Download Eight weeks of moderate-intensity exercise training increases heart

Eight weeks of moderate-intensity exercise training
increases heart rate variability in sedentary
postmenopausal women
Radim Jurca, PhD, Timothy S. Church, MD, PhD, Gina M. Morss, MA, Alexander N. Jordan, MS, and
Conrad P. Earnest, PhD Dallas, Tex
Background
Regular exercise is associated with increased heart rate variability (HRV). However, results from studies examining the effect of exercise training on HRV in postmenopausal women are inconclusive. In addition, the effect of
hormone replacement therapy (HRT) on HRV remains a subject of speculation.
Methods
We examined 88 sedentary postmenopausal women in a randomized controlled trial who were assigned
to exercise (n ⫽ 49) or control (n ⫽ 39) groups. The exercising women performed 8 weeks of aerobic exercise training at
a heart rate equivalent to 50% of VO2max, consisting on average of 44 minutes per session, 3 to 4 times per week. Resting HRV was measured in each participant at baseline and after 8 weeks of intervention. Ten minutes of resting R-R intervals were analyzed by time (standard deviation of mean R-R intervals, root of mean square successive differences) and
frequency domain methods: low-frequency (LF) was defined as 0.04 to 0.15 Hz, high-frequency (HF) as 0.15 to 0.40 Hz,
and total spectral power as 0.00 to 0.40 Hz. The LF and HF components in normalized units were also calculated.
Results At baseline, there were no significant differences in HRV between control and exercise groups. Additionally,
there were no differences in any HRV variables when women were grouped by HRT use (no HRT, estrogen-only HRT, and
progestin-containing HRT). After 8 weeks, women randomly assigned to the exercise group increased all absolute time
and frequency domain indexes (all P ⬍ .001) and reduced resting heart rate (P ⫽ .002) compared with women in the
control group. The LF and HF components expressed as normalized units remained unchanged after exercise intervention.
Additionally, HRT use did not modify the exercise-induced changes in HRV.
Conclusions
We conclude that moderate aerobic exercise increases HRV in sedentary postmenopausal women.
This benefit is not influenced by the use of HRT. (Am Heart J 2004;147:e21.)
Cardiovascular disease (CVD) is the leading cause of
death in women.1,2 Risk of death caused by CVD in
women markedly increases with the onset of menopause.3 Heart rate variability (HRV) provides a noninvasive measurement of the cardiac autonomic regulation
of the heart.4 Enhanced efferent vagal activity is characterized by increasing the variability of the heart rate
(HR), whereas sympathetic stimulation decreases
HRV.5 Reduced HRV is associated with increased risk
of cardiac events and death in healthy individuals.6,7
Additionally, reduced HRV is an independent predictor
of arrhythmic death after myocardial infarction.8 PostFrom The Cooper Institute, Dallas, Tex.
Supported in part by American Heart Association Texas Affiliate award 02651404
and by National Institutes of Health grant HL-66262.
Submitted May 5, 2003; accepted October 17, 2003.
Reprint requests: Radim Jurca, PhD, The Cooper Institute, 12330 Preston Road, Dallas,
TX 75230.
E-mail: [email protected]
0002-8703/$ - see front matter
© 2004, Elsevier Inc. All rights reserved.
doi:10.1016/j.ahj.2003.10.024
menopausal women have reduced HRV compared with
premenopausal women.9
Although cross-sectional reports suggest that regular
exercise is associated with improved HRV, training
studies examining the effect of exercise on HRV are
inconclusive.10 –19 Moderate- to vigorous-intensity aerobic exercise training in elderly men and women resulted in an improvement of the autonomic modulation to the sinoatrial node, as assessed by HRV.10 –12
Conversely, other studies reported no change in HRV
in elderly populations after an exercise intervention.13–16 Studies conducted on middle-aged populations show an increase in parasympathetic tone after
aerobic exercise training,17,18 whereas other studies in
middle-aged individuals show exercise training to have
no effect on HRV.13,19 The limited exercise-training
studies conducted on postmenopausal women report
no change in HRV after exercise intervention.14 –16
However, spontaneous baroreflex function was increased after moderate-intensity aerobic exercise.15 All
previous training studies of postmenopausal women
American Heart Journal
May 2004
828.e9 Jurca et al
are limited by a small sample size (n ⬍ 10). Thus, data
from a large sample size are needed in this area.
