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Effects of endurance training on resting and

post-exercise cardiac autonomic control

Article in Medicine & Science in Sports & Exercise · October 2001

DOI: 10.1097/00005768-200109000-00012 · Source: PubMed

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Effects of endurance training on resting and
post-exercise cardiac autonomic control
KENTA YAMAMOTO, MOTOHIKO MIYACHI, TAKESHI SAITOH, AKIRA YOSHIOKA, and SHO ONODERA
Department of Health and Sports Sciences, Kawasaki University of Medical Welfare, 288 Matsushima, Kurashiki,
Okayama, JAPAN

ABSTRACT
YAMAMOTO, K., M. MIYACHI, T. SAITOH, A. YOSHIOKA, and S. ONODERA. Effects of endurance training on resting and
post-exercise cardiac autonomic control. Med. Sci. Sports Exerc., Vol. 33, No. 9, 2001, pp. 1496 –1502. Purpose: Endurance training
induces reductions in both resting and postexercise heart rate (HR). If adaptation in cardiac autonomic regulation is a contributing factor
in these reductions, changes in cardiac autonomic nervous system (ANS) should correspond to those in HR during an endurance-
training program. We investigated the changes in resting and postexercise HR variabilities (both in the time and frequency domain)
over a 6-wk training program. Methods: HR variability was measured five times in an endurance-training group (N ⫽ 7) and four times
in a control group (N ⫽ 5) during the course of study. Results: Endurance training decreased HR and increased indices of
parasympathetic modulation measured both at rest and during postexercise recovery periods. Noteworthy is that no changes in either
HR or indices of ANS modulation measured during postexercise recovery periods were detectable after the first 7 d of the study despite
continued changes in resting HR and indices in ANS modulation measured between the 7th and 42nd days of the endurance-training
program. Conclusions: The study demonstrates that with endurance-training changes in cardiac ANS modulation partly contribute to
a decrease in HR at rest and during postexercise recovery period, and that adaptation of the cardiac autonomic control occurs sooner
in immediate postexercise periods than at rest. Key Words: HEART RATE VARIABILITY, BRADYCARDIA, AUTONOMIC
NERVOUS SYSTEM, ADAPTATION

I
t is well known that endurance training induces brady-
cardia: reduction in heart rate (HR) at rest (5). Many
previous studies have suggested that bradycardia at rest
may be caused by decreased cardiac sympathetic modula-
tion and increased cardiac parasympathetic modulation
(5,10,12,27,28). On the other hand, there are very few
studies on the effects of endurance training on the cardiac
autonomic control measured during a postexercise recovery
period as opposed to studies done at rest (10). Darr et al. (9)
reported that trained subjects in both younger and older age
groups exhibited more rapid HR recovery than their un-
trained counterparts after exercise at similar relative work-
loads. During exercise, HR increases through a combined
effect of sympathetic activation and parasympathetic with-
drawal. Immediately after exercise, HR recovery is mainly
attributed to vagal reaction (2). Therefore, there is a possi-
bility that an adaptation of the cardiac autonomic nervous
system (ANS) to endurance training contributes to a more
rapid HR recovery after exercise. If adaptation in cardiac
autonomic modulation is a major contributing factor in the
reduction of resting and postexercise HR after endurance-
training sessions, then changes in cardiac ANS modulation
during training periods should correspond to the changes in
HR reduction. However, the changes over time in cardiac
0195-9131/01/3309-1496/$3.00/0
MEDICINE & SCIENCE IN SPORTS & EXERCISE®
Copyright © 2001 by the American College of Sports Medicine
Submitted for publication February 2000.
Accepted for publication November 2000.
1496
ANS modulation and HR during an endurance-training pro-
gram have never been reported.
HR variability analysis has proven to be a simple nonin-
vasive technique for the evaluation of autonomic modula-
tion of HR through the measurement of instantaneous beat
to beat variations in R-R interval length. Thus, it furnishes
a tool to noninvasively explore the sympathovagal interac-
tion under varying conditions (19). An additional advantage
of this method is the possibility of repeated measurements
with the same subject. Using analysis of HR variability, we
investigated the changes over time in HR and ANS modu-
lation measured both at rest and during postexercise recov-
ery periods over a 6-wk endurance-training program.
