercise training may favorably alter the reflex activation of cardiac autonomic responses. Thus the present study was designed to test the following hypotheses. 1) Endurance exercise training attenuates the sympathetic component of the arterial baroreflex control of HR. 2) Endurance exercise training enhances the parasympathetic component of the arterial baroreflex control of HR.

    METHODS
Top
Abstract
Introduction
Methods
Results
Discussion
References

Design. Female Long-Evans rats were weaned at 3 wk of age and randomly assigned to a sedentary (SED, n = 8) or daily spontaneous running (DSR, n = 8) group. DSR rats were housed in cages with free access to running wheels. SED rats were housed in standard wire suspended cages. After 8-9 wk of DSR or SED control, rats were chronically instrumented with arterial and venous catheters. After surgery (2 days), the arterial baroreflex regulation of HR was examined under the following three experimental conditions: 1) control, 2) after beta 1-adrenergic receptor blockade (parasympathetic component), and 3) after muscarinic-cholinergic receptor blockade (sympathetic component).

Surgical procedures. All instrumentation was performed using sterile surgical procedures. Rats were anesthetized with an intramuscular injection of "rat cocktail" (8 mg/kg xylazine, 4 mg/kg chlorpromazine hydrochloride, and 40 mg/kg ketamine hydrochloride). Supplemental doses were administered as needed. A Teflon catheter was placed into the thoracic aorta via the left common carotid artery for measurements of arterial pressure (AP) and HR. Two polythethylene (PE-50) catheters were placed into the inferior vena cava via the right jugular vein for the infusion of drugs. Two venous catheters were required to alternately increase and decrease AP in a random order without flushing the line. One catheter was used for the infusion of phenylephrine (PE), and the other catheter was used for the infusion of sodium nitroprusside (SNP). The arterial and venous catheters were tunneled beneath the skin and exteriorized at the back of the neck. The catheters were flushed daily with heparinized saline, filled with heparin (1,000 U/ml), and plugged with a paraffin-filled obturator. The animals were allowed 2 days to recover from the surgery. During the recovery period, all animals were familiarized with the experimental environment and procedures.

Experimental measurements. AP was measured by connecting the arterial catheter to a Gould P23 XL pressure transducer. Mean arterial pressure (MAP) was derived electronically, using a low-pass filter with a time constant of 3.2 s. HR was determined with a Gould electrocardiogram/Biotach that was triggered from the AP pulse. AP analog signals were digitized at 400 samples/s by a MacLab 8 analog-to-digital converter and laboratory computer (Macintosh Performa 5200CD) for subsequent analysis.

Experimental protocols. On day 1 (protocol 1), the rats were placed unrestrained in a large Plexiglas box. The animals were allowed to acclimate to the laboratory environment for at least 40 min to ensure a stable resting hemodynamic condition. After all variables reached a steady state, control AP and HR were recorded over a 30-s interval. MAP was alternately increased and subsequently decreased by progressive infusions of PE (concentration: 100 µg/ml, infusion rate: 20-60 µl/min) and SNP (concentration: 100 µg/ml, infusion rate: 20-60 µl/min). The data were generated during two to five increases or decreases in MAP for each animal for two reasons: 1) to demonstrate reproducibility of the responses and 2) to account for failures when the rate of change was not consistent or if the animal moved. However, only data obtained from one increase and one decrease were subsequently analyzed. Approximately 30 s were required to increase and decrease MAP over the 25- to 30-mmHg pressure range. This range of pressure was required to obtain maximum decreases and increases in HR. At least 15 min were allowed after the PE infusion and 30 min were allowed after the SNP infusion for hemodyamic parameters to return to control levels. The increases and decreases in MAP were generated in random order. To evaluate the sympathetic component of the arterial baroreflex regulation of HR, these procedures were repeated 20 min after cardiac autonomic parasympathetic blockade (muscarinic-cholinergic receptor blockade). Cardiac muscarinic-cholinergic receptor blockade was achieved by injection of the nonspecific muscarinic-cholinergic receptor antagonist methylatropine (3 mg/kg ia). Supplemental doses were administered every 20 min.