A further complication in studying the effect of exercise on HRV in postmenopausal women is the use of
hormone replacement therapy (HRT) and the various
combinations of HRT use, which have been suggested
by some to modify HRV. However, the available literature is conflicting and inconclusive. Some groups have
reported estrogen HRT to increase parasympathetic
tone20,21 and decrease sympathetic nerve discharge,22,23 whereas others reported that estrogen has
a minimal effect on autonomic tone.24,25 Short-term
(up to 6 months) application of progestin-containing
HRT is reported to increase parasympathetic tone,25
whereas others report no effect on HRV.26 Another
report found that women taking HRT with progestin
for at least 6 months had reduced HRV compared with
women on HRT without progestin.27 Thus, the available data examining the effect of various types of HRT
on HRV are equivocal, and more data are needed. The
lack of a consensus in regard to the effect of HRT on
HRV necessitates the careful consideration of HRT use
in any study that examines HRV in postmenopausal
women.
The primary goal of this study was to investigate the
effect of an 8-week exercise training intervention on
HRV in sedentary, postmenopausal women participating in a large, supervised, aerobic exercise study. Secondary goals are to examine the association between
HRT use and HRV and whether HRT use modifies the
exercise-induced changes in HRV.
Methods
Participants
We recruited sedentary postmenopausal women from the
Dallas metropolitan area through television, radio, and newspaper advertisements. Study inclusion criteria included
women who were nonsmokers, sedentary over the previous
6 months,28,29 with body mass index 25 to 40 kg/m2, systolic
blood pressure between 120 to 159 mm Hg (diastolic blood
pressure ⬍100 mm Hg), and HRT status stable for the past 6
months. The Institutional Review Board of The Cooper Institute approved all methods and procedures, and all participants provided written informed consent to participate.
Women who met the inclusion criteria were randomly assigned to either the exercise group (n ⫽ 49) or the control
group (n ⫽ 39). All participants were screened for medications known to alter HR and had no history of respiratory or
cardiac diseases. Forty-nine of the participants were taking
HRT. Before initiation into the study, all participants were
assessed at baseline for height, body mass, resting blood pressure, cardiorespiratory fitness, and resting R-R intervals. The
R-R interval assessment was repeated for all women after 8
weeks. This report only presents HRV data. Other outcomes
are presented elsewhere as part of a larger clinical trial.
Heart rate variability measurement
Participants were asked to fast for at least 3 hours, not to
consume caffeine-containing products for 12 hours, and to
abstain from alcohol use and heavy exercise for 48 hours before testing. Participants rested quietly in the supine position
for 25 minutes in a semidark room with a temperature between 22 to 23°C. Participants controlled their respiration
rate by breathing with a metronome at a fixed rate of 12
breaths per minute (0.2 Hz). Beat-to-beat measurements of
R-R intervals were made during the entire period. The R-R
interval measurements were conducted at the same time of
day for each participant.
We used an IBM-compatible PC equipped with a program
for signal processing and heart rate variability analysis (Polar
Precision Performance SW 3.02, Polar Electro OY, Kempele,
Finland). The 2-channel electrocardiographic signal was detected by a Polar Heart Rate Monitor and transmitted online
to a PC through a Polar Advantage Interface receiver. The
QRS timing accuracy of Polar Advantage Interface is fixed to
1 ms. The computer program labeled each QRS complex,
and the resulting signal was passed through a filter that eliminates ectopic beats and artifacts. Additionally, an R-R interval
tachogram was displayed for manual editing, and areas of
ectopy or artifacts were identified and removed by manual
deletion. Each edited R-R interval was replaced with an average value. Segments containing ⬎15% of edited R-R intervals
were interpreted as premature beats and were excluded from
data analysis. These segments accounted for ⬍2% of edited
10-minute intervals in every subject. The filtering techniques
are described in earlier reports.30,31 HRV was quantified from
the last 10 minutes of the R-R interval recording.