METHODS
Subjects. Twelve healthy male students majoring in
physical education volunteered for the study. They were
assigned to either an endurance-training group (ET, N ⫽ 7)
or a control group (C, N ⫽ 5) and were matched as closely
as possible with regard to age, height, weight, and peak
oxygen uptake (peak V̇O2). All subjects were nonsmokers.
The subjects had no history of any respiratory or cardiac
diseases. All subjects provided informed written consent for
their participation with the experimental procedures con-
ducted in conformance with the human subjects policy state-
ment published by Medicine and Science in Sports and
Exercise. Table 1 shows the physical characteristics of the
respective ET and C groups measured before and after the
6-wk training period.
TABLE 1. The characteristics and echocardiographic data of the respective ET and C groups before and after the 6-wk training period.
Control Group Endurance-Trained Group
Before After Before After
Age (yr) 22 ⫾ 1 22 ⫾ 1 21 ⫾ 1 21 ⫾ 1
Height (cm) 170.2 ⫾ 2.2 170.2 ⫾ 2.2 174.6 ⫾ 4.1 174.6 ⫾ 4.1
Weight (kg) 65.4 ⫾ 6.5 66.1 ⫾ 7.1 72.5 ⫾ 10.4 70.7 ⫾ 10.0*
Peak V̇O2 (L䡠min⫺1) 3.26 ⫾ 0.43 3.17 ⫾ 0.41 3.43 ⫾ 0.31 3.73 ⫾ 0.21*
Peak V̇O2 per body weight (mL䡠min⫺1䡠kg⫺1) 50.0 ⫾ 6.1 48.2 ⫾ 6.7 48.2 ⫾ 8.5 53.8 ⫾ 9.1*
Resting HR (bpm) 67.5 ⫾ 2.7 66.2 ⫾ 3.8 68.1 ⫾ 3.7 53.2 ⫾ 2.8*
Resting SBP (mm Hg) 113 ⫾ 3.7 110 ⫾ 1.7 120 ⫾ 4.7 112 ⫾ 3.3
Resting DBP (mm Hg) 72.8 ⫾ 5.0 73.6 ⫾ 2.3 69.7 ⫾ 3.4 64.9 ⫾ 1.9
LVEDD (cm) 4.92 ⫾ 0.08 4.96 ⫾ 0.09 4.79 ⫾ 0.09 4.97 ⫾ 0.10*
LVESD (cm) 3.06 ⫾ 0.15 3.14 ⫾ 0.15 3.21 ⫾ 0.13 3.24 ⫾ 0.07
LVEDV per body surface area (mL䡠m⫺2) 66.7 ⫾ 2.4 68.2 ⫾ 3.1 59.1 ⫾ 2.9 65.2 ⫾ 3.8*
LVESV per body surface area (mL䡠m⫺2) 21.8 ⫾ 2.4 23.2 ⫾ 2.5 23.0 ⫾ 2.1 23.5 ⫾ 1.1
* Shows the significant difference to the value before the training period, as analyzed by the paired t-test.
Peak V̇O2, peak oxygen uptake; HR, heart rate; SBP and DBP, systolic and diastolic blood pressure; LVEDD and LVEDV, left ventricular end-diastolic dimension and volume;
LVESD and LVESV, left ventricular end-systolic dimension and volume.

Procedure. The ET group underwent cycle-endurance
training for 6 wk. The C group led normal lives during the
6-wk period. To record changes in HR variability both at
rest and during postexercise recovery periods, the ET
group was measured five times: before the training, on
the 4th day, on the 7th day, on the 28th day, and on the
42nd day of the training period. The C group was mea-
sured four times: before the training, and on the 7th, 28th,
and 42nd days of the 6-wk period. All measurements
were made at the same time of day for each subject.
Measurement of HR variability was performed in a quiet,
air-conditioned (22–25°C) room. All subjects were in-
structed to fast for at least 3 h before testing on the day
of the experiment. After 15 min of quiet rest in the sitting
position, the subject’s electrocardiogram (ECG, CM5
lead, Nihonkoden WEP-7404, Tokyo, Japan) was sam-
pled by a computer that measured and stored each R-R
interval over a 5-min period. Then, the subjects per-
formed cycle exercise for 40 min at the individual 80%
peak V̇O2. At 10- and 20-min intervals after exercise, the
subject’s ECG also was sampled over a 5-min period in
the sitting position. Respiration was controlled at fre-
quencies 0.25 Hz during the measurement of HR vari-
ability both at rest and during postexercise recovery periods.
