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1 Division of Cardiology, University of Pittsburgh, Pittsburgh, Pennsylvania 15213; 2 Department of Human Kinetics, University of Wisconsin-Milwaukee, Milwaukee, Wisconsin 53201; and 3 Department of Kinesiology, University of Maryland, College Park, Maryland 20742
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ABSTRACT |
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 TOP
 ABSTRACT
 INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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We sought to determine the cardiovascular responses to increasing exercise intensities in postmenopausal women with different physical activity levels and hormone replacement therapy (HRT) status. Forty-four women (11 sedentary, 19 physically active, 14 master athletes; 24 not on HRT, 20 on HRT) completed treadmill exercise at 40, 60, 80, and 100% of maximal oxygen consumption. Oxygen consumption, heart rate, blood pressure, and cardiac output, determined via acetylene rebreathing, were measured at each exercise intensity. HRT did not affect cardiovascular hemodynamics. Stroke volume (SV) decreased significantly between 40 and 100% of maximal oxygen consumption in all groups, and the decrease did not differ among groups. The greater oxygen consumption of the athletes at each intensity was due to their significantly greater cardiac output, which was the result of a significantly greater SV, compared with both of the less active groups. The athletes had significantly lower total peripheral resistance at each exercise intensity than did the two less active groups. There were no consistent significant hemodynamic differences between the physically active and sedentary women. These results indicate that SV decreases in postmenopausal women as exercise intensity increases to maximum, regardless of their habitual physical activity levels or HRT status.
cardiac output; stroke volume; oxygen consumption; estrogen
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INTRODUCTION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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IN THE LAST 10-15 years, several reports have
questioned the traditional concept that stroke volume (SV) attains a
plateau at exercise intensities above 40-60% of maximal oxygen
consumption (
O2 max)
(2). Some reports indicate that SV may decrease in untrained
individuals as the exercise approaches maximal intensity (3, 8, 31). It
has also been reported that endurance exercise training can prevent
this decline in SV (31) and that trained individuals may increase SV as
intensity increases (5). A recent study in endurance-trained
postmenopausal women reported that SV decreased between 70 and 90%
O2 max (25). However,
sedentary postmenopausal women and elite endurance-trained
postmenopausal athletes were not studied. Thus it is not clear whether
sedentary and elite postmenopausal female athletes would respond
similarly. We hypothesized that SV responses to increasing exercise
intensity would not decline in elite endurance-trained
postmenopausal women. Most physically active postmenopausal women,
however, do not perform the level of training necessary to be a
competitive athlete. Therefore, we also sought to determine whether the
hemodynamic responses to increasing exercise intensity were similar in
women participating in an exercise program that would be typical of
what older, sedentary women might initiate and maintain (20).
Several studies have reported differences between older men and women in their hemodynamic responses to acute exercise and aerobic training (7, 10, 11, 30, 32). The estrogen deficiency that accompanies menopause has been cited as a potential factor explaining these gender differences. This decline in estrogen has been linked to increased incidence of heart disease and has wide-ranging effects on the cardiovascular (CV) system (9, 22, 29). Many studies have documented the physiological benefits gained from hormone replacement therapy (HRT) (9, 12, 13, 15, 16, 18, 21, 23, 24, 26, 29). However, there are limited data indicating whether the CV hemodynamic response to increases in exercise intensity differs between postmenopausal women on HRT and not on HRT (25). Thus we also sought to determine whether HRT use was associated with altered hemodynamics during exercise.
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METHODS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Subjects
Forty-four healthy postmenopausal women were recruited on the basis of their habitual level of physical activity (sedentary, physically active, or competitive master athletes) and hormone replacement status (on HRT or not on HRT). Postmenopausal status was determined by self-reported lack of menses for >2 yr and elevated levels of follicle-stimulating hormone and luteinizing hormone. Sedentary women had not participated in regular aerobic activity for >2 yr. Women who participated in aerobic exercise for >90 min/wk, >3 days/wk, but who were not training for endurance-based competitive events were classified as physically active (20). The female athletes were competitive distance runners who were training vigorously and regularly placed in regional, national, and international competitions. The HRT group consisted of a majority of women on oral combined estrogen and progestin (16 of the 20 women on HRT); 10 of these women were taking progesterone continuously, while the remaining 6 were on a cyclic regimen (Table 1). The ranges of estrogen and progestin dosages were similar in all groups. The physical activity level and HRT status of all subjects had been constant for at least the 2 yr before the study. Whereas the sedentary and physically active women were recruited from the Pittsburgh metropolitan area, it was necessary to recruit the female athletes from across the United States to achieve sufficient numbers for study. All subjects were free of known heart disease and were not taking medications that could affect their response to exercise. The Institutional Review Board of the University of Pittsburgh approved this study, and all subjects provided their informed voluntary consent before testing.