We used an autoregressive model to estimate the power
spectrum densities for the frequency domain. The power
spectra were quantified by measuring the area in 3 frequency
bands: high-frequency power (HF, 0.15 to 0.40 Hz), lowfrequency power (LF, 0.04 to 0.15 Hz), and total-frequency
power (PT, 0.00 to 0.40 Hz). Although it is generally accepted that HF is mediated by variations in parasympathetic
activity, the LF power reflects both parasympathetic and sympathetic modulations.32 In addition, the LF and HF oscillatory
components are presented in normalized units (nu). The normalized unit expresses the power centered in the frequency
of interest divided by total power less very-low-frequency
power.
In addition to frequency domain indexes of HRV, we analyzed time-domain measures of HRV, which are derived from
direct measurements of R-R intervals. We calculated the standard deviation of all R-R intervals (SDNN) over the given
measurement period and the square root of the mean of the
sum of the squares of differences between adjacent R-R intervals (rMSSD). SDNN reflects all the cyclic components responsible for variability in the period of recording, whereas
rMSSD is considered to be an index of parasympathetic modulations in HR.32
Blood pressure measurement
Baseline blood pressure measurements were obtained after
25 minutes of R-R interval collection. We discarded the first
value from each sequence, subsequently averaging the last 3
values (⫾5 mm Hg) to determine resting blood pressure. All
blood pressure measurements were obtained through the use
American Heart Journal
Volume 147, Number 5
of a Colin STBP-780 automated BP monitor (San Antonio,
Tex).
Jurca et al 828.e10
Table I. Baseline characteristics of the study participants
Determination of VO2max
Participants performed an exercise test on a bicycle ergometer (Lode Excalibur Sport Cycle Ergometer, Lode BV,
Groningen, Netherlands). Each test started with an initial tension load of 30 W for 2 minutes. After this first stage, tension
was increased to 50 W for 4 minutes, followed by 20 W increases every 2 minutes until exhaustion. Open-circuit spirometry measurements were obtained with the use of a Parvomedics True Max 2400 Metabolic Measurement Cart (Salt
Lake City, Utah). VO2max was determined as the greatest
quantity of oxygen consumed for the last 30-second period
of a completed stage and corresponding to a respiratory exchange ratio ⬎1.1 and a HR ⬎85% of age-predicted maximum. All participants met the inclusion criteria.
Exercise training program
Participants in the control group did not participate in any
supervised exercise and were asked not to change their physical activity habits during the study. All participants in the
exercise group completed 8 weeks of supervised aerobic exercise, alternating exercise sessions on a treadmill and a recumbent leg ergometer (Life Fitness, Franklin Park, Ill) each
session. Exercise intensity was kept within ⫾5 beats to HR
equivalent to 50% of VO2max. HR was monitored during the
entire exercise session by an HR transmitter (Polar Vantage
NV). Participants in the exercise group were asked not to
exercise outside of the study.
All women randomly assigned to an exercise group began
exercising for 60 minutes per week, equivalent to 4 kcal/kg
per week. Participants extended their caloric expenditure by
adding 15 extra minutes each week, equivalent to 1 kcal/kg
per week, until they accumulated 120 to 165 minutes of exercise during each week. Participants exercised 3 to 4 times
per week. Rationale for the gradual increase of caloric expenditure was to prevent soreness, fatigue, injuries, and to enhance participant compliance. Participants were weighed
each week, and their weight was multiplied by the exercise
dosage to determine the number of calories to be expended
for the week. Power output was calculated at 3-minute increments by speed and grade combinations for the treadmill and
Watts for the recumbent leg ergometer. When HR fell outside the prescribed training zone, power output was increased or decreased to keep HR within the desired exercise
intensity.
Age (y)
Ethnicity % (n)
White
African American
Hispanic
Asian
VO2max (mL/kg/min)
Body mass index (kg/m2)
Systolic blood pressure (mm Hg)
Diastolic blood pressure (mm Hg)
HRT use % (n)
No HRT
Estrogen only
Progestin ⫹ estrogen
Progestin only
Control
(n ⴝ 39)
Exercise
(n ⴝ 49)
57.4 ⫾ 6.2
56.5 ⫾ 6.2
79.5 (31)
5.1 (2)
15.4 (6)
–
15.9 ⫾ 3.0
32.1 ⫾ 4.3
139.2 ⫾ 10.5
78.3 ⫾ 7.7
87.7 (43)
10.2 (5)
–
2.1 (1)
16.0 ⫾ 2.9
32.0 ⫾ 3.9
139.8 ⫾ 11.7
82.1 ⫾ 8.7*
43.6 (17)
41.0 (16)
15.4 (6)
–
44.9 (22)
38.8 (19)
12.2 (6)
4.1 (2)
Values are mean ⫾ SD. HRT, Hormone replacement therapy.