HR both at rest and during the postexercise recovery period
were determined by the average R-R interval over the entire
5-min measurement period. Before and after the training
period, left ventricular end systolic (LVESD) and diastolic
(LVEDD) diameters were measured by M-mode echocardi-
ography according to the American Society of Echocardi-
ography (23). The echocardiographic measurement was
taken in supine position at rest. Additionally, left ventricular
end systolic (LVESV) and diastolic (LVEDV) volumes
were calculated with Teichholz’s conventional method (32).
Determination of peak V̇O2. The peak V̇O2 was mea-
sured by an incremental cycle exercise test using a cycle
ergometer (Monark, Varberg, Sweden). The incremental
cycle exercise began at a work rate of 120 W (60 rpm), and
power output was increased by 30 W·min⫺1 until the sub-
jects could not maintain the fixed pedaling frequency. The
subjects were encouraged during the ergometer test to ex-
ercise at as high a level of intensity as possible. HR and a
TRAINING AND CARDIAC AUTONOMIC CONTROL
rating of perceived exertion (RPE) were monitored minute
by minute during exercise. Oxygen uptake (V̇O2) was mon-
itored during the last 30 s of each increase in the work rate
after the RPE reached 18. RPE was obtained using the
modified Borg scale (7). Subjects breathed through a low-
resistance two-way valve, and the expired air was collected
in Douglas bags. Expired O2 and CO2 gas concentrations
were measured by mass spectrometry (Westron WSMR-
1400, Chiba, Japan), and gas volume was determined using
a dry gas meter (Shinagawa Dev. NDS-2A-T, Tokyo, Ja-
pan). The highest value of V̇O2 during the exercise test was
designated peak V̇O2.
Training protocol. The ET group underwent cycle-
endurance training for 6 wk. Subjects exercised 4 d·wk⫺1 at
an intensity that elicited 80% of each subject’s peak V̇O2.
The pedaling rate was 60 rpm, and the duration of training
was 40 min. As each ET, subjects’ peak V̇O2 increased
during the training period, exercise intensity was increased
every week as required to elicit 80% of the actual peak V̇O2
that was measured every week.
Estimation of the cardiac ANS modulation. HR
variability was sampled at 1000 samples per second with an
A/D converter (AD instruments Maclab/400, New South
Wales, Australia) from ECG to computer. Before analysis,
all R-R intervals were visually inspected for artifacts that
could affect the result. The power spectra were estimated
from the sampled HR variability for 5 min using fast Fourier
transform algorithm (FFT). Sampling points for spectral
analysis were 1024 points. Power spectra obtained by spec-
tral analysis were defined as two components: 0.04 – 0.15
Hz (low frequency: LF) and 0.15– 0.4 Hz (high frequency:
HF). The very low frequency (0 – 0.04 Hz) is not addressed
in the present study. HF power is almost entirely mediated
by the vagal activity in the sinoatrial node directly associ-
ated with respiratory activity (1,3,21), whereas LF power
reflects the mixed modulation of vagal and sympathetic
activities (4). The ratio of LF power to HF power (LF/HF)
is considered to reflect the sympathovagal balance, and high
values suggest a sympathetic predominance (20). The
LF/HF ratio, HF power, and total power (LF power plus HF
power) were transformed into their natural logarithms (ln)
before statistical analysis. The logarithmic transformations
Medicine & Science in Sports & Exercise姞 1497

FIGURE 1—Instantaneous power of high-frequency component ob-
tained by complex demodulation during postexercise recovery periods.
Values are shown as mean (thick line) ⴞ SE (thin line). HF ⴝ high
frequency; ln ⴝ natural logarithm.
produced approximately symmetric distributions and thus
allowed for the use of parametric statistics that require near
normal distribution. In addition to frequency domain indices
FIGURE 2—Examples of power spectral plots before (A–C)
and after (D–E) training program of 6 wk. (A and D) ⴝ at
rest; (B and E) ⴝ 10 min after exercise; (C and F) ⴝ 20 min
after exercise.
1498 Official Journal of the American College of Sports Medicine
of HR variability, the standard deviation of normal R-R
intervals (SDNN) was calculated from sampled HR vari-
ability for 5 min.
