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-adrenergic cardiovascular responses to
training in older women
Division of Geriatrics and Gerontology, Claude D. Pepper Older Americans Independence Center, and Cardiovascular Division, Department of Medicine, Washington University School of Medicine, St. Louis, Missouri 63110
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ABSTRACT |
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 TOP
 ABSTRACT
 INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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To determine whether endurance exercise training
can alter the 
-adrenergic-stimulated inotropic response in older
women, we studied 10 postmenopausal healthy women (65.4 ± 0.9 yr
old) who exercised for 11 mo. Left ventricular (LV) function was
evaluated with two-dimensional echocardiography during infusion of
isoproterenol after atropine. Maximal O2 consumption
increased 23% in response to training (from 1.35 ± 0.06 to
1.66 ± 0.07 l/min; P = 0.004). Training had no
effect on baseline LV function, end-diastolic diameter, LV wall
thickness, or LV mass. The increase in LV systolic function in response
to isoproterenol was unaffected by training. Furthermore, neither the
systolic shortening-to-end-systolic wall stress relationship nor the
end-systolic wall stress-to-end-systolic diameter relationship during
isoproterenol infusion changed with training. We conclude that older
postmenopausal women can increase their maximal O2
consumption with exercise training without eccentric LV hypertrophy or
enhancement of -adrenergic-mediated LV contractile function. These
observations provide an explanation for the finding that maximal
cardiac output and stroke volume are not increased in older women in
response to training.
aging; cardiac function; exercise; gender
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INTRODUCTION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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RECENT EVIDENCE SUGGESTS
THAT, in older adults, gender plays a significant role in the
physiological adaptations to endurance exercise training (1, 18,
20, 21). Both older men and women increase their aerobic
power [maximal O2 consumption
(
O2 max)] in response to training
(3, 20). However, it appears that in the older women
adaptations in skeletal muscles are mostly responsible for the
training-induced gain in O2 max, as
reflected by a significant increase in arteriovenous O2
content difference without appreciably higher cardiac output or stroke volume during maximal exercise in the trained state (20).
In contrast, in older men, a large portion of the training-induced gain
in O2 max is due to higher cardiac
output and stroke volume during maximal exercise (20).
Among the potential mechanisms responsible for the increases in maximal
cardiac output and stroke volume in response to training are a greater
inotropic sensitivity to -adrenergic agonists and physiological left
ventricular (LV) hypertrophy, as evidenced by enhancement of LV
contractile response to isoproterenol and LV enlargement in
endurance-trained older men and younger subjects (11, 12, 15, 18,
19, 22). Therefore, it is plausible that the absence of
increases in maximal cardiac output and stroke volume in older
postmenopausal women in response to training reported previously may be
a consequence of lack of -adrenergic-mediated increase in
LV function in the older women. Accordingly, this study was designed to
determine whether endurance exercise training can influence the
isoproterenol-stimulated increase in LV contractile function in the
older postmenopausal women.
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METHODS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Subjects
We studied 10 women [65.4 ± 0.9 (SE) yr old] who completed 11 mo of supervised endurance exercise training. These 10 women were among 12 women who were initially recruited for the study. The other two dropped out for nonmedical reasons. The selection criteria were age between 60 and 70 yr and absence of the following: 1) coronary risk factors, including elevated blood pressure, high plasma cholesterol and low-density-lipoprotein cholesterol concentrations, low high-density-lipoprotein cholesterol level, abnormal glucose tolerance, smoking, and family history for coronary artery disease; 2) pulmonary diseases; 3) angina; 4) significant cardiac arrhythmias; 5) congestive heart failure; and 6) orthopedic or musculoskeletal problems that could interfere with exercise training. No woman was on any medications, including cardiac medications or hormone replacement therapy. All women were sedentary (defined as lack of any regular physical activity more than twice a month) and nonsmokers. All had a normal cardiovascular examination, a negative exercise electrocardiogram (ECG) for myocardial ischemia and a normal thallium-201 myocardial perfusion exercise test. All subjects gave their informed consent, and the study was approved by the Washington University Human Studies Committee.Exercise Tests and O2 max
O2 max, as previously described
(8). O2 was measured continuously by open-circuit spirometry with the use of an automated on-line system (8). Inspiratory volume was measured by a
dry-gas meter (model CD-4, Parkinson-Cowan). The fractional
concentrations of expired O2 and CO2 were
measured with the use of O2 (model S3-A, Applied
Electrochemistry) and CO2 (model JB-2, Beckman) analyzers,
respectively. The following criteria were used for determining
O2 max: 1) no further
increase in O2 despite an increase in
exercise intensity, 2) a respiratory exchange ratio of
1.10, and 3) a heart rate within 10 beats/min of the
age-predicted maximal heart rate. The subjects were also tested
on a cycle ergometer to evaluate adaptive responses to training during
submaximal exercise at an absolute work rate.