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To ensure that they were free of CV disease, sedentary and physically
active subjects underwent a screening graded maximal exercise test
according to a modified Naughton protocol (6). O2 max was measured
in a subsequent exercise test in those women completing the screening
test without evidence of CV disease. The female athletes completed a
single maximal treadmill exercise test for both screening and to
measure O2 max. Blood
pressure (via auscultation of the brachial artery), heart rate (HR),
and electrocardiogram (ECG) were monitored before, during, and after and oxygen consumption (O2)
was measured during all exercise tests. Exercise continued until the
subject reached exhaustion or signs or symptoms of CV decompensation
occurred (1). Body composition was determined with dual-energy X-ray
absorptiometry (DPX-L, Lunar, Madison, WI).
Cardiac output was measured at 40, 60, 80, and 100% of
O2 max
during treadmill exercise by using an acetylene rebreathing technique
on the basis of the procedures of Triebwasser et al. (33). During
submaximal exercise, cardiac output was measured after ~6 min at the
desired O2. During maximal
exercise the cardiac output determination began when the subject's
O2 was within 5% of her
O2 max or she
indicated that she was unable to complete another 60 s of exercise.
O2 and ECG were monitored throughout exercise, and blood pressure was measured immediately preceding each cardiac output determination. SV, total peripheral resistance (TPR), and arteriovenous
O2 difference were calculated by
using standard equations.
Statistics
All data are reported as means ± SD. Differences among groups at each intensity were determined by ANOVA with Bonferroni adjustments made on all significant F-values. To evaluate differences in the response to increases in exercise intensity among the different groups, a two-factor ANOVA with repeated measures on one factor (exercise intensity) was performed. Contrast statements were used to determine differences in the response to exercise between exercise intensities. P < 0.05 was considered statistically significant.| |
RESULTS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Subject Characteristics (Table 2)
The 44 women in the study averaged 63 ± 5 yr of age (range 53-75 yr). There were no significant differences among groups in the length of time the women had been postmenopausal or their duration of HRT. The physically active and athlete groups exercised for a similar number of hours per week and had been exercising for a similar number of years. The athletes averaged 29.0 ± 9.6 miles/wk of running at the time of the study.
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There were no differences in age, height, or weight among any of the different physical activity or HRT groups (Table 2). The female athletes had significantly lower body fat and fat mass than did the other two groups of women and significantly greater lean mass than did the sedentary, but not the physically active, women. There were no significant body composition differences between the physically active and sedentary women.
The athletic women had a significantly greater
O2 max than
did the less active groups. The
O2 max of the phy-
sically active women was greater than that of the sedentary group, but the difference was only significant when
O2 max was expressed in
liters per minute (Fig. 1). There were no
differences in maximal HR among the different habitual physical
activity groups.
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CV Hemodynamics
Effects of HRT.
HRT status was not associated with any differences in
O2, cardiac output, HR, SV,
arteriovenous O2 difference, blood
pressure, or TPR across the 40-100% of
O2 max range of
exercise intensities. HRT status also did not affect the change in
these variables as exercise intensity increased. Figure
2 demonstrates the similarity of the SV
response in the women on and not on HRT. Furthermore, subgroup analyses
indicated that there were no significant differences between those
women on and not on HRT within any physical activity group. Therefore,
women on and not on HRT were combined for the remainder of the
analyses.
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Effects of habitual physical activity levels.
As a result of their higher
O2 max, the female
athletes had a greater O2
than did either of the less active groups at each of the four exercise
intensities (40, 60, 80, and 100% of O2 max; Fig.
1). The physically active women had a greater
O2 than did the sedentary
women only at 80 and 100% of
O2 max and only when
expressed as liters per minute.
O2 max. The increase in
cardiac output from 80 to 100% of
O2 max was significant
in the sedentary and physically active groups but not in the athletes.
The athletic women had a significantly greater cardiac output than did
the two less active groups of women at each exercise intensity. There
were no differences in cardiac output between the physically active and
sedentary women at any exercise intensity. Arteriovenous oxygen
difference increased significantly for each group over the range of
exercise intensities, but there were no significant differences between groups at any of the exercise intensities. Thus, at each intensity, the
greater O2 of the athletes
was due solely to their significantly larger cardiac output.