Complex demodulation analysis. To standardize
physiological and clinical studies, short-term recordings of
5 min should be made under physiologically stable condi-
tions when processed by FFT (31). Cardiac autonomic con-
trol and HR are dramatically changed during exercise and
immediately after heavy exercise. Thus, it is difficult to
estimate cardiac autonomic control when processed by FFT
algorithm under these situations, due to the limitation in
time resolution of FFT. Therefore, we designed that the
postexercise measurements to be made during 10 –15 min
and 20 –25 min after exercise. However, the frequency anal-
ysis of HR response during recovery phase should confirm
whether sympathovagal balance was dynamically changed
during 10 –15 min and 20 –25 min after exercise in the
present study. Complex demodulation (CDM) can measure
time-dependent changes in the amplitude of specific fre-
quency domain components (13,14). Thus, the time-depen-
dent changes in ln HF power, obtained from all subject’s
ECG data before training period, during postexercise recov-
ery periods were assessed by CDM analysis. For the anal-
ysis of HF component of the R-R interval, reference fre-
quency was set at 0.30 Hz. The low-pass corner frequency
was set at 0.16 Hz for HF component, so that the frequency
band for demodulating the HF component was 0.14 – 0.46
Hz. Figure 1 shows instantaneous power of HF component
obtained by CDM during postexercise recovery periods. The
power of HF component did not change during 10 –15 and
20 –25 min after exercise. In addition, HR decreased ~3 bpm
during 10 –15 min and did not change during 20 –25 min
after exercise. These results show that the 5-min sampling
period for FFT analysis was in stable condition at 10 and 20
min during the postexercise recovery phase of the present
study.
http://www.acsm-msse.org

Statistical analysis. Values are shown as mean ⫾ SE.
The differences between the change in the ET group and
change in the C group during the training periods were
statistically analyzed using two-way ANOVA with repeated
measurements and Scheffe post hoc test. The correlation
coefficients between ⌬ HR and ⌬ ln LF/HF or ⌬ ln HF
power in the ET group were determined by the Pearson
correlation. The ⌬ HR, ⌬ ln LF/HF, and ⌬ ln HF power were
estimated as the difference between the measurements be-
fore the training and on the 4th, 7th, 28th, or 42nd day of
training period. The level of significance was established at
P ⬍ 0.05.
RESULTS
Peak V̇O2 after the training program was significantly
higher than peak V̇O2 measured before the training program
began in the ET group. The increase in peak V̇O2 for seven
subjects of the ET group averaged 5.7 mL·min⫺1·kg⫺1
(12%, Table 1).
Figure 2 (A–F) illustrates examples of power spectral
plots measured at rest (A, D) and at 10-min (B, E) and
20-min (C, F) intervals after 80% peak V̇O2 exercise in a
sitting position before and after the 6-wk training program.
At rest, there was a higher HF component after training (Fig.
2D) as compared with before the training (Fig. 2A). During
postexercise recovery periods, the HF component after
training (Fig. 2, E and F) was higher than that before
training (Fig. 2, B and C). Conversely, the LF component
decreased after the training program.
Figure 3 shows the changes in HR and the indices of
TRAINING AND CARDIAC AUTONOMIC CONTROL
FIGURE 3—Changes in heart rate and indices of cardiac
autonomic nervous system modulation in both endurance-
training (black) and control (white) groups measured (left)
at rest and (center) at 10-min and (right) 20-min intervals
after 80% peak V̇O2 exercise in a sitting position over a
training program of 6 wk; * shows the significant difference
to the value before the training program; HR ⴝ heart rate;
HF ⴝ high frequency; LF/HF ⴝ low to high frequency ratio;
ln ⴝ natural logarithm; SDNN ⴝ standard deviation of
normal R-R intervals.
cardiac ANS modulation measured both at rest and at 10-
and 20-min intervals after 80% peak V̇O2 exercise ses-
sions over a total training program of 6 wk. At rest (Fig.
3, left), HR at 28 d was significantly lower than HR
measured before the training program began in the ET
group. Furthermore, HR (53.1 ⫾ 2.7) at 42 d was signif-
icantly lower than HR (58.8 ⫾ 2.9) at 28 d (P ⬍ 0.05).