*P ⫽ .03 versus control.
natural logarithmic transformation was used to normalize the
data. An ␣-level of 0.05 was considered significant. All statistical analyses were performed by SAS Software, Version 8.2
(Cary, NC).
Results
Baseline characteristics
At baseline, participants in the exercise group had
significantly higher diastolic blood pressure than did
the participants in the control group. Other variables
were similar in the 2 groups (Table I). Baseline demographic and physiologic variables were additionally
categorized in the 3 groups on the basis of HRT use
(Table II). The HRT users and nonusers groups were
similar in age, ethnicity, body mass index, blood pressure, and HRV indexes. Baseline VO2max was significantly lower in women abstaining from HRT compared
with women using HRT. Women using progestin-containing replacement therapy had higher baseline HR
than women using estrogen only or women without
HRT.
Statistical analysis
Compliance with the exercise training program
Baseline and follow-up characteristics of the study groups
are presented as mean ⫾ SD. Participants’ baseline characteristics were examined within randomized groups and categories of HRT use. An unpaired t test was used for comparison
between the 2 randomized groups. One-way analysis of variance was used for comparison among the 3 HRT groups at
baseline. The Student paired t test was used for comparison
within groups. The mean change in each variable was compared between treatment groups by using analysis of covariance with adjustment for baseline value. All frequency components presented in absolute units (ms2) were skewed; a
Mean total time spent exercising for individuals randomly assigned into the exercise training group was
1133 ⫾ 149 minutes over the 8-week program. Participants averaged 3.2 ⫾ 0.6 exercise sessions per week,
with the average exercise session lasting 44 ⫾ 11 minutes. Exercise compliance was excellent, with the average amount of energy expenditure prescribed (4902
⫾ 665 kcal/8wk) very closely matching the actual
amount (4859 ⫾ 607 kcal/8wk) of energy expenditure
(P for difference ⫽ .31).
American Heart Journal
May 2004
828.e11 Jurca et al
Table II. Baseline characteristics and heart rate variability variables of the participants categorized by hormone replacement therapy use
Age (y)
Ethnicity % (n)
White
African American
Hispanic
Asian
VO2max (mL/kg/min)
Body mass index (kg/m2)
Systolic blood pressure (mm Hg)
Diastolic blood pressure (mm Hg)
Heart rate (beats/min)
Time domain measures
rMSSD (ms)
SDNN (ms)
Frequency domain measures
lnPHF (ms2)
lnPLF (ms2)
lnPT (ms2)
HF (nu)
LF (nu)
No HRT
(n ⴝ 39)
Estrogen
only
(n ⴝ 35)
Progestin ⴙ estrogen
(n ⴝ 12), progestin only
(n ⴝ 2)
57.3 ⫾ 6.6
56.9 ⫾ 6.4
56.0 ⫾ 4.2
84.6 (33)
7.7 (3)
5.1 (2)
2.6 (1)
15.0 ⫾ 2.6
32.8 ⫾ 3.9
140.7 ⫾ 10.3
80.9 ⫾ 8.6
66.9 ⫾ 8.1
80.0 (28)
8.6 (3)
11.4 (4)
–
16.5 ⫾ 3.1*
31.1 ⫾ 4.2
137.7 ⫾ 12.8
78.7 ⫾ 7.9
65.3 ⫾ 7.1
92.9 (13)
7.1 (1)
–
–
17.3 ⫾ 2.7*
32.3 ⫾ 3.9
140.6 ⫾ 8.6
83.3 ⫾ 8.9
72.4 ⫾ 5.3*†
20.34 ⫾ 9.51
29.21 ⫾ 9.36
19.18 ⫾ 7.19
26.36 ⫾ 6.54
15.79 ⫾ 4.38
25.94 ⫾ 5.78
5.02 ⫾ 1.10
4.82 ⫾ 0.84
6.55 ⫾ 0.85
53.4 ⫾ 17.5
44.6 ⫾ 16.9
4.95 ⫾ 0.88
4.78 ⫾ 0.68
6.49 ⫾ 0.56
52.9 ⫾ 18.2
45.3 ⫾ 17.2
4.66 ⫾ 0.86
4.95 ⫾ 0.55
6.44 ⫾ 0.41
43.1 ⫾ 16.1
54.3 ⫾ 21.6
Values are mean ⫾ SD. rMSSD, The root mean square successive difference of R-R intervals; SDNN, standard deviation of R-R intervals; lnPHF, log high-frequency spectral
power (0.15– 0.40 Hz); lnPLF, log low-frequency spectral power (0.04 – 0.15 Hz); lnPT, log total frequency spectral power (0.00 – 0.40 Hz); nu, normalized units.