Echocardiographic and Transmitral Doppler Studies
Two-dimensional and two-dimensional-guided M-mode (model 2000, Hewlett-Packard) echocardiographic images were obtained according to the guidelines recommended by the American Society of Echocardiography (16). The end-diastolic diameter (EDD) and end-systolic diameter (ESD) were measured, and fractional shortening (FS) was calculated using standard guidelines (16). LV end-systolic wall stress (
es) was measured as described by Grossman
et al. (2). LV mass was calculated from the M-mode images
and was normalized for fat-free mass and body surface area.
End-systolic pressure (ESP) was estimated from the equation ESP = (2 × systolic blood pressure + diastolic blood pressure)/3,
as reported by Kelly et al. (7). An average of six cardiac
cycles was used for the analysis. LV contractile performance was
assessed with the analyses of the FS-es and
ESD-es relationships by plotting FS as a function of
es and es as a function of ESD,
respectively, during graded doses of isoproterenol infusion after vagal
blockade (1.0 mg atropine iv), taking into consideration the changes in
EDD and heart rate. Nine of ten subjects had a strong inverse
relationship between FS and es. All had a strong
positive relationship between es and ESD. Pulsed-wave
Doppler transmitral diastolic flow velocity was measured to assess LV
diastolic filling dynamics. The early (E)-to-late (A) diastolic flow
velocity ratio was used to evaluate the effects of isoproterenol and
training on overall LV filling. E/A was normalized
(E/Ac) for heart rate and EDD: (E/A)/[EDD × (R-R)0.5], where R-R indicates cardiac cycle length
expressed in seconds, to reduce the confounding effects of preload and
heart rate. The echocardiograms were analyzed blindly with
respect to the subjects' status (i.e., before or after training). The
intraobserver variability for the measurement of EDD was 1%, for ESD
was 0.9%, for LV posterior wall was 4.7%, and for LV septal thickness
was 4.9%.
Isoproterenol Infusion
The subjects rested in the recumbent position for at least 30 min after insertion of an intravenous catheter. After baseline echocardiographic and transmitral Doppler images were acquired, each subject received atropine (1.0 mg). Intravenous isoproterenol infusion was given ~4 min after atropine at successive doses of 0.01, 0.02, 0.025, and 0.03 µg · kg
1 · min1 with the
use of an infusion pump (model 122, Harvard Apparatus, South Natick,
MA) with ECG and blood pressure monitoring. Each stage of infusion
lasted for 5 min. Repeat two-dimensional echocardiographic and
transmitral Doppler images and blood pressure measurements were
obtained 2 min after atropine administration and in the last 2 min of
each stage of the isoproterenol infusion. Transmitral Doppler diastolic
flow-velocity profile data were available in six women during
isoproterenol infusion.