The greater exercise cardiac output in the athletes was due to their
significantly larger SV at each intensity because there was no
differences in HR among any of the groups at any of the four exercise
intensities (Fig. 1). Although there were no differences in HR among
the groups, HR increased significantly in all groups with each increase
in intensity. SV was not significantly different between the physically
active and sedentary women at any exercise intensity. There were no
significant differences between SV at 40 and 60% of
O2 max in any of the
physical activity groups. However, SV decreased significantly in each
group of women as exercise intensity increased from 60 to 100% of
O2 max. This decrease
in SV was similar in all three physical activity groups. Cardiac output
was increased, or at least maintained, because the increase in HR
compensated for the reduction in SV.
In general, the groups had similar systolic blood pressure (SBP),
diastolic blood pressure (DBP), and mean arterial pressure (MAP) at all
of the exercise intensities (Fig. 3). As
exercise intensity increased both SBP and MAP increased significantly
for each group. DBP did not change as exercise intensity increased. Although each group significantly reduced their TPR with the increase in exercise intensity from 40 to 100% of
O2 max, the TPR of the
athletes was, with one exception, significantly lower than either of
the other two groups of women at each exercise intensity (Fig. 3).
There were no differences in TPR between the physically active and
sedentary women.
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DISCUSSION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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The major finding of this study is that the SVs of postmenopausal women
decrease significantly as exercise intensity increases to maximal,
regardless of the level of habitual physical activity. In the present
study, SV was maximal at 40-60% of
O2 max and then
decreased significantly in all three physical activity groups as
exercise intensity approached maximum. Although such a decline in SV
has been reported in sedentary individuals (31), such a finding is not
typically seen in trained individuals. Previous studies in young,
trained men and women have reported that SV either plateaus or
increases as exercise intensity approaches maximum (5, 27, 28).
Similarly, in studies of male athletes of the same age as the women in
the present study, SV has been reported to either plateau (27) or to
continue to increase as exercise intensity increases (4). Only Proctor
et al. (25) have reported a decline in SV in trained subjects as
exercise intensity increased. Like the present study, the subjects
studied by Proctor and colleagues were endurance-trained postmenopausal women. Thus it appears that postmenopausal female athletes, unlike young men and women and older men, are unable to maintain SV as exercise intensity increases to maximum. Furthermore, the decline in SV
was similar for all three physical activity groups. This similarity
between the physical activity groups is not typically seen in older men
or young men or women (4, 5, 27, 28, 31).
In previous studies in untrained individuals, the decline in SV as exercise approaches maximal intensity has generally been attributed to a decrease in left ventricular filling that results from the higher HRs. It is typically assumed that endurance training compensates for this decrease, thus preventing the decline in SV. Gledhill et al. (5) reported that the greater SV in young trained men was the result of enhanced left ventricular filling rather than their enhanced emptying, which was also present. Fleg et al. (4) suggest that in older male athletes the greater SV was the result of a combination of an increase in end-diastolic volume and a decrease in end-systolic volume. Proctor et al. (25) suggest that the decline in SV that was seen in their postmenopausal women may have been related to the estrogen deficiency associated with menopause because the four postmenopausal women not receiving estrogen replacement appeared to demonstrate more of a decline in SV than did the four women that were receiving estrogen replacement (25). However, in the present study, with 20 of the 44 subjects receiving HRT, HRT use was not associated with different hemodynamic responses to the increase in exercise intensity (Fig. 2). Nor was HRT status associated with differing responses when examined separately within each of the three physical activity groups. Proctor and colleagues (25) also suggest that the decline in SV was more evident in their older subjects. It may be that the advanced age of our subjects (63 ± 5 yr) contributed to the decline in SV. Further study is necessary to address this potential gender-specific age effect seen in women but not men.
The increase in cardiac output that occurs as exercise intensity
increases beyond 60% of
O2 max was solely the
result of the increase in HR that occurs as intensity increases. Even
though there was a decrease in SV, the increase in HR was sufficiently large between each of the submaximal exercise intensities to result in
a significantly greater cardiac output. However, when the intensity was
increased from 80 to 100% of
O2 max, the increase in
HR was not great enough to result in a significantly greater cardiac output in the athletic women.
The greater O2, at each
exercise intensity, of the athletic women was due to their
significantly larger cardiac output since arteriovenous oxygen
difference was not significantly different among physical activity
groups at any exercise intensity. The greater cardiac output, in turn,
was the result of a significantly greater SV, because there was no
difference in HR among the groups. In addition, there were no
differences in SBP, DBP, or MAP among groups at any of the four
exercise intensities. This suggests that the greater SV of the athletes
is the result of enhanced central, rather than peripheral, CV factors,
which may have resulted from their prolonged endurance training. An
enhancement of either contractility or the Frank-Starling mechanism, or
both, could potentially contribute to the enhanced central factors.
Similar findings previously have been reported in training studies in young men and women and older men (14, 17, 30, 31). Such a finding
might also be expected in women who have undergone vigorous endurance
training for an average of 15 yr. Spina et al. (30) reported that
previously sedentary postmenopausal women who undergo an
endurance-training program of 9-12 mo do not improve central CV
function (i.e., cardiac output and SV) (30). Clearly it is possible,
because of the cross-sectional nature of the present study, that the
athletes' greater SV and cardiac output are the result of differences
that were present before the initiation of training. A second
possibility, however, is that the years of training performed by the
athletes in the present study provided a sufficiently greater stimulus
to induce beneficial adaptations to the CV system than might be
achieved with the 6-12 mo of training typically used in
longitudinal studies.
With few exceptions, the physically active women were not significantly
different from the sedentary women in any of the CV variables measured
in the present study. This is perhaps not unexpected as the Centers for
Disease Control (CDC)/American College of Sports Medicine (ACSM) report
indicates that meeting the minimum exercise guidelines may not be
sufficient to improve CV fitness, but would likely reduce one's risk
for heart disease (20). And while none of the differences was
significant in the present study, the data generally indicate trends
toward greater SV, cardiac output, and O2 and lower TPR in the
physically active compared with the sedentary women throughout the
range of exercise intensities in the current study.
HRT status was not associated with altered CV hemodynamics at any of the exercise intensities in the present study. This agrees with our previous findings that HRT was not associated with altered hemodynamics during maximal exercise (19). These results suggest that HRT use may not improve CV function during exercise. A randomized, longitudinal trial will be necessary to provide a definitive answer to this question. Our results also suggest that the gender differences in response to exercise in older men and women reported in previous studies may not necessarily have been due to the estrogen deficiency that is associated with menopause.
In conclusion, the results of the present study demonstrate that SV
declines in postmenopausal women as exercise intensity approaches
maximum, regardless of the level of habitual physical activity or HRT
status. In addition, the greater
O2 attained by postmenopausal
female athletes during submaximal and maximal exercise is the result of
their greater SV and lower TPR. Furthermore, postmenopausal women who
perform regular exercise in sufficient quantity to meet the guidelines
of the CDC/ACSM do not have significantly different hemodynamics during
exercise than do sedentary postmenopausal women who do not undergo
regular exercise (20).
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ACKNOWLEDGEMENTS |
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The authors acknowledge Dr. Lurng-Kuo Liu for his computer expertise in the development of the customized metabolic software. The authors also acknowledge the enthusiastic and dedicated volunteers who participated in this project.
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FOOTNOTES |
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This research was supported by grants from the American Heart Association, Pennsylvania Affiliate, and the Andrus Foundation American Association of Retired Persons. M. D. Brown was supported by National Institutes of Health (NIH) Grant RO3 AG-12781, and G. E. Moore was supported by NIH Grant KO8 HL-03029. This work was also conducted with the assistance of the University of Pittsburgh General Clinical Research Center (GCRC) (NIH/National Center for Research Resources/GCRC Grant 5M01 RR-00056).
The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. §1734 solely to indicate this fact.
Address for reprint requests and other correspondence: S. D. McCole, Dept. of Human Kinetics, P.O. Box 413, Univ. of Wisconsin-Milwaukee, Milwaukee, WI 53201 (E-mail: smccole{at}uwm.edu).
Received 14 December 1998; accepted in final form 6 August 1999.
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TOP
ABSTRACT
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METHODS
RESULTS
DISCUSSION
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S. D. McCole, A. R. Shuldiner, M. D. Brown, G. E. Moore, R. E. Ferrell, K. R. Wilund, A. Huberty, L. W. Douglass, and J. M. Hagberg {beta}2- and {beta}3-Adrenergic receptor polymorphisms and exercise hemodynamics in postmenopausal women J Appl Physiol, February 1, 2004; 96(2): 526 - 530. [Abstract] [Full Text] [PDF]
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J. M. Hagberg, S. D. McCole, M. D. Brown, R. E. Ferrell, K. R. Wilund, A. Huberty, L. W. Douglass, and G. E. Moore ACE insertion/deletion polymorphism and submaximal exercise hemodynamics in postmenopausal women J Appl Physiol, March 1, 2002; 92(3): 1083 - 1088. [Abstract] [Full Text] [PDF]
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), physically active (
), and master athlete (
) postmenopausal
women. bpm, Beats/min. For an explanation of the significant changes as
exercise intensity increased, see text. * Significantly different
from sedentary group at same exercise intensity,
P < 0.05. # Significantly different
from physically active group at same exercise intensity,
P < 0.05.
)
postmenopausal women. For an explanation of the significant changes as
exercise intensity increased, see text. * Significantly different
from sedentary group at same exercise intensity,
P < 0.05. # Significantly different
from physically active group at same exercise intensity,
P < 0.05.