*P ⬍ .05 versus No HRT group
†P ⬍ .05 versus estrogen only group
Effect of aerobic exercise training on heart rate
variability
At baseline, there were no significant differences
between the exercise group and the control group for
any HRV indexes. Individuals randomly assigned to the
exercise training groups had significant increases in all
HRV indexes presented in absolute units: rMSSD
(⫹25%), SDNN (⫹18%), lnPHF (⫹11%), lnPLF (⫹9%),
and lnPT (⫹6%), respectively. The normalized HF and
LF powers remained unchanged after exercise intervention. Additionally, all HRV variables remained unchanged in the control group. To control for regression to the mean, we adjusted for baseline HRV values.
The difference in changes adjusted for baseline value
between groups was highly significant for all HRV variables (Table III).
Resting HR decreased in the exercise group and remained unchanged in the control group. To evaluate
whether the decrease in resting HR was responsible
for the improvement in HRV variables in the exercise
group, we further adjusted for change in resting HR
(Table III). All observed HRV changes in the exercise
group remained statistically significant (all P ⱕ .05).
Because weight loss has been associated with HRV
enhancement, we further adjusted for change in
weight in the exercise group and found no effect on
the direction or magnitude of change for all HRV variables in the exercise group (data not shown).
To examine the effect of HRT use on the exerciseinduced changes in HRV, we categorized the exercise
group on the basis of HRT use (no-HRT group and
HRT group). The differences in HRV changes were
compared between HRT groups (Table IV). All HRV
variables calculated in absolute units significantly increased in both groups after 8 weeks of moderate exercise, whereas normalized HF and LF powers remained unchanged in both HRT groups. The observed
HRV changes did not significantly differ between
groups (Table IV). In addition, we categorized all HRT
users from the exercise group into estrogen-only or
progestin-containing groups because the impact of estrogen and progesterone on cardiac autonomic regulation is inconclusive. All HRV variables increased in
both groups, and the mean HRV changes did not significantly differ between the 2 groups (data not
shown).
Discussion
The primary finding of the study is that 8 weeks of
moderate-intensity aerobic exercise training can increase HRV in postmenopausal women. Furthermore,
we did not find HRT use to be associated with any
HRV indexes, nor did HRT use modify the exerciseinduced improvements in HRV.