Body Composition
We used hydrodensitometry to estimate changes in body composition (9).Exercise Training Program
The exercise training consisted of an initial flexibility and light stretching exercise component followed by 9 mo of endurance exercise training, as previously described (20). The flexibility portion of the exercise program lasted for 2 mo and was intended to prepare the older women for endurance exercise training and to reduce the likelihood of musculoskeletal complications. The endurance exercise training program consisted of walking, running, cycle ergometer, and treadmill exercises, as described previously in detail (20). The subjects were expected to exercise 5 days/wk for 1 h/session under supervision. The intensity of exercise was initially adjusted to require 60-70% of the subject'sO2 max and was increased
progressively to 70-80% of
O2 max, supplemented by additional
bouts of interval exercise requiring 90-95% of
O2 max 2 days/wk.
O2 max was measured at 3-mo intervals
to monitor the effectiveness of the training intensity to maintain a
constant training stimulus.
Study Design
We evaluated LV size and function with the use of two-dimensional echocardiography at baseline and during infusion of isoproterenol after cardiac muscarinic-receptor blockade with atropine. The studies were performed before and after 11 mo of endurance exercise training at the same time of day and using the same intercostal space and body position for the echocardiographic studies.Statistics
The differences in physiological variables before and after training were compared with the use of Student's t-test for paired observations when appropriate. In addition, two-way repeated-measures ANOVA (dose × time) was used to evaluate the responses during the isoproterenol infusion. Significance of differences was further evaluated with the use of the pairwise multiple-comparison procedures (Tukey's test). When the data were not normally distributed, nonparametric (ranked-order) two-way repeated-measures ANOVA was used. Least squares linear regression was used to determine the slopes of FS-es and
es-ESD relationships for each subject. Data are
presented as means ± SE.
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RESULTS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Exercise Training
The women exercised 3.7 ± 0.18 days/wk for ~9 mo. Exercise intensity averaged 86 ± 3% of maximal heart rate in the last 3 mo of the training program.O2 max, Heart Rate, and
Blood Pressure Responses to Training
O2 max, normalized for fat-free
mass or expressed in absolute terms, increased 23% in response to
training (Table 1). This increase
was greater (31%) when O2 max was normalized for body weight (Table 1). The respiratory exchange ratio
during the O2 max test was 1.21 ± 0.02 before and 1.22 ± 0.02 after training, indicating the
subjects attained their O2 max (Table
1). Resting as well as maximal heart rate, systolic blood pressure, and
diastolic blood pressure did not change significantly in response to
training (Tables 1 and 2). The women lost a modest amount of weight in
response to training (Table 1). Fat-free mass did not change
significantly (Table 1). The decrease in percent body fat did not
attain statistical significance (before: 35 ± 1.5% vs. after:
32 ± 1.7%; P = 0.09).
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During submaximal exercise at the same absolute work rate
(O2, before: 0.92 ± 0.08 l/min,
after: 0.88 ± 0.08; P = 0.23), heart rate was
significantly slower (129 ± 5 vs. 111 ± 6 beats/min; P = 0.012), but the reduction in systolic
(185 ± 8 vs. 172 ± 8 mmHg; P = 0.1)
or diastolic blood pressure (85 ± 3 vs. 80 ± 4 mmHg;
P = 0.13) did not attain statistical significance.
There was no relationship between the magnitude of increase in
O2 max and the extent of decrease in
heart rate during submaximal exercise in response to training.
LV Size, Geometry, and Function
Baseline data.
Exercise training induced no significant changes in EDD, ESD, FS,
es, and E/Ac (Table
2). LV septal and posterior wall
thicknesses, the LV wall thickness-to-radius ratio, or LV mass
expressed in absolute terms or when normalized for fat-free mass or
body surface area did not differ between the untrained and trained
states (Table 1).
Responses to cardiac muscarinic blockade. Atropine increased heart rate (Table 2). The effects of atropine on echocardiographic measures of LV systolic function as well as systolic and diastolic blood pressure were not statistically significant (Table 2). However, E/Ac decreased 29 and 32% with atropine before and after training, respectively (Table 2). Training had no significant effect on the cardiovascular responses to cardiac muscarinic blockade (Table 2). The dose of atropine normalized for body weight was 16.8 ± 0.9 µg/kg before and 17.4 ± 0.9 µg/kg after training (P = 0.01).