On an alternate day (>48 h), protocol 2 was conducted. Rats were treated identically as described for protocol 1 with the exception that the control baroreflex function curve was not generated. However, the parasympathetic component of the baroreflex control of HR was evaluated. This was achieved by generating baroreflex function curves 20 min after cardiac autonomic sympathetic blockade (beta 1-adrenergic receptor blockade). Cardiac beta 1-adrenergic receptor blockade was achieved by injection of the specific beta 1-adrenergic receptor antagonist metoprolol (3 mg/kg ia). The order of cardiac autonomic blocking agents between the two protocols was randomized. Resting AP in SED or DSR rats was not altered by either metoprolol or methylatropine.

The effectiveness of muscarinic-cholinergic and beta 1-adrenergic receptor blockade was judged by the absence of an HR response to changes in AP. Before blockade, a 19 ± 1 mmHg increase in MAP was associated with a decrease in HR of 30 ± 1 beats/min. A 25 ± 8 mmHg decrease in MAP was associated with an increase in HR of 30 ± 10 beats/min. After muscarinic-cholinergic receptor blockade, a 24 ± 5 mmHg increase in MAP decreased HR only 5 ± 3 beats/min. After beta 1-adrenergic receptor blockade, a 24 ± 3 mmHg decrease in MAP increased HR only 7 ± 3 beats/min.

Data analysis. Although the data for increases and decreases in MAP were generated separately in each protocol, the baroreflex control of HR is generally a sigmoid curve. Therefore, the data from each animal were fitted to a sigmoid logistic function as described by Kent et al. (17), using a nonlinear regression program (Systat 5.2.1) run on a Macintosh computer. This analysis evaluates the relationship between HR and MAP, where
HR = P<SUB>4</SUB> + {(P<SUB>1</SUB>)/1 + exp[P<SUB>2</SUB>(MAP − P<SUB>3</SUB>)]}
where P1 is the range of HR (maximum response minus minimum response), P2 is the coefficient to calculate the gain as a function of pressure, P3 is the pressure at the midrange of the curve, and P4 is the minimum response of HR. The gain at any given MAP was calculated from the first derivative of the sigmoid function using the following equation
gain = P<SUB>1</SUB> P<SUB>2</SUB>{exp[P<SUB>2</SUB>(MAP − P<SUB>3</SUB>)]}/{1 + exp[P<SUB>2</SUB>(MAP − P<SUB>3</SUB>)]}<SUP>2</SUP>
The maximum HR achieved by lowering AP was calculated as P1 + P4 (Table 1).

                              
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  		Table 1.   Baroreflex function parameters for arterial baroreflex control of HR in SED and DSR rats under 3 experimental conditions of preblockade (arterial baroreflex function), muscarinic-cholinergic receptor blockade (sympathetic component), and beta 1-adrenergic receptor blockade (parasympathetic component)

To illustrate this analysis and the "goodness of fit," Fig. 1 presents actual data points from one increase and one decrease in AP from one SED rat. All data points were fitted to the sigmoid logistic function. The corresponding curve and logistic parameters are included.


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  		Fig. 1.   Actual data points illustrating the relationship between mean arterial pressure (MAP) and heart rate (HR) from 1 sedentary (SED) rat. All data points were fitted to the sigmoid logistic function. Corresponding fitted curve and logistic parameters are presented. MAP was increased by an intravenous infusion of phenenylephrine and was decreased by an intravenous infusion of nitroprusside. P1, range of HR (maximum response minus minimum response); P2, coefficient to calculate the gain as a function of pressure; P3, pressure at the midrange of the curve; and P4, minimum response of HR; bpm, beats/min.

A two-way analysis of variance (ANOVA) was also used to evaluate differences in baroreflex function parameters (P1, P3, and P4), maximum HR (P1 + P4), Gmax, and the average rate of change in blood pressure during generation of baroreflex function curves (Table 1). When significant differences were observed, between-group and within-group multiple comparisons were made using a test of Simple Effect (Systat 5.2.1). The rates of change of blood pressure were obtained by averaging the rate from one increase or decrease in AP from each animal used in the analysis of the blood pressure-HR relationship (Table 1).

Differences in resting hemodynamic variables between SED and DSR rats were evaluated using a two-way ANOVA with repeated measures. Resting HR and MAP before generation of baroreflex function curves were not significantly different within the SED and DSR groups; therefore, HR and MAP were averaged and are presented in Table 2. A Student's unpaired t-test was used to evaluate differences in age, body weight, heart weight-to-body weight ratio (HW/BW), resting HR, and resting MAP between SED and DSR rats. A Student's unpaired t-test was also used to evaluate differences in pulse pressure between SED and DSR rats under the three experimental conditions (Table 3). All values are expressed as means ± SE. Significant differences were determined at the 0.05 level.

                              
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  		Table 2.   Number of animals, age, body weight, HW/BW, resting MAP, and resting HR in SED and DSR rats

                              
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  		Table 3.   Pulse pressure before (control) and in response to PE and SNP in SED and DSR rats under the 3 experimental conditions of preblockade, muscarinic-cholinergic receptor blockade, and beta 1-adrenergic receptor blockade

Determination of training effect. Exercise training has been shown to elicit a resting bradycardia and an increase in the HW/BW (7, 8, 10, 11, 24, 28). Resting HR and MAP, determined before generation of baroreflex function curves under the three experimental conditions, were averaged and compared between the SED and DSR groups (Table 2). After completion of the studies, the hearts of the rats were excised, and the cardiac chambers were opened, rinsed clean of all clots, and weighed. HW/BW was calculated and compared between groups (Table 2).

    RESULTS
Top
Abstract
Introduction
Methods
Results
Discussion
References

Figure 2 is an analog recording of AP, MAP, and HR during intravenous infusions of PE in one SED and one DSR rat. The rates of increase in MAP were 0.97 and 0.94 mmHg/s, respectively. DSR reduced the maximum bradycardic response to an increase in AP (Delta 122 vs. Delta 58 beats/min for SED vs. DSR, respectively).


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  		Fig. 2.   Analog recording of arterial pressure, mean arterial pressure, and heart rate during an intravenous infusion of phenylephrine in one SED and one daily spontaneous running (DSR) rat.

Figures 3, A-C, and 4, A-C, illustrate the relationship between MAP and HR fitted to the sigmoid logistic function and gain of the arterial baroreflex control of HR in SED and DSR rats under the three experimental conditions. The baroreflex function parameters calculated from data in these figures are presented in Table 1. In the control condition (both sympathetic and parasympathetic components intact), DSR attenuated the range (32%), maximum HR (15%), and Gmax (42%; Figs. 3A and 4A and Table 1). DSR attenuated the sympathetic component of the arterial baroreflex control of HR. Specifically, DSR attenuated the range (26%), maximum (8%), and Gmax (42%; Figs. 3B and 4B and Table 1). Finally, DSR did not alter the parasympathetic component. DSR did not alter the range, maximum, or Gmax (Figs. 3C and 4C and Table 1). There were no differences in the rates of change in MAP or pulse pressure for PE or SNP under the three experimental conditions between SED and DSR rats (Tables 1 and 3).


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  		Fig. 3.   Relationship between MAP and HR, fitted to the sigmoid logistic function, in SED and DSR rats under the 3 experimental conditions of control (A), after muscarinic-cholinergic receptor blockade (B), and after beta 1-adrenergic receptor blockade (C).


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  		Fig. 4.   Gain of arterial baroreflex control of HR in SED and DSR rats under the 3 experimental conditions of control (A), after muscarinic-cholinergic receptor blockade (B), and after beta 1-adrenergic receptor blockade (C).

Intragroup comparisons were made regarding the effect of beta 1-adrenergic receptor and muscarinic-cholinergic receptor blockade on the arterial baroreflex control of HR. In SED rats, both cardiac autonomic receptor antagonists significantly decreased the Gmax. In DSR rats, the Gmax was reduced after muscarinic-cholinergic receptor blockade only (Table 1).

    DISCUSSION
Top
Abstract
Introduction
Methods
Results
Discussion
References

The influence of endurance exercise training on the sympathetic and parasympathetic components of the arterial baroreflex control of HR was evaluated in female normotensive rats. The major findings of this study are 1) DSR attenuated the arterial baroreflex control of HR, 2) DSR attenuated the sympathetic component of the arterial baroreflex control of HR, and 3) DSR did not alter the parasympathetic component of the arterial baroreflex control of HR. The attenuated arterial baroreflex control of HR was due to training, since factors that influence reflex responses (rate of change of AP and pulse pressure) were not different between SED and DSR rats.

Training adaptations on reflex sympathetic and parasympathetic components. In the present study, DSR was used as the training stimulus. Spontaneous wheel running has been reported to result in significant increases in maximum O2 uptake, HW/BW, and a resting bradycardia (6, 8, 19, 24, 28). There are several advantages of using a DSR training program, including 1) the animals run spontaneously during their active hours, i.e., at night; 2) no stress or adversive stimuli are used to force the animals to run; and 3) because running occurs in the animal's cage, the running environment is not changed between running and nonrunning situations.

DSR was monitored from a cyclometer attached to each running wheel apparatus. The average running distance during the 8-9 wk of DSR is similar to distances recently reported for female rats (6, 28). During the first 4 wk, the animals rapidly increased their DSR distance, reaching a plateau between weeks 4 and 9. The average weekly running distance over the plateau period was 70 ± 3 km/wk. These distances produced cardiovascular adaptations as demonstrated by a 14% increase in HW/BW and a 13% decrease in resting HR. Furthermore, the increase in HW/BW was a genuine training adaptation, since SED and DSR rats did not differ in body weight (Table 2). Thus, the results of this study were due to the effects of training and not due to the stress associated with a forced training program.

DSR attenuated the arterial baroreflex control of HR. Specifically, DSR attenuated the maximum HR response and range 15 and 32%, respectively. These data suggest that the reserve to increase HR during a hypotensive stimulus was substantially reduced after training. The gain of the arterial baroreflex was also significantly attenuated 42% in DSR rats. The reduction in gain indicates that the ability to change HR to compensate for a given blood pressure disturbance is attenuated. This suggests that compensation for blood pressure disturbances by changing HR would be substantially reduced after training.

The sympathetic component of the arterial baroreflex control of HR was also attenuated in DSR rats. Specifically, DSR attenuated the maximum HR response, range, and Gmax 8, 26, and 42%, respectively. The reduction in the sympathetic component is consistent with studies that examined the effect of exercise training on the arterial baroreflex control of directly measured peripheral sympathetic nerve activity (6, 10, 11, 21). The range, maximum nerve activity, and Gmax of the arterial baroreflex control of directly measured renal and lumbar sympathetic nerve activity are reduced in trained animals (6, 10, 11, 21). Taken together, these data suggest that training reduced the reflex control of sympathetic activity to the kidney (10, 11, 21), hindlimb (6), and heart.

The parasympathetic component of the arterial baroreflex control of HR was not different between SED and DSR rats. There are no studies that have directly examined the effect of endurance exercise training on the parasympathetic component of the arterial baroreflex control of HR. However, Billman and colleagues (3) reported that 6 wk of daily treadmill running enhanced the bradycardic response to an increase in AP in dogs with a healed anterior wall myocardial infarction. These results suggest that exercise training enhanced the parasympathetic component of the arterial baroreflex control of HR. Reasons for the disparate results regarding the effect of exercise training on the parasympathetic component of the arterial baroreflex control of HR are unknown; however, two possible explanations exist. 1) At rest, dogs are vagally dominated, whereas rats are sympathetically dominated. Thus increases in the parasympathetic component of the arterial baroreflex control of HR after training may be related to the resting level of parasympathetic activity (23). 2) The effect of myocardial infarction on the arterial baroreflex control of HR may also account for the disparate results. It is well known that myocardial infarction alters the arterial baroreflex control of HR (27). However, it is unknown to what extent myocardial infarction affects the mechanisms responsible for the training-induced enhancement of the parasympathetic component of the arterial baroreflex control of HR.

Intragroup comparisons were made regarding the effect of beta 1-adrenergic receptor and muscarinic-cholinergic receptor blockade on the arterial baroreflex control of HR. In SED rats, both cardiac autonomic receptor antagonists significantly decreased the Gmax. However, in DSR rats, the Gmax was reduced after muscarinic-cholinergic receptor blockade only. These data suggest that nearly all of the reflex changes in HR around the Gmax in DSR rats were mediated by the parasympathetic nervous system.

It is known that muscarinic-cholinergic receptors exert a presynaptic inhibition on sympathetic efferent nerves. Thus interpretation of the results must be considered with this concern in mind. Specifically, the sympathetic component was determined after muscarinic-cholinergic receptor blockade. Because muscarinic-cholinergic receptor blockade has the potential to increase the influence of the sympathetic nervous system, our determination of the sympathetic component of the arterial baroreflex control of HR may have been slightly enhanced. However, the major comparison is between SED and DSR rats. It is assumed that the potential overestimation of the sympathetic component is constant between groups.

Mechanisms mediating the reduction in the sympathetic component. The mechanism(s) responsible for the attenuation in the sympathetic component without an alteration in the parasympathetic component of the arterial baroreflex control of HR is unknown; however, at least three possibilities exist: 1) alterations at the effector organ (beta 1-adrenergic or muscarinic-cholinergic receptor-mediated responses), 2) an altered central response to arterial baroreceptor afferent activity, and 3) an increased afferent input from cardiac receptors.

It is possible that DSR caused a reduction in postsynaptic mechanisms. It is well known that prolonged exposure of a receptor to its agonist results in loss of responsiveness of the tissue to subsequent stimulation by the agonist. This phenomenon, termed desensitization, refractoriness, tolerance, or tachyphylaxis, leads to a loss in the ability to induce a maximal biological response (20). During exercise, catecholamine concentrations are significantly increased (16). Repetitive, short-term exposure to elevated catecholamine concentrations that occur during a training program may provide an adequate stimulus for desensitization of cardiac beta 1-adrenergic receptor responsiveness. In support of this hypothesis, previous reports have demonstrated a decrease in adenylate cyclase activity (12) and a reduction in beta 1-adrenergic receptor number (30) in hearts obtained from trained rats. Furthermore, Friedman and colleagues (13) demonstrated that the tachycardic response to the beta 1- and beta 2-adrenergic receptor agonist isoproterenol was attenuated after a single bout of treadmill running in dogs. A decreased sensitivity of cardiac beta -adrenergic receptors was postulated. Taken together, these data suggest that the heart is less responsive to a catecholamine stimulus after training.

Alternatively, exercise training may result in an altered integration of arterial baroreceptor afferent activity within the nucleus tractis solitarius or elsewhere. Recently, Chen et al. (8) evaluated aortic afferent reactivity and the central gain of the aortic baroreflex in SED control and DSR rats. The investigators reported that training reduced the central gain of the arterial baroreflex without changes in reactivity of aortic baroreceptor afferents. These results are consistent with the hypothesis that the reduced ability of the baroreflex to regulate HR may be due to an attenuated central processing of arterial baroreceptor afferent signals.

Finally, an increase in the tonic inhibitory influence of the cardiopulmonary baroreflex may also contribute to the reduction in the reflex control of HR. Several lines of evidence support this hypothesis. Cardiac vagal afferents exert a tonic inhibitory influence on the arterial baroreflex (4). Factors associated with exercise training, such as increased blood volume (10), increased HW/BW (6, 8, 10, 11, 28), and increased systolic performance (5), enhance the discharge frequency of cardiac afferents (4). DiCarlo and Bishop (11) have previously reported that the training-induced attenuation of the arterial baroreflex control of renal sympathetic nerve activity was the result of an enhanced inhibitory influence of cardiac afferents. This was suggested because reversible denervation of cardiac afferents in trained animals restored the range and gain of the arterial baroreflex to levels observed in the untrained state.

Clinical perspectives. Interventions that decrease the reflex activation of cardiac sympathetic or increase the reflex activation of cardiac parasympathetic components are known to reduce the incidence of sudden cardiac death (3, 22). For example, Billman and colleagues (3) utilized a model in which ventricular fibrillaton could be induced by a combination of acute myocardial ischemia and exercise in dogs with a healed myocardial infarction. With the use of this model, the effects of endurance exercise training on the arterial baroreflex control of the heart were examined. The investigators demonstrated that exercise training decreased the development of VF. An increase in reflex vagal and decrease in reflex sympathetic tone were postulated. We have extended these findings and demonstrated that, like dogs with a healed myocardial infarction, exercise training decreased the sympathetic component of the arterial baroreflex control of HR in healthy female rats. Thus a reduction of the sympathetic component of the arterial baroreflex control of HR, as observed in DSR rats, may also contribute to the prevention of sudden cardiac death.

Potential limitations. In the present study, ramp increases and decreases in AP were used to generate baroreflex function curves. Approximately 30 s were required to either increase or decrease MAP by 30 mmHg. Coleman (9) has demonstrated in conscious rats that the relative roles of the sympathetic and parasympathetic nervous systems are dependent on the duration of the change in AP. The contribution of the parasympathetic nervous system to the reflex control of HR is greatest at 1 s, whereas sympathetic effects are revealed between 1 and 30 s. However, because of this significant delay for the full expression of the sympathetic nervous system, it may be argued that we did not record the full effect of the sympathetic nervous system. However, this concern was minimized because we used the relationship between MAP and HR. MAP was determined with a low-pass filter having a delay (time constant) of 3.2 s behind pulsatile pressure. In addition, the fact that HR plateaued during generation of the baroreflex function curves also suggests that we obtained full expression of the sympathetic nervous system.

Summary. This is the first investigation to assess the sympathetic and parasympathetic components of the arterial baroreflex control of HR in SED and DSR rats. Consistent with previous findings, these results demonstrate that the arterial baroreflex control of HR is attenuated after training. Importantly, the attenuation is due to a reduction in the reflex control of the sympathetic component of the arterial baroreflex control of HR. This reduction in the sympathetic component may be beneficial to patients at high risk for sudden cardiac death by preventing the development of ventricular tachyarrhythmias during acute myocardial ischemia. Thus exercise training may lead to an additional measure calculated to lower the incidence of sudden cardiac death.

    ACKNOWLEDGEMENTS

This study was supported by the American Physiological Society, Porter Physiology Development Program, and the American Heart Association, Ohio Affiliate, Grant AK-95-02-S.

    FOOTNOTES

Address for reprint requests: S. E. DiCarlo, Dept. of Physiology, Northeastern Ohio Universities, College of Medicine, PO Box 95, Rootstown, OH 44272.

Received 4 April 1997; accepted in final form 7 August 1997.

    REFERENCES
Top
Abstract
Introduction
Methods
Results
Discussion
References

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AJP Heart Circ Physiol 273(6):H2613-H2619
0363-6135/97 $5.00 Copyright © 1997 the American Physiological Society


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