American Heart Journal
Volume 147, Number 5
Jurca et al 828.e12
Table III. Heart rate variability at baseline and after training
Control (n ⴝ 39)
Pre
Heart rate (beats/min)
Time domain measures
rMSSD (ms)
SDNN (ms)
Frequency domain measures
lnPHF (ms2)
lnPLF (ms2)
lnPT (ms2)
HF (nu)
LF (nu)
Change exercise
vs control
Exercise (n ⴝ 49)
Post
Pre
Post
P†
P‡
66.0 ⫾ 6.4
65.8 ⫾ 6.3
68.1 ⫾ 8.5
65.0 ⫾ 7.4*
.08
20.5 ⫾ 8.0
29.0 ⫾ 8.1
19.5 ⫾ 7.5
30.1 ⫾ 8.8
18.1 ⫾ 8.0
26.4 ⫾ 7.6
22.6 ⫾ 9.6*
31.2 ⫾ 8.7*
.001
.01
.006
.05
5.19 ⫾ 0.86
4.96 ⫾ 0.65
6.65 ⫾ 0.62
54.2 ⫾ 14.9
44.2 ⫾ 14.6
5.05 ⫾ 0.79
5.04 ⫾ 0.63
6.67 ⫾ 0.58
49.5 ⫾ 15.1
48.8 ⫾ 14.9
4.73 ⫾ 1.03
4.72 ⫾ 0.78
6.40 ⫾ 0.72
49.4 ⫾ 19.6
48.2 ⫾ 18.8
5.23 ⫾ 1.07*
5.13 ⫾ 0.86*
6.79 ⫾ 0.79*
51.7 ⫾ 19.3
46.8 ⫾ 19.0
.002
.03
.001
.30
.36
.008
.05
.008
.58
.64
Values are mean ⫾ SD.
*P ⬍ .001 versus baseline.
†Adjusted for baseline value.
‡Adjusted for baseline value and heart rate change.
Table IV. Heart rate variability at baseline and after training in exercise group categorized by hormone replacement therapy use
No HRT (n ⴝ 22)
Pre
Heart rate (beats/min)
Time domain measures
rMSSD (ms)
SDNN (ms)
Frequency domain measures
lnPHF (ms2)
lnPLF (ms2)
lnPT (ms2)
HF (nu)
LF (nu)
Post
HRT (n ⴝ 27)
Pre
Post
Change No
HRT vs HRT
P§
68.4 ⫾ 9.1
64.7 ⫾ 7.1*
67.8 ⫾ 8.1
65.2 ⫾ 7.7*
.56
18.6 ⫾ 10.0
26.9 ⫾ 8.7
22.8 ⫾ 9.8*
31.2 ⫾ 9.9†
17.8 ⫾ 6.1
25.9 ⫾ 6.7
22.5 ⫾ 9.6‡
31.2 ⫾ 7.7‡
.92
.67
4.69 ⫾ 1.14
4.66 ⫾ 0.91
6.38 ⫾ 0.93
49.7 ⫾ 18.8
47.8 ⫾ 17.9
5.23 ⫾ 1.07†
5.07 ⫾ 1.05*
6.74 ⫾ 0.99†
52.8 ⫾ 15.4
45.8 ⫾ 14.9
4.77 ⫾ 0.96
4.78 ⫾ 0.68
6.42 ⫾ 0.49
49.3 ⫾ 20.7
48.4 ⫾ 19.7
5.23 ⫾ 1.09†
5.18 ⫾ 0.69*
6.83 ⫾ 0.66‡
50.8 ⫾ 22.2
47.6 ⫾ 22.0
.78
.87
.68
.71
.77
Values are mean ⫾ SD.
*P ⬍ .05 versus baseline.
†P ⬍ .01 versus baseline.
‡P ⬍ .001 versus baseline.
§Adjusted for baseline value.
Population studies have found impaired HRV to be
associated with increased risk for acute cardiovascular
events and development of metabolic syndrome.6,7,33–36 Numerous studies have reported regular
physical activity and increased fitness to be associated
with reduced risk of CVD death.37 However, the
mechanisms whereby regular exercise reduces the risk
of death are only partially explained by traditional
CVD risk factors. Previous studies, as supported by our
observation, have reported significant improvement in
both time-domain and frequency-domain markers of
vagal modulation with exercise training, suggesting
that positive benefits of regular exercise on the autonomic balance may be one additional mechanism
whereby exercise provides CVD benefit.38 – 40
We have reported improvement in all absolute spectral frequency components. However, we found no
effect of exercise on normalized frequency components. One way to interpret this is that the increase in
absolute HF was accompanied by an increase in absolute LF and total power without redistribution of spectral frequency components. It is unclear whether either an increase in parasympathetic activity or both
the increase in parasympathetic and a decrease in sympathetic activity are responsible for an increase in
power of the LF component. We found greater LF
power with exercise training in sedentary postmenopausal women, which is in agreement with other interventional studies and studies conducted on athletes.11,18,41 An enhancement of the parasympathetic
tone might be one of the possible adaptations to aerobic exercise, as seen in greater HF power after the exercise intervention. The additional explanation of
higher HRV after aerobic exercise might be an im-
American Heart Journal
May 2004
828.e13 Jurca et al
provement of cardiovagal baroreflex sensitivity reported in sedentary middle-aged and older men.42
It is significant that the positive changes in HRV occurred within a relatively short period of exercise (2
months) and from a relatively modest amount of exercise at moderate intensity. For example, during the last
2 weeks of the exercise program, the average participant was only exercising 169 minutes per week. The
selected intensity of 50% VO2max is obtainable for
nearly all individuals. Thus, both the weekly time commitment and exercise intensity were well within the
consensus recommendation of 150 to 180 minutes per
week of moderate intensity,43 yet resulted in substantial improvements in HRV. Whether greater exercise
doses or longer trial periods result in greater change in
HRV are areas for future work.