Responses to -adrenergic stimulation.
dose effect
. Isoproterenol resulted in significant increases in heart rate,
systolic blood pressure, and LV systolic shortening (Table 2).
There were significant decreases in es, ESD, and
diastolic blood pressure in response to isoproterenol (Table 2).
E/Ac approached the baseline levels with higher doses of
isoproterenol (Table 2).
es or
ESD induced by isoproterenol (Table 2). The changes in EDD were not
significant (Table 2). Diastolic blood pressure was significantly lower
in the trained state (Table 2). However, the slopes of the fall in
diastolic blood pressure in response to isoproterenol were similar
before and after training (before: 
5.2 ± 0.8 mmHg · µg1 · kg1 · min1,
after: 4.4 ± 0.7 mmHg · µg1 · kg1 · min1;
P = not significant). The training had no effect
on the magnitude of the maximal decrease in diastolic blood pressure in
response to isoproterenol (before: 14.0 ± 2.4 mmHg, after:
11.6 ± 2.2; P = 0.28). Furthermore, the
2-adrenergic sensitivity (5), defined as
the dose of isoproterenol needed to reduce diastolic blood pressure to
one-half of its lowest level, was unchanged with training (before:
0.0140 ± 0.002 µg · kg1 · min1, after:
0.0145 ± 0.002 µg · kg1 · min1;
P = 0.81).
DOSE × TRAINING INTERACTION.
There were no statistically significant interactions in the
physiological variables (Table 2), except for the heart rate response to isoproterenol which was slower after training (Table 2).
Effects of training on the -adrenergic-mediated changes in LV
contractile function.
We found that in 9 of the 10 women the FS-es
relationship was linear, with an r value of 0.943 ± 0.015 for the initial and 0.884 ± 0.041 for the final
evaluations. Therefore, for the analysis of the FS-es
slopes, data from those nine subjects were used. For all other
analyses, the data from the entire group (n = 10) are
reported. The average of the individual slopes of the
FS-es relationships was 0.673 ± 0.104 for the
initial evaluation and 0.722 ± 0.102 (P = 0.61)
for the final assessment (Fig.
1A). The
y-intercept of the FS-es relationship was
unaffected by training (initial: 69.4 ± 3.4% vs. final:
72.8 ± 3.8%; P = 0.36; Fig. 1A).
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es both before (r = 0.89 ± 0.03) and
after (r = 0.91 ± 0.02) in all 10 women. The
slopes and y-intercepts of the es-ESD
relationship during -adrenergic stimulation were similar in the
trained and untrained states (slope, before: 3.2 ± 0.3, after:
2.7 ± 0.5, P = 0.32; y-intercept,
before: 41 ± 8 g/cm2, after: 30 ± 12 g/cm2; P = 0.40; Fig. 1B).
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DISCUSSION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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The findings of this study provide evidence that, although older
postmenopausal women can attain a significant increase in aerobic
power, they do not show significant cardiac adaptations to endurance
exercise training. This is reflected in the absence of
physiological LV eccentric hypertrophy and remodeling and
-adrenergic-mediated enhancement of LV diastolic filling and
systolic function. These adaptations are considered among the
mechanisms accounting for the larger cardiac output and stroke volume
during maximal exercise in young subjects and older men in the trained
state (6, 22). In two recent studies, older postmenopausal
women did not exhibit significant increases in exercise cardiac output,
stroke volume, LV ejection fraction, and diastolic filling in response
to training (18, 20). Our findings provide an explanation
for the lack of these adaptive responses and suggest that one of the
reasons for the lack of increase in stroke volume during maximal
exercise in older women is the absence of -adrenergic-mediated
enhancement of LV systolic function.
Exercise training induced a greater decrease in diastolic blood
pressure in response to isoproterenol in these women. This finding
suggests that training may have been associated with vascular adaptations. The role of the 2-adrenergic agonist in
this adaptive response, however, is unclear because baseline diastolic
blood pressure was lower in the trained state, the magnitude of the maximal reduction in diastolic blood pressure in response to
isoproterenol was similar before and after training, and the
2-mediated vasodilatory sensitivity was unaffected by
training. Additional studies are needed to delineate the mechanisms
involved in this adaptation.
The reasons for the lack of -adrenergic-mediated cardiac adaptations
to exercise training in older postmenopausal women are unknown. One
possibility is that in women estrogen is necessary for exercise-induced
cardiac adaptations and physiological hypertrophy, because
premenopausal women show cardiovascular adaptations that are similar to
those in men even in response to short-term (as brief as 10 days)
endurance exercise training (14). However, a recent
cross-sectional study reported that hormone replacement therapy had no
effect on cardiac output during maximal exercise in the older
postmenopausal endurance-trained women (13). The other
possibility is that these women could have had occult cardiac disorders
such as ischemic heart disease or cardiomyopathy that could have
prevented the physiological adaptations in cardiovascular system. This
possibility is unlikely because of the vigorous screening procedure we
used in this study. All of the women had normal thallium-201 and
negative ECG responses to exercise, and none had clinical or
echocardiographic evidence of dilated or hypertrophic cardiomyopathy or
of valvular heart disease. A smaller increase in heart rate in response
to isoproterenol in the trained state may have contributed to the
absence of enhanced LV contractile function during -adrenergic stimulation. However, this interpretation does not provide a
satisfactory explanation for our findings because older men who adapt
to training with a significant enhancement of the
isoproterenol-stimulated increase in LV systolic performance also
exhibit diminished chronotropic responses to isoproterenol
(22).
Another possibility is the gender-related differences in cardiac
-adrenergic activity in older adults. In support of this notion are
a previous study that reported gender-related differences in cardiac
response to exercise (4) and a recent report that suggests
that the age-associated alterations in contractile responses to
isoproterenol appear to be gender specific (25). Because the age-associated decline in the -adrenergic sensitivity appears to
be less pronounced in women than in men (25), the
-adrenergic-mediated cardiac adaptations to training may also be
less conspicuous in the older women compared with older men. The
relative intensity and duration of the training in these women were
similar to the training protocol used in older men in our previous
studies (18, 20). Therefore, the absence of
cardiovascular adaptations cannot be attributed to the differences in
the training stimulus.
Men in the 60- to 75-yr-old age range show significant cardiovascular
adaptations to endurance exercise training. These include physiological
LV eccentric remodeling and enhanced systolic and diastolic LV function
during exercise (10, 18, 24) mediated, in part, by an
increase in inotropic response to -adrenergic stimulation
(22). These adaptations are likely to attenuate the age-associated decline in cardiovascular function attributed to
physical inactivity (23) and provide a mechanism for the increase in maximal cardiac output induced by training (17, 22). Our data demonstrate that older women can attain as large an increase in aerobic power, in relative terms, as the older men even
without enhancement of -adrenergic-mediated increases in inotropic
sensitivity, LV diastolic filling, or physiological cardiac hypertrophy
in response to 9 mo of endurance exercise training. These observations
suggest that neither LV eccentric hypertrophy nor enhancement of
cardiac function is necessary to bring about a significant
increase in aerobic power in response to endurance exercise
training in older healthy women. It appears that adaptations in
skeletal muscle can, at least partially, compensate for the lack of
central adaptations to induce a relatively large increase in
O2 max in older healthy women.
Nevertheless, it seems probable that the adaptive response in
performance to the very intense training necessary to be
successful in competition in athletic endurance events would be
limited by the absence of central cardiovascular adaptations.
The limitations of our study are as follows. 1) We used a
relatively small number of subjects, making it difficult to generalize our findings to all older women. However, it is likely that the absence
of adaptive -adrenergic responses in our study is not due to an
inadequate sample size because the increase in LV systolