Japanese Circulation Society

CLINICAL INVESTIGATIONS

Jpn Circ J 2000; 64:809-813

Effects of Physical Training on the Recovery of theAutonomic Nervous Activity During
Exercise After Coronary Artery Bypass Grafting
Effects of Physical Training After CABG

Junichiro Takeyama, MD*; Haruki Itoh, MD; Makoto Kato, MD;

Akira Koike, MD; Keiichi Aoki, MD; Long Tai Fu, MD;
Hiroshi Watanabe, MD; Masatoshi Nagayama, MD*; Takashi Katagiri, MD*

Analysis of heart rate variability (HRV) can identify patients at risk of sudden cardiac death after myocardial
infarction. The present study examined the effect of 2 weeks of supervised aerobic exercise training on the recov
ery of the autonomic nervous activity, exercise capacity, and cardiac output (CO) after coronary artery bypass
grafting (CABG). Twenty-eight patients were randomly divided into the training group or the control group andperformed exercise tests at 1 week, 3 weeks, 3 months, 6 months and 1 year after CABG. The HRV was measured,and the high-frequency component of HRV was used as an index of parasympathetic nerve activity (PNA); theplasma norepinephrine concentration (NE) was used as an index of sympathetic nervous activity. Cardiac output
was also measured. In the training group, peak VO2, peak CO and PNA during exercise had improved at 3 weeks,
but there was no improvement in these indices in the control group. NE decreased 1 week after CABG in bothgroups. These results indicate that physical training soon after CABG improves not only the exercise capacity,
but also PNA. (Jpn Ore J 2000; 64: 809-813)
Key Words: Aerobic exercise training; Coronary artery bypass grafting; Heart rate variability; Norepinephrine

Analysis of heart rate variability (HRV) is a noninvasive
method of evaluating autonomic nervous systemk effects on the heart1'2 It can identify patients at
risk of sudden cardiac death after myocardial infarction(MI) independently of other risk factors, including clinicalfeatures, ventricular arrhythmias, ventricular late potentials
and the left ventricular ejection fraction (LVEF)?-5
Coronary artery bypass grafting (CABG) is an establishedtreatment in patients with ischemic heart disease, but inpost-CABG patients the status of sympathetic nervous
activity (SNA) and parasympathetic nervous activity (PNA)
is not fully understood. We used HRV analysis to investi
gate the effects of short-term supervised aerobic exercise
training on the autonomic nervous system, exercise capacity
and cardiac output (CO) at rest and during exercise in postCABG patients. We also examined the difference between
the time course of the recovery of SNA and that of PNA.

Methods
The study was approved by the Ethics Committee of the
Cardiovascular Institute Hospital and all subjects gave
informed consent.

Patients (Table 1)
We studied 28 consecutive cases from the Cardiovascular
Institute Hospital (26 men, 2 women; age, 60.4±7.8 years)
in which CABG provided complete revascularization. The
study population included 8 patients with angina pectorisand 20 patients with previous MI. All subjects underwent abaseline cardiopulmonary exercise test 1 week after CABG
and were then randomly assigned to either the training orcontrol group.
The training group consisted of 13 men (3 with angina
pectoris and 10 with previous MI) aged 58.8±6.3 years. The
mean number of grafts was 2.8±0.8, and the mean LVEF
measured by left ventriculography performed before CABG
was 62.5±12.7%. The control group consisted of 13 men
and 2 women, (5 patients with angina pectoris and 10 withprevious MI) aged 61.7±8.7 years. The mean number ofgrafts was 2.7±1.1, and the mean LVEF before CABG was

Ibble 1

Clinical Characteristics

Mean age (years)(Received February 17, 2000; revised manuscript received July 19,
2000; accepted July 21,2000)
Cardiovascular Institute Hospital and *Third Department of Internal
Medicine, Showa University School ofMedicine, Tokyo, Japan
Mailing address: Junichiro Takeyama, MD, Third Department of Inter
nal Medicine, Showa University School of Medicine, 1-5-8 Hatanodai,
Shinagawa-Ku, Tokyo 142-8666, Japan

Japanese Circulation Journal

M/F

AP/previous Ml
No. ofgrafts
LVEF(%)

Training group

Control group(n=13)(n=15)

58.8±6.3
13/0

61.7±8.7
13/2
5/10

3/10

2.8±0.862.5±12.7

p valueNSNS

2.7±1.1NSNS

61.6±1J.1

NS

Values are expressed as the mean ± SD.
AP, angina pectoris; LVEF, left ventricular ejectionfraction; MI, myocardial
infarction.

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810

All subjects were stable and were being treated with
diuretics, nitrates, Ca antagonists and anti-coagulants.
Angiotensin-converting enzyme inhibitors were used in 6
patients in the training group and in 8 patients in the control
group. We excluded patients receiving /?-blockers and thosewith arrhythmias (atrial fibrillation, frequent extrasystole).
There were no significant differences in the age, number ofgrafts, LVEF or in the use of angiotensin-converting enzyme
inhibitors between the 2 groups.
ProtocolThe subjects underwent cardiopulmonary exercise tests
with expired gas analysis and measurement of CO at 1
week after surgery, when they no longer had a fever andwere able to walk at least 200 m without symptoms orsignificant ECG changes.
All patients in both groups began a rehabilitation program
1 week after CABG. In the training group, the exercise
program consisted of 30min of training on a cycle ergometer
twice daily for 2 weeks. The exercise training was performedat the anaerobic threshold that was determined 1 week after

CABG. One week later, the exercise test for a new exercise
program was done, and patients did the training based on
the new prescription for 1 more week. The patients in thecontrol group were asked to walk 200 m 3 times daily; thewalking distance was increased up to 500 m within 2 weeks.
After 2 weeks of rehabilitation in the hospital, all patients
underwent an exercise test and were then discharged. Noneof the subjects followed any special physical training
program after discharge from the hospital.
Cardiopulmonary exercise tests were performed to evaluate the exercise capacity, CO and autonomic nervous
activity at 1 week, 3 weeks, 3 months, 6 months and 1 year
after surgery.
Cardiopulmonary Exercise Test
Cardiopulmonary exercise tests were performed with anelectromagnetically controlled cycle ergometer (CPE-2000,
MedGraphic Co, Minneapolis, MN, USA). After restingfor 4min on the ergometer, the subject began exercisingwith a 4-min warm-up at 20 W at 60rpm; the work rate wasincreased by 1W every 6 s until exhaustion. A 12-lead

HRV spectra were analyzed, we screened 3 min of HRV
data, excluding the first minute from the rest period and
20 W of the warm-up period, for extra or missing beats that
could affect the results of spectral analysis. Abnormalintervals were corrected by either omitting (those <300ms)
or inserting beats (those with double or triple length ofpreceding intervals)? with less than 2% of the total beats
being corrected manually in this way. Spectral HRV isexpressed as a low-frequency (LF: 0.04-0.15 Hz) component
and a high-frequency (HF: 0.15-0.80Hz) component; inthis study the power of the HF component was used as anindex of PNA.
Assay ofNorepinephrine (NE)
Blood samples for NE were obtained at rest and the end of
the 4-min warm-up. Samples were transferred immediately
into ice-cold tubes containing ethylenediamine tetraacetic
acid and centrifuged at 4°C. Plasma was separated andstored at -80°C until assayed. The plasma concentration ofendogenous NE was determined using an HLA-725CA
automated catecholamine analyzer (Tosoh, Tokyo, Japan),which consists of a high-performance liquid chromatography column with fluorescence detection using 1,2-diphenylethylenediamine as the fluorescence derivation reagent. The
plasma NE concentration was used as an index of SNA.
Measurement of CO
Cardiac output was measured at rest and at peak exercise

by the dye dilution method with indocyanine green? using

an ear photoelectric transducer. Analysis was performed bya special purpose computer (Cardiac Output Computer
MLC-4200, Nihon-Koden, Tokyo, Japan), a method that is

considered comparable to measuring CO during exercise.10

Statistical Analysis
Data are expressed as the mean±SD. The statisticalsignificance of differences were analyzed with unpaired t
test and 2-way analysis of variance (ANOVA) followed by
Tukey-Kramer's test for between-group comparisons andDunnett's test for individual comparisons of values at 1 week
versus those at 3 weeks, 3 months, 6 months, and 1 year. A pvalue less than 0.05 was considered statistically significant.

ECG and the HR were monitored throughout the test using
the Stress Test System (ML-5000, Fukuda Denshi, Tokyo,
Japan). The cuff blood pressure was measured every minutewith an automatic indirect manometer (Stress Test Blood
Pressure Monitor STBP-780, Colin Denshi, Aichi, Japan).
Respiratory gas analysis was performed using the Aero
Monitor AE-280 (Minato Medical Science, Osaka, Japan),which consists of a zirconia 02 analyzer, an infrared CO2
analyzer and a hot-wire spirometer. The system was carefully
calibrated before each study and O2 uptake (VO2), CO2
output (VCO2), and expired tidal volume were continuously
measured on a breath-by-breath basis.
The anaerobic threshold was determined from the gas
exchange data by the V-slope method6 using softwaredeveloped at our institute that determines the turning pointof the VO2-VCO2 relation curve using 2 linear regression
lines. The peak O2 was denned as the mean VO2 during thelast 30 s of each test.
Power Spectral Analysis and HRV
HRV data were analyzed by fast Fourier transformation.
Spectral analysis of HRV was performed according to themethods described by Yamamoto and Hughson? Before theResults
None of the 28 patients had any major complications,such as worsening of heart failure, worsening of ischemia,
sudden cardiac death or other cardiac events, during thestudy.
Exercise Capacity

The anaerobic threshold increased significantly in the
training group at 3 weeks after surgery compared with 1
week after surgery (from 10.6±1.6 to 11.9±1.6ml-min-1kg-1, p=0.04). In the control group, the anaerobic thresholdshowed no increase at 3 months after surgery, and the eventual increase did not become significant until 6 months after
surgery (from 11.6±1.3 to 13.1±1.3ml-miirl-kg-|,p=0.01).
The change from baseline was significantly greater in the
training group than in the control group at 3 weeks after

surgery (1.3±1.2 vs -0.2±0.9ml-miir1-kg-1, p=0.02).

The peak VO2 increased significantly at 3 weeks after

surgery compared with 1 week after surgery in the training

group only (from 13.1±1.7 to 16.1±2.0ml*min-1-kg-|1
p=0.001). The control group exhibited a significant increase
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Exercise and Recovery of SNA and PNA

Table 2811

Changes in the Anaerobic Threshold, Peak VOj and Body Weight
1 week3 weeks

3 months

6 months

I year

14.4+2.1*
13.2±0.9*

Anaerobic threshold (ml-minr1 -kg-1)
Training groupJ0.6±1.6

H.9±l.6*13.2±1.6*

13.6*1.0*

Control group

11.6*13U.4±L512.5±1.9

13.1*1.3*

Training group13.1±1.719.8±2.8*t

13.7±2.5

16.1±2.0*
14.8±2.3

18.9±2.5*

Control group17.2±2.8*17.6±2.4*

62.3+6.8

64.0i6.4
66.7110.264.9±6.464.5±10.9

64.2+7.0

59.8±8.6

3 months

6 months

1 year

4.32+0.38
4.59+0.40

4.24+0.27

14.4+3.7*

15.0+3.5*
13.1*1.6

PeakVCh(mlmitr>kg-*)

21.7+2.6*
18.0+2.0*

Body weight (kg)Training group
Control group64.3±6.3
63.2±10.7

65.3*12.1

Values are expressed as the meaniSD. *p<0.05 vs 1 week, fp<0.05 vs Control group.

Table 3

Changes in the Cardiac Output (CO) at Rest and Peak CO
1 week3 weeks

3.94±0.63
4.48±0.80

4.61*0.37

4.33+0.41

4.41+0.71

4.43+0.53

10.6+2.4

13.4+2.1*
12.0+2.5

13.7+2.7*
13.4+2.0

CO at Rest
Training group

Control group
Peak CO
Training group
Control group

11.9+2.8

13.1+2.4431±0.56

Values are expressed as the mean±SD, *p<0.05 vs 1 week. *p<0.05 vs Control group.

Table 4

Changes in the Plasma Norepinephrine (NE) Concentration and High-Frequency (HF) Component
1 week3 weeks

3 months

6 monthslyear

618*195
536*184

358*90*370*168*

381*176*

327*86*315*108*

329*100*

374*126*

24.8*14.7
20.4*13.9

35.3*22.3
35.0*17.0

42.4*14.3*
43.0*9.2*

50.9*30.6*
46.6*19.0*

70.6*52.9*
52.0*16.7*

840+380

470*90*550*310*430*210*550*230*

380*150*

360*150*510*200*

21.0*19.9*
9.4*8.7

31.5*22.7*t

32.1±24.7*t

18.5*12.7*

17.3+15.4

At restNE(pg/ml)
Training group

Control group
HF component (ms2)Training group
Control group
At 20 W ofconstant load exercise
NE(pg/ml)
Training group
Control group
HF component (ms2)
Draining group
Control group980*490
9.6*6.2

8.8*7.5500*0.18*

333*115*36.0*20.7*f
19.4*17.6*

Values are expressed as the mean*SD. *p<0.05 vs 1 week, *p<0.05 vs Control group.

in the peak VO2 at 3 months after surgery compared with 1
week after surgery (from 13.7±2.5 to 17.2±2.8ml-min-1kg~l, p=0.003). The change from baseline was greater in the
training group than hi the control group at all measurement
points.
There were no significant body weight changes throughout the study in either group (Table 2).

Plasma NE Concentration
The plasma NE concentration at rest decreased early after
surgery (at 3 weeks) in both groups; there was no significant
difference in the change in the NE concentration between
the groups. In the overall study population, the plasma NE
concentration decreased significantly at 3 weeks after
surgery (1 week=565±192,3 weeks=365±141* 3 months=

377±150* 6 months=320±100* 1 year=331±108*pg/ml,

CO
The CO at rest showed no significant increase from 1
week to 1 year after surgery in either group and there wasno significant difference between the groups. The peak CO
increased significantly from 1 week to 3 weeks after surgery(from 10.6±2.4 to 13.4±2.1L/min, p=0.01) and increasedslightly thereafter in the training group. The control group
showed no significant increase in the peak CO from 1 week
to 1 year after surgery (Table 3). The change in CO frombaseline was significantly greater in the training group thanin the control group at 3 weeks after surgery (2.8±2.2 vs*p<0.05 vs 1 week).
The plasma NE concentration at 20 W of constant load
exercise showed the same pattern as that of at rest In theoverall study population, the plasma NE concentration
decreased significantly at 3 weeks after surgery (1 week=
917±450, 3weeks = 509±236* 3 months = 494±225* 6months=442±177* 1 year=439±189*pg/ml, *p<0.05 vs 1
week). The age-matched normal value (21 men and 3
women) of the NE concentration at 20 W of constant load
exercise was 29Q±110pg/ml in our laboratory.

0.1±1.5L/min,p=0.02).

HRV

The HF component at rest increased significantly at 3
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812
Table 5

Changes in the Respiratory Rate (RR) and Tidal Volume (TV)
1 week3 weeks

3 months

6 months

1 year

20.413.922.3±4.0

19.914.1

19.314.0

19.712.5

19.113.7

19.313.5

18.712.5*

18.113.6*

19.212.0

6I7.5±86.7
594.1±107.2

636.71115.6
581.71117.8

625.7±138.5
601.0192.5

624.41120.9

655.71106.2
607.31101.0

23.914.2

21.613.3
23.012.5

22.314.1
22.616.7

22M3.323.413.6
1036.31129.9
1004.91142.8

1021.81170.4
1033.11158.2

1121.51226.0
1096.41128.5

1160.01157.5
1065.41150.5

At restRR
Training group

Control groupTVl V

Training group

Control group635.5187.1

At 20 W ofconstant load exercise
RR
Training group
Control group24.9±4.1
25.914.6.

23.113.8

TV

Training group

Control group1005.11155.5
993.8U39.3

Values are expressed as the meant SD. *p<0.05 vs 1 week, *p<0.05 vs Control group.

months after surgery compared with 1 week after surgery inboth groups (from 24.8±14.7 to 42.4±14.3ms2 in the train
ing group, p=0.02; from 20.4±13.9 to 43.0±9.2ms2 in thecontrol group, p=0.013). There was no significant difference
between the groups. In the overall study population, the HF
component increased significantly at 3 weeks after surgery(1 week=21.4±14.6, 3 weeks=35.1 ±19.4* 3 months=
42.7±12.0* 6 months=49.1±26.4* 1 year=61.6±40.2*ms2,*p<0.05 vs 1 week). The age-matched normal value (18men and 2 women) of the HF component at rest determinedin our laboratory was 159.8±96.0ms2.
The HF component at 20 W of constant load exercise
increased significantly at 3 weeks after surgery comparedwith 1 week after surgery in the training group (from9.6±6.2 to 21.0±19.9ms2, p=0.04). In the control group, the
HF component did not increase significantly until 3 months
after surgery (from 8.8±7.5 to 18.5±12.7ms2, p=0.04)(Table 4). The improvement from baseline was smaller inthe control group than in the training group at all measure
ment points. In the overall study population, the HF compo
nent increased significantly at 3 months after surgery (1week=9.2±8.2,3 weeks=14.9±13.0,3 months=24.3±19.0*

6months=24.3±21.6* 1 year=26.4±20.7*ms2, *p<005 vs

1 week). The age-matched normal value (18 men and 2
women) of the HF component at 20 W of constant load
exercise determined in our laboratory was 74.5±56.3 ms2.

Discussion
A decrease in PNA in patients with ischemic heart disease
may be associated with sudden cardiac death, which makes
PNA a prognostic marker in these patients? SNA reflects
the severity of heart failure and is closely associated withprognosis.11 The present study assessed SNA and PNA at
rest and during 20 W of constant load exercise in patients
after CABG by measuring the plasma NE concentrationand HRV, and previous data supported the concept thatphysical training improves not only the exercise capacity
but also PNA.

The measurement of HRV during exercise has beenreported as useful for evaluating the autonomic nervous
function during low-intensity exercise.12-13 In the present
study, the ratio of the LF to HF components of HRV, which
has been shown to be an index of SNA,14 showed no association with the plasma NE concentration, and this may havebeen partly a result of the short sampling period.

It has also been reported that the HF component is influ
enced by the ventilatory pattern;15 that is, a higher respiratory rate reduces the HF component, and a larger tidal
volume increases it. In the present study, the respiratory
rate tended to decrease slightly and the tidal volume tended
to increase slightly at rest and at 20 W of exercise in bothgroups (Table5); there were no significant differences inthese parameters between the 2 groups at any measurement
point. The ventilatory pattern might affect the value of the
HF component, but the difference in the HF component
between the present groups was not because of the ventila
tory pattern.

The time courses of the recovery of SNA and PNA weredifferent. In the overall study population, SNA improved
soon after surgery, whereas PNA improved at 3 months
after surgery.
Arterial and cardiopulmonary baroreflex control, both ofwhich are reduced in patients with acute MI, gradually

recovers during the chronic phase.16-17 Exercise training inyoung athletes increases the cardiopulmonary baroreflex

control,18 and PNA has been shown to be decreased insedentary healthy subjects!9-20 These results suggest thataerobic exercise training soon after CABG could correct
the autonomic imbalance observed after this operation,
probably by improving the baroreflex sensitivity. We also
speculate that the effects of exercise training on autonomic
nervous activity may not differ between the diseased state
and the state of deconditioning without disease; however,these speculations will have to be tested in future studies.
In the training group the anaerobic threshold, peak VO2,
HF component during exercise and peak CO increased
significantly at 3 weeks after surgery compared with thebaseline values, whereas in the control group these indices
did not improve. Moreover, the improvements of the peakVO2 and the HF component in the training group persisted
for months. The reason for this is unknown, but it is possiblethat the physical training before discharge encouraged
patients to continue exercising after they left the hospital.
No significant difference was noted between the groups inthe change of the plasma NE concentration. The aerobic
exercise training did not affect the recovery of SNA, eventhough SNA was activated during exercise.
We conclude that aerobic exercise training early after
CABG was associated with early and long-term improvements in exercise capacity and PNA during exercise without
affecting the recovery of SNA. The present data also indicate
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Exercise and Recovery of SNA and PNA

813

that SNA improved soon after surgery, but PNA recovered
later.

9.

Acknowledgments

10.

We thank Mr Yoshio Nakamurafor technical assistance in measuring
and evaluating HRV, and Mr Tokujiro Ohuchi and Mr Yuji Kawamoto forstatistical assistance. We also thank Mr Akihiko Tajima, Mrs Naomi
Harada and Miss Tomoko Maedafor technical assistance in performing
the cardiopulmonary exercise tests.

11.

12.

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