Our training program significantly reduced resting
HR. Both resting HR and HRV depend on the autonomic nervous system, so they are not independent
variables. To examine if the positive changes in HRV
were the result of lower resting HR, we adjusted the
changes in HRV for the changes in resting HR. This
adjustment had minimal effect on change in HRV, suggesting that the exercise training–induced changes in
HRV are not the result of lower resting HR. Furthermore, this suggests that HRV measures may be of
greater sensitivity to detect changes in cardiac autonomic modulation on HR rather than evaluation of HR
rhythm alone.
Previous training studies conducted on sedentary
postmenopausal women have failed to show an increase in HRV with exercise training.14 –16 However,
Myslivecek et al15 showed an improvement in spontaneous baroreflex function, used as an index of parasympathetic modulation, and a decrease in sympathetic modulation after 12 weeks of a moderateintensity walking program. Conversely, Davy et al14
demonstrated that 12 weeks of moderate-intensity aerobic exercise had no effect on HRV, spontaneous
baroreflex sensitivity, VO2max, or body weight, despite
producing a reduction in resting BP in postmenopausal
women with elevated BP. Moreover, Perini et al16
found that 8 weeks of supervised aerobic training did
not affect HRV in older postmenopausal women (70 to
80 years old). Importantly, none of these studies had
more than 8 subjects in the training group, limiting
their ability to draw conclusions. To our knowledge,
our study is the first with adequate sample size to rigorously examine the effect of aerobic exercise training
on HRV in postmenopausal women.
The effect of HRT on the autonomic nervous system
remains inconclusive because of the variety of HRT
therapies available and a limited number of studies
examining this issue. At baseline, we did not find HRV
to differ among groups of women using and not using
HRT. Furthermore, HRT use did not modify the posi-
tive benefits of exercise training on HRV, and this was
evident regardless of the type of HRT used. However,
these findings must be taken cautiously because there
was a small number of women in the progestin-containing category.
Our observation of the short-term adaptation to aerobic training associated with enhanced cardiac vagal
activity in sedentary postmenopausal women may be
caused by several metabolic, biochemical, hormonal,
and neural changes in the body. An adequate shortterm exercise training program may reduce daily
stress, regulate body fat metabolism, slow resting HR,
and improve cardiorespiratory capacity, all of which
are associated with increases in cardiac vagal tone.
Exercise has a beneficial effect on several risk factors
for CVD, such as insulin resistance, lipid profiles, and
arterial blood pressure, which may associate with the
improvement in autonomic balance. Further studies
are needed to define the mechanisms that underlie
these interactions.
A limitation of the current study is the lack of ethnic
diversity. The effect of race on HRV has been reported
in the ARIC Study,44 in which black women have
higher cardiac vagal tone than white women. Although
our groups did not significantly differ by ethnicity, additional studies with a larger number of minority participants would be helpful in examining any potential
interaction between ethnicity, exercise, and HRV. The
current study does have important strengths such as a
large sample size, a tightly controlled protocol, and a
well-quantified, supervised exercise program.
In summary, the current study established that 8
weeks of a moderate-intensity aerobic exercise training
program increases overall HRV in sedentary postmenopausal women. This benefit is not influenced by the
use of HRT.
We thank Life Fitness for the donation of aerobic
exercise training equipment to our exercise physiology laboratory.
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