(Circulation. 2000;102:2588.)
© 2000 American Heart Association, Inc.
Clinical Investigation and Reports |
Effects of a Residential Exercise Training on Baroreflex Sensitivity and Heart Rate Variability in Patients With Coronary Artery Disease
A Randomized, Controlled Study
From Dipartimento di Medicina Interna, Centro di Riabilitazione Madonna della Letizia, Università di Roma, Tor Vergata, Rome, Italy.
Correspondence to Ferdinando Iellamo, MD, Dipartimento Medicina Interna, Università di Roma, Tor Vergata, Via O. Raimondo, 8, 00173 Roma, Italy. E-mail iellamo{at}med.uniroma2.it
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Abstract |
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Background—Myocardial ischemia and infarction impair baroreflex sensitivity (BRS), which when depressed is predictive of future cardiac events after myocardial infarction (MI). The main objective of this study was to determine whether exercise training improves BRS in patients with coronary artery disease.
Methods and Results—Ninety-seven male patients with and without a previous MI were recruited after myocardial revascularization surgery and randomized into trained (TR) or untrained (UTR) groups. TR patients underwent a residential exercise program at 85% of maximum heart rate (HRmax) consisting of 2 daily sessions 6 times a week for 2 weeks. Eighty-six patients (45 TR and 41 UTR) completed the study. BRS was assessed at baseline and at the end of the protocol by the spontaneous baroreflex method. The standard deviation of mean R-R interval (RRSD) was also assessed as a measure of heart rate variability. At baseline, there were no significant differences between TR and UTR patients in any variable. In TR patients, BRS increased from 3.0±0.3 to 5.3±0.7 ms/mm Hg (P<0.001), RRSD from 18.7±1.4 to 23.6±1.6 ms (P<0.01), and R-R interval from 792.0±15.5 to 851.3±20.5 ms (P<0.001). No significant changes occurred in UTR patients. Increases in BRS and RRSD were significant in patients either with or without a previous MI.
Conclusions—Exercise training increases BRS and heart rate variability in patients with coronary artery disease. Improved cardiac autonomic function might add to the other benefits of exercise training in secondary prevention of ischemic heart disease.
Key Words: reflex • heart rate • exercise • coronary disease
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Introduction |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Patients with extensive coronary artery disease are at risk for life-threatening arrhythmias and sudden death.1 It is well recognized that alterations in the neural control of the heart characterized by decreased vagal activity and relative sympathetic predominance play a major role in the occurrence of arrhythmic events during myocardial ischemia or infarction.2 3 4 5 6 7 More specifically, several animal studies have indicated that a depressed baroreflex sensitivity (BRS), an index of the reflex vagal control of the sinoatrial node, and a reduced heart rate variability (HRV), considered as a measure of the tonic vagal control of the heart,7 are associated with a greater risk for ventricular fibrillation during transient ischemia after myocardial infarction (MI).6 8 9 10 The unfavorable effect of a depressed BRS on ventricular arrhythmias during myocardial ischemia also extends to animals without prior MI.6 Clinical studies have clearly demonstrated that both BRS and HRV are reduced after MI11 12 13 and that BRS is markedly depressed during spontaneous episodes of transient myocardial ischemia14 and in patients without an MI who experienced out-of-hospital ventricular fibrillation.15 Finally, a recent large prospective trial has definitively indicated that a reduced BRS has prognostic value for cardiac mortality and cardiac events after MI,16 independent of other risk factors (eg, low ejection fraction and serious arrhythmias). An emerging concept from the above studies is that strategies that increase these indirect markers of autonomic activity might be an important target for intervention in coronary artery disease.
Exercise training, as a part of a comprehensive rehabilitation program, has been shown to produce beneficial effects in many cardiovascular diseases17 and to improve prognosis after MI.18 In conscious dogs with or without a healed MI, exercise training was able to increase BRS and HRV, effects associated with a protective action against ventricular fibrillation during myocardial ischemia.19 20 Small clinical studies seem to confirm the effectiveness of exercise training in improving some measures of HRV in post-MI patients.21 22 To date, there has been only 1 published study on the effect of exercise training on BRS in post-MI patients, and the results were not definitive.22 The effects of exercise training on cardiac autonomic function in coronary patients without previous MI have not been addressed.
The primary objective of the present study, therefore, was to determine whether a structured exercise training program improves BRS in coronary patients with or without a previous MI who had been referred to a formal rehabilitation program. The effect on HRV was also assessed.
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Methods |
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The study population consisted of patients with coronary artery disease referred after myocardial revascularization surgery to our cardiac rehabilitation center between January and December 1997. Patients had undergone CABG on the basis of symptomatic and/or abnormal findings on diagnostic procedures and arteriographically documented coronary artery disease. All patients came from the same cardiac surgery division, so that they had undergone the same surgical procedures and preoperative and postoperative clinical management.
Criteria for eligibility were male sex, in sinus rhythm, and
with left ventricular ejection fraction 
50%, as determined by
preoperative cardiac catheterization and by echocardiographic
examination before hospital discharge and at the rehabilitation center.
Exclusion criteria were age >70 years, coexisting valvular and/or
peripheral vascular diseases, concomitant endarterectomy,
contraindications to exercise stress testing, frequent atrial or
ventricular premature beats, conduction defects, insulin-dependent
diabetes, arterial blood pressure >160/90 mm Hg, pericarditis,
peripheral neuropathy, orthopedic or neurological limitations, and
perioperative MI or any serious postoperative complication.
The patients were admitted to the rehabilitation center during the first postoperative week, and after the initial screening, which included a 24-hour Holter recording, they were randomly assigned to a supervised, residential exercise training program (TR) or to an untrained group (UTR). Initially, 97 patients met the study criteria, but 7 dropped out from the study because of personal reasons (n=5) or intercurrent illness (n=2). Four patients were also excluded because of discomfort in breathing within the face mask that prevented measurements of gas exchange during the exercise stress test (n=2) or for unexpected frequent premature beats at the time of recordings for autonomic evaluation (n=2).
Eighty-six patients (45 TR and 41 UTR) completed the study.
In post-MI patients, the time elapsed after MI ranged from 9 years to 2
months. However, in 66% of patients, MI occurred in the last year
before the study. Clinical characteristics of the patients are
summarized in
Table 1
. Medications were not altered throughout the study.
All patients gave written informed consent to participate in this
study, which was approved by the Scientific and Ethical Committee of
the rehabilitation center.
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Protocol
Fourteen to 16 days after CABG, all patients
underwent a functional (symptom-limited) incremental exercise test in
the upright position on a bicycle ergometer (Corival 400, Lode) with
monitoring of gas exchange (CPX). Exercise started with 1 minute of
unloaded pedaling and increased by 20 W every 2 minutes. A 12-lead ECG
and oxygen consumption (Vmax 29 C, SensorMedics) were recorded
continuously. At the end of the study, all patients repeated the
symptom-limited exercise test.
BRS and HRV Assessment
BRS and HRV assessment was made the day before CPX
and repeated after the training period. The patients were studied in
the morning 2 hours after breakfast. Patients were studied at rest
while supine in a quiet room at ambient temperature and were asked to
relax and to avoid sleeping or talking. Recordings were begun after 10
to 15 minutes of acclimatization and were continued for 10 minutes.
Patients were connected to an analogue multichannel signal conditioner
and amplifier/filter (Marazza). The ECG signal was recorded from a
precordial chest lead. Arterial blood pressure was continuously and
noninvasively measured by Finapres (Finapres 2300, Ohmeda). This device
provides accurate estimates of changes of intra-arterial pressure
during laboratory tests, including the BRS testing used in the present
investigation.23 The
analogue signals were sampled at 300 Hz per channel and stored on hard
disk for subsequent analyses.
BRS was dynamically assessed by the spontaneous baroreflex
method.24 Details of
this technique have been described
previously.25 26 27
Briefly, beat-by-beat time series of systolic arterial pressure (SAP)
and R-R interval are scanned by a computer to identify sequences of 3
consecutive beats in which SAP and R-R interval change in the same
direction (either increasing or decreasing). A linear regression is
applied to each individual sequence, similar to the technique that uses
bolus injections of phenylephrine, and the mean slope of the SAP/R-R
interval relationship, obtained by averaging all slopes computed within
a given test period, is calculated and taken as a measure of
spontaneous BRS for that period. This method allows a quantification of
the BRS-cardiac reflex sensitivity at the current prevailing levels of
arterial pressure and R-R interval and reflects vagally mediated
baroreflex
responses.24 28
The time-domain measure of HRV considered in the present study was the standard deviation of mean R-R interval (RRSD).
Exercise Training Program
All patients resided at the rehabilitation center for
a period of 3 weeks. Cardiac rehabilitation regimens lasting 2 to 4
weeks for patients in residential programs after a coronary event are
standard in the Italian National Health Service. Before CPX, the
program consisted of 2 daily sessions of calisthenics and walking.
After CPX, the training program consisted of 2 daily sessions of 30
minutes of stationary cycling 6 times a week for 2 weeks (24 sessions
overall) combined with calisthenics. Training intensity was graded
according to 85% of the maximum heart rate (HRmax) attained in the
initial CPX (or to 75% of HRmax in patients older than 65 years).
Heart rate (HR) was tracked by a Polar chest-belt HR monitor (Polar
Electro Oy) that simultaneously controlled the computer-driven workload
of the bicycle ergometer (Bikerace, Technogym) to maintain the target
HR.
Subjects in the control group continued to perform walking and calisthenics with the same daily schedule as the TR group for 2 weeks as inpatients. The activity for the control group was not designed to improve cardiovascular performance. All sessions were held under the supervision of a cardiologist.
Statistical Analysis
Differences in baseline characteristics between TR
and UTR groups were evaluated by 
2 and
unpaired t tests. Within-group changes in the reported
variables were evaluated by paired t test or Wilcoxon
signed rank test for nonnormally distributed variables. Between-group
comparisons were performed by unpaired t tests and
Mann-Whitney rank sum test. Relations between variables were assessed
by Pearson product-moment correlation. Data were expressed as mean±SE
unless otherwise specified. Statistical significance was assumed at
P<0.05.
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Results |
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There were no significant differences in baseline characteristics between TR and UTR patients with respect to all variables, including peak
O2, arterial
pressure, R-R interval, RRSD, and BRS
(Tables 1
and 2).
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Exercise training resulted in a significant increase in peak
O2
(Table 2). A small increase in peak
O2 was also
observed in the UTR group and can be explained in part by normal
recovery from surgery and by the fact that our controls performed some
amount of daily physical activity. However, the magnitude of
O2 increase
was significantly and markedly greater in the TR group (181.3±27.2
versus 73.9±18.0 mL/min, P=0.001). In TR patients,
resting R-R interval was significantly increased by 7%, BRS by 73%,
and RRSD by 26%. No significant changes in these variables were
observed in UTR patients
(Table 2).
No correlations were found between peak
O2 and BRS
either at baseline for the study population as a whole
(r=0.18, P=0.10) or after training in
the TR group (r=0.09, P=0.55).
Similarly, no relationships were found between peak
O2 and RRSD
at baseline in the whole population or after training in the TR group
(r=0.15, P=0.16 and
r=0.11, P=0.49,
respectively).
No significant differences were observed in baseline BRS and
RRSD between MI and non-MI patients in the overall population. BRS was
3.4±0.4 versus 3.0±0.3 ms/mm Hg and RRSD was 18.0±1.3 versus
17.9±1.3 ms in MI and non-MI patients, respectively. Mean age did not
differ significantly between MI and non-MI patients (59.0±6.6 versus
58.9±8.5 years), nor did the number of coronary vessels with a
critical stenosis (2.4±0.7 versus 2.6±0.6). BRS increased
significantly in both MI and non-MI trained patients, as did RRSD
(Figure),
and the magnitude of the increase in both variables did not differ
significantly between the 2 groups (2.8±1.0 versus 1.7±0.5 ms/mm Hg,
P=0.53 and 5.4±2.3 versus 4.3±1.8 ms,
P=0.72, for BRS and RRSD, respectively).
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P<0.01,
and 
P<0.001 vs baseline. Rehab indicates
rehabilitation.No significant cardiovascular events occurred during the training sessions.
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Discussion |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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The present study indicates that a structured exercise training program is able to enhance BRS and increase HRV in patients with coronary artery disease. The relevance of this finding should be placed in the context of the growing evidence indicating the adverse effect of a depressed vagal cardiac modulation and the protective role exerted by high vagal activity in the setting of ischemic heart disease.
Animal studies have clearly indicated that the presence of depressed vagal reflexes and enhanced sympathetic activation is associated with a greater risk for life-threatening arrhythmias during myocardial ischemia.6 8 9 10 Clinical studies confirmed the adverse effect of impaired vagal modulation by showing that both BRS and HRV are reduced early after MI11 12 13 and that this has an independent prognostic value.16 Moreover, a depressed BRS may play a role in the occurrence of malignant arrhythmias, even long after MI.29 30
Conversely, interventions capable of increasing vagal activity exert a protective effect against ischemia-related arrhythmias.31 32 Among these interventions, exercise training has been shown to increase both BRS and HRV and to prevent ventricular fibrillation, concomitantly improving cardiac electrical stability, in conscious dogs with and without healed MI.19 20 Thus, exercise training might be an effective nonpharmacological tool to increase the vagal contribution to autonomic control of the heart in patients with coronary artery disease, as has been observed in other pathological states.33 34 Indeed, recent studies have suggested the effectiveness of exercise training in improving HRV in post-MI patients,21 22 and this was confirmed by the present investigation. However, the potential for exercise training to improve BRS in patients with coronary artery disease had not been clearly established. One small study22 reported an improvement in BRS after exercise training in post-MI patients, but the lack of an untrained control group prevented a definitive conclusion from being reached. Thus, this is the first randomized, controlled study obtained in a relatively large population showing that exercise training results in marked enhancement of both BRS and HRV in patients with coronary artery disease. This is important information, because BRS and HRV reflect different, although possibly related,35 aspects of the autonomic modulation of the heart and are not clinically redundant.16 36 Although both BRS and HRV effectively discriminate individuals at high and low risk for cardiac mortality,16 experimental and clinical studies have indicated that BRS is more useful in the prediction of future events. In an animal model, analysis of BRS before MI was able to predict outcome during ischemic episodes that occurred after MI, whereas HRV was not.6 10 Similarly, BRS but not HRV was reduced in patients who developed malignant arrhythmias long after MI.29 30 Thus, the increase in BRS induced by exercise training, reflecting more powerful vagally mediated baroreflex responses, might result in a condition less favorable for the development of malignant arrhythmias in the event of ischemic episodes by conferring protection against increases in sympathetic activity.4 19 20
The results of the present study also indicate that the improvement of BRS associated with exercise training is not limited to patients with prior MI but extends to coronary patients without MI, in whom measures that could reduce the risk of subsequent lethal events might be of paramount importance.1 37 The potential clinical relevance of increasing BRS in coronary patients without MI is also outlined by the observation that a depressed BRS present before MI affected the susceptibility to ventricular fibrillation during myocardial ischemia that occurred after MI in an animal model of sudden death.6
No significant differences were observed in baseline BRS between patients with and without a previous MI. This finding could be explained by the severity of coronary artery disease, which was similar in MI and non-MI patients, as evaluated by the number of vessels with critical stenosis, because the extent of coronary narrowing negatively affects BRS.11 12 38
Our study confirms the improvement in cardiovascular
performance induced by exercise, and the 14% increase in peak
O2 obtained
after this short-term yet intensive, concentrated endurance exercise
training is in line with expectations. However, no relationship was
observed between changes in functional capacity and indexes of
autonomic function after training, a finding that is in line with the
hypothesis that the mechanisms responsible for the improvements may
differ for each
variable.39 The
mechanisms through which exercise training affects these markers of
cardiac vagal modulation are still unclear and cannot be defined by the
present investigation. They may involve adaptations in peripheral and
central neural pathways, although modifications in the responsiveness
of the heart might also contribute.
Some possible limitations of the present investigation deserve comment. The first is the generalization of the reported effects to other coronary patient populations, namely, those who have not undergone CABG. However, it is reasonable to speculate that the benefits of exercise training should also extend to patients who have not undergone CABG but are eligible for a formal exercise training program. Moreover, there are no data indicative that CABG per se positively affects BRS and HRV in patients without MI or in the recovery phase after MI. Consistent with this assumption is the lack of spontaneous increase in BRS and HRV in the control group. In any case, the patients of the present study are representative of a large population of ischemic patients for whom cardiac rehabilitation is highly recommended40 and who could benefit from improved cardiac autonomic function.
Second, we do not know whether improving markers of autonomic activity by exercise actually affects the outcome of patients with coronary artery disease. The present study was not designed for this purpose. Instead, it was aimed at addressing the question of whether exercise training improves autonomic markers that have been shown to carry adverse effects and negative prognosis in ischemic heart disease. The answer to this question is affirmative. In fact, the increase in BRS is in a direction that has been associated with a better outcome in coronary patients.11 16 29 30 However, the potential for exercise-induced enhancement of BRS and HRV to improve the risk profile in coronary artery patients remains to be demonstrated. This would require a large, multicenter trial. Nevertheless, among the many beneficial effects of exercise training in secondary prevention of ischemic heart disease, improvement in markers of cardiac autonomic function should also be considered.
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Acknowledgments |
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The authors wish to thank the physical therapist, Oriana Moroni, for her care of the patients. We also thank the cardiac surgeons of Policlinico Universitario Agostino Gemelli-Università Cattolica del Sacro Cuore, Roma, for their cooperation.
Received June 27, 2000; revision received July 7, 2000; accepted July 7, 2000.
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 M.-W. Tsai, W.-C. Chie, T. B. Kuo, M.-F. Chen, J.-P. Liu, T. H.-H. Chen, and Y.-T. Wu Effects of Exercise Training on Heart Rate Variability After Coronary Angioplasty Physical Therapy, May 1, 2006; 86(5): 626 - 635. [Abstract] [Full Text] [PDF]
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 Z. Lenard, P. Studinger, B. Mersich, G. Pavlik, and M. Kollai Cardiovagal autonomic function in sedentary and trained offspring of hypertensive parents J. Physiol., June 15, 2005; 565(3): 1031 - 1038. [Abstract] [Full Text] [PDF]
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 J. Mimura, F. Yuasa, R. Yuyama, A. Kawamura, M. Iwasaki, T. Sugiura, and T. Iwasaka The Effect of Residential Exercise Training on Baroreflex Control of Heart Rate and Sympathetic Nerve Activity in Patients With Acute Myocardial Infarction Chest, April 1, 2005; 127(4): 1108 - 1115. [Abstract] [Full Text] [PDF]
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 A. S. Leon, B. A. Franklin, F. Costa, G. J. Balady, K. A. Berra, K. J. Stewart, P. D. Thompson, M. A. Williams, and M. S. Lauer Cardiac Rehabilitation and Secondary Prevention of Coronary Heart Disease: An American Heart Association Scientific Statement From the Council on Clinical Cardiology (Subcommittee on Exercise, Cardiac Rehabilitation, and Prevention) and the Council on Nutrition, Physical Activity, and Metabolism (Subcommittee on Physical Activity), in Collaboration With the American Association of Cardiovascular and Pulmonary Rehabilitation Circulation, January 25, 2005; 111(3): 369 - 376. [Abstract] [Full Text] [PDF]
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I. Fietze, D. Romberg, M. Glos, S. Endres, H. Theres, C. Witt, and V. K. Somers Effects of positive-pressure ventilation on the spontaneous baroreflex in healthy subjects J Appl Physiol, March 1, 2004; 96(3): 1155 - 1160. [Abstract] [Full Text] [PDF]
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 A. Loimaala, H. V. Huikuri, T. Koobi, M. Rinne, A. Nenonen, and I. Vuori Exercise Training Improves Baroreflex Sensitivity in Type 2 Diabetes Diabetes, July 1, 2003; 52(7): 1837 - 1842. [Abstract] [Full Text] [PDF]
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 P. A. Lanfranchi and V. K Somers Arterial baroreflex function and cardiovascular variability: interactions and implications Am J Physiol Regulatory Integrative Comp Physiol, October 1, 2002; 283(4): R815 - R826. [Abstract] [Full Text] [PDF]
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M. T. La Rovere, C. Bersano, M. Gnemmi, G. Specchia, and P. J. Schwartz Exercise-Induced Increase in Baroreflex Sensitivity Predicts Improved Prognosis After Myocardial Infarction Circulation, August 20, 2002; 106(8): 945 - 949. [Abstract] [Full Text] [PDF]
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F. Iellamo, J. M. Legramante, F. Pigozzi, A. Spataro, G. Norbiato, D. Lucini, and M. Pagani Conversion From Vagal to Sympathetic Predominance With Strenuous Training in High-Performance World Class Athletes Circulation, June 11, 2002; 105(23): 2719 - 2724. [Abstract] [Full Text] [PDF]
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J.-L. Liu, J. Kulakofsky, and I. H. Zucker Exercise training enhances baroreflex control of heart rate by a vagal mechanism in rabbits with heart failure J Appl Physiol, June 1, 2002; 92(6): 2403 - 2408. [Abstract] [Full Text] [PDF]
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G. E. Billman Aerobic exercise conditioning: a nonpharmacological antiarrhythmic intervention J Appl Physiol, February 1, 2002; 92(2): 446 - 454. [Abstract] [Full Text] [PDF]
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 B. M. Curtis and J. H. O'Keefe Jr Autonomic Tone as a Cardiovascular Risk Factor: The Dangers of Chronic Fight or Flight Mayo Clin. Proc., January 1, 2002; 77(1): 45 - 54. [Abstract] [PDF]
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