The ln LF/HF tended to decrease with training, but there
was no statistical significance (P ⫽ 0.09). The ln HF
power and SDNN at 7 d were significantly larger than
those before the training period began in the ET group.
Although HR at 42 d was significantly lower than HR at
28 d, there were no significant differences in the cardiac
ANS parameters between those at 28 d and those at 42 d
in the ET group.
At 10 min after 80% peak V̇O2 exercise (Fig. 3, center),
HR at 7 d was significantly lower than HR before the
training program began in the ET group. Although ln LF/HF
showed changes similar to HR in the ET group, there was no
statistical significance. ln HF power and SDNN at 7 d were
significantly larger than those before the training program
began. There were no significant changes in any parameters
of the ET group between 7 d and 42 d in the training
program.
In both ET and C groups measured at 20 min after 80%
peak V̇O2 exercise (Fig. 3, right), changes in HR, ln HF
power, and SDNN during the training program were similar
to those at 10 min after exercise. However, ln LF/HF mea-
sured at 7 d was significantly lower than the ln LF/HF
before the training program began in the ET group.
Medicine & Science in Sports & Exercise姞 1499
TABLE 2. Correlation coefficients (r) of changes during training period between heart
rate and indices of cardiac autonomic nervous system modulation measured both at
rest and during postexercise recovery periods.
Preexercise Postexercise Recovery
10 Min after 20 Min after
Rest Exercise Exercise
ln LF/HF 0.326 0.268 0.666*
ln HF power ⫺0.681* ⫺0.809* ⫺0.704*
* P ⬍ 0.05.
HR, heart rate; HF, high frequency; LF/HF, low to high frequency ratio; ln, natural
logarithm.
At rest, the total power (6.63 ⫾ 0.28 ms2) at 7 d was
significantly larger than before (5.99 ⫾ 0.33 ms2) the train-
ing period began in the ET group (P ⬍ 0.05). Subsequently,
the total power slightly increased throughout the remainder
of the training program, but there was no statistical signif-
icance (before the training, 5.99 ⫾ 0.33 ms2; on the 4th day,
6.45 ⫾ 0.29 ms2; on the 7th day, 6.63 ⫾ 0.28 ms2; on the
28th day, 6.79 ⫾ 0.26 ms2; and on the 42nd day of training
period, 6.85 ⫾ 0.24 ms2; mean ⫾ SE). However, when
measured at both 10- and 20-min intervals after 80% peak
V̇O2 exercise, there were no significant changes in ln total
power in the ET group at any time during the 6-wk program.
There were no significant changes in any parameter in the C
group at any time during the 6-wk program.
Table 2 shows the correlation coefficients of changes
during training period between HR and ln LF/HF or ln HF
power measured both at rest and at 10 min and 20 min
after 80% peak V̇O2 exercise. These were obtained from
all measurements of ET group during the training pro-
gram. There were significant relationships between ⌬ HR
and ⌬ ln HF power measured at rest and at 10 min and 20
min after 80% peak V̇O2 exercise. Significant relation-
ship between ⌬ HR and ⌬ ln LF/HF existed at 20 min
after exercise only.
DISCUSSION
Training state, peak V̇O2, and HR. The present train-
ing program significantly increased peak V̇O2 and LVEDD,
and decreased resting HR. In a review of the interactions of
intensity, frequency, and duration of exercise training by
Wenger and Bell (33), the increase in V̇O2max induced by
70 –90% V̇O2max exercise intensity training was as follows:
6.5% when frequency was 4 d·wk⫺1; 7.8% when duration was
35– 45 min and 4.5% when program length was 5–7 wk. The
increase in peak V̇O2 of ET group in the present training
program of 6 wk, 4 d·wk⫺1, for 40 min per training session, at
80% peak V̇O2 was 12%. Also, the present training program
decreased resting HR of approximately 15 bpm. Recently,
Wilmore et al. (34) reported effects of a 20-wk cardiorespira-
tory endurance-training program at 55–75% of the initial
V̇O2max on resting HR as determined under highly controlled
conditions. After the training, the resting HR decreased ap-
proximately 3 bpm. On the other hand, a reduction in resting
HR induced by high exercise intensity training (80% V̇O2max)
was reported at approximately 10 bpm (26). Our belief is that
the rather large reduction in resting HR in the present study was
1500 Official Journal of the American College of Sports Medicine
due to the relatively high training intensity. Thus, the present
training program was effective in improving aerobic work
capacity and reducing resting HR.
Changes in cardiac autonomic control induced
by endurance training measured at rest. In the ET
group, the present training program significantly decreased HR
and increased ln HF power and SDNN measured at rest with a
simultaneous increase in aerobic work capacity. Cardiac neural
control was first evaluated in athletes by spectral analysis of
HR variability of short length recordings by Dixon et al. (10).
These investigators observed a higher cardiac vagal control and
lower cardiac sympathetic control in endurance athletes than in
sedentary controls. Goldsmith et al. (12), using HR variability
analysis by 24-h Holter monitoring, also found greater para-
sympathetic modulation of HR in trained than untrained sub-
jects. Other investigators (5,28) have reported that cardiac
vagal modulation, which was assessed by either respiratory
sinus arrhythmia or pharmacologic maneuvers, was enhanced
at rest in long-term physically trained athletes. They have
speculated that enhanced cardiac vagal modulation might in
part contribute to resting bradycardia in these athletes. These
findings support the present results. On the other hand, the ln
LF/HF tended to decrease with present training, but there was
no statistical significance (P ⫽ 0.09). Shin et al. (27) reported
that the index of parasympathetic modulation in R-R interval
spectra was significantly higher in athletes than in nonathletes,
whereas the index of sympathetic modulation tended to be
lower in athletes than that in nonathletes, but there was no
statistical significance. Furthermore, present training program
increased ln total power. An increased total power of HR
variability, i.e., LF power plus HF power, induced by endur-
ance training indicates both improved cardiac sympathetic and
parasympathetic modulation (11,16). These findings suggest
that endurance training may either increase both cardiac sym-
pathetic and parasympathetic modulation at rest, or that it has
no effect on sympathetic modulation and only increases para-
sympathetic modulation. In either situation, this causes a pre-
dominance of parasympathetic control in the sympathovagal
balance.
We investigated the contributory rates of alteration in ln
LF/HF and ln HF power to bradycardia induced by the present
training methodology. As shown in Table 2, there was a sig-
nificant relationship between ⌬ HR and ⌬ ln HF power mea-
sured at rest during the training program. However, significant
correlation was not found between ⌬ HR and ⌬ ln LF/HF.
Significant difference before and after the training program
was not found in the ln LF/HF. These findings suggest that the
enhanced parasympathetic modulation contributes in part to
decreased resting HR due to endurance training and the ln
LF/HF has no effect on resting bradycardia.
Other mechanisms have been proposed to explain resting
bradycardia induced by endurance training. Katona et al.
(17), using sympathetic and parasympathetic blocking
agents, found that the lower HR in athletes results from a
reduction in intrinsic cardiac rate and not from an increase
in parasympathetic tone and decrease in sympathetic tone.
Bonaduce et al. (6) reported that detrained athletes showed
a higher cardiac parasympathetic modulation with slower
http://www.acsm-msse.org
HR than controls, but after vigorous training no further
increase in parasympathetic modulation was detectable in
athletes despite further decreases in HR and increases in
LVEDD. In the present study, after the 28th day of training,
no further changes in the indices of cardiac ANS modulation
were detectable despite a continued decrease in HR. The
present training program also significantly increased
LVEDD and LVEDV, which is corrected for individual
body surface area when measured at rest. Taken together,
these observations support the hypothesis that resting bra-
dycardia induced by endurance training was, in part, a
consequence of a decrease in intrinsic HR.
Changes in cardiac autonomic control induced
by endurance training measured during postexer-
cise recovery periods. The ln LF/HF measured 10 min
after cessation of exercise tended to decrease with continued
endurance training, but there was no statistical significance.
However, HR was significantly decreased and the ln HF
power and SDNN were significantly increased by endurance
training when measured 10 min after cessation of exercise.
These findings indicate that enhanced cardiac parasympa-
thetic modulation is a major contributor to the decrease in
HR measured 10 min after cessation of exercise in the
present study. On the other hand, the ln LF/HF measured 20
min after exercise cessation was significantly decreased by
the endurance training with a decrease in HR and increases
in the ln HF power and SDNN. As shown in Table 2, ⌬ ln
HF power measured both 10 min and 20 min after exercise
was correlated with ⌬ HR. The relationship between ⌬ HR
and ⌬ ln LF/HF existed only when measured 20 min after
exercise. These data suggest that the effects of cardiac
autonomic controls on a more rapid recovery in HR induced
by endurance training may be different when measured 10
min and 20 min after exercise cessation.
Comparison of changes in cardiac autonomic
control measured at rest and during postexercise
recovery periods. It is interesting that endurance training
resulted in no significant changes in any parameters mea-
sured during the postexercise recovery periods from the 7th
day to the 42nd day of the training period despite the
measured-at-rest changes which occurred between that time.
This result suggests that adaptations of HR and cardiac ANS
modulation measured during postexercise recovery periods
may be achieved in the short term, such as the first 7 d of the
training program. In all measurements taken at rest and 10
min and 20 min after exercise cessation, the amount of
change in HR before and after the training period was about
15 bpm. In other words, the amount of change in HR during
the postexercise recovery periods for the first 7 d of the
training program corresponded to the adaptation, which was
needed for 42 d at rest. Obviously, the adaptations of HR
and cardiac ANS modulation that occur during the postex-
ercise recovery period occur quickly when compared with
those measured at rest. These results suggest that under
conditions of endurance training there are differences in the
adaptabilities of cardiac autonomic control between at rest
and postexercise recovery periods.
TRAINING AND CARDIAC AUTONOMIC CONTROL
Although the factors that exerts an influence on cardiac
autonomic control are central command and afferent stim-
ulation from chemoreflex or baroreflex functions, the mech-
anisms of cardiac autonomic adaptation at rest and during
postexercise recovery periods after endurance training re-
main unclear. Training-associated changes in baroreflex
control of HR have been proposed. Although the experi-
mental findings have been remarkably inconsistent
(22,24,25), the possibility of the adaptation in baroreflex
function cannot be removed as a possible factor in the
differences between the cardiac autonomic adaptation at rest
and during recovery. Furthermore, previous studies (18,29)
suggest that endurance training induces a lower level of
muscle chemoreflex stimulation as the result of the in-
creased oxidative metabolic capacity of the exercising mus-
cle during exercise. We, therefore, speculate that the differ-
ence in the adaptabilities of cardiac autonomic control at rest
and during recovery phases is due to the difference in the
mechanism of the adaptation between these phases.
Methodological limitations in the present study.
The present study used HR variability analysis for estima-
tion of cardiac ANS modulation. A major advantage of this
method is the possibility of repeated measurements with the
same subject, because it can explore noninvasively the sym-
pathovagal interaction under different conditions. The
present study observed changes in HR and cardiac ANS
modulation measured at rest and during postexercise recov-
ery periods over the training program of 6 wk. However,
breathing patterns and changes in tidal volume can affect a
respiratory sinus arrhythmia, i.e., the HF power as index of
parasympathetic modulation (8,15). Also, Strano et al. (30)
concluded that because athletes usually breathe slowly, and
because slow breathing influences spectral LF component,
HR variability power spectra in athletes should be assessed
under controlled respiration, which does not alter ANS
modulation. In the present study, the breathing pattern does
not affect the HF power because all subjects maintained
respiratory rates of 0.25 Hz during all measurements. How-
ever, ventilatory tidal volumes were not directly measured.
When measured during the postexercise recovery periods,
the effect of changes in tidal volume on the HF power may
be larger than that at rest. Because there is the possibility
that the acceleration of ventilation is retained during the
recovery phase after intense exercise as used in the present
study. Thus, if the tidal volume is controlled, cardiac ANS
modulation could be measured more accurately both at rest
and during the postexercise recovery periods.
CONCLUSIONS
The present study, using analysis of HR variability, lon-
gitudinally examined the effects of endurance training on
HR and cardiac ANS modulation measured at rest and
during postexercise recovery periods. With endurance train-
ing, changes in cardiac ANS modulation partly contribute to
a decrease in HR measured at rest and during postexercise
recovery periods. The effects of adaptability of the cardiac
Medicine & Science in Sports & Exercise姞 1501
autonomic control to endurance training occurs sooner in
immediate postexercise recovery periods than at rest.
The authors gratefully acknowledge Dr. Junichiro Hayano
(Nagoya City University Medical School) for advice on this research.
This study was partly supported by grant-in-aid for scientific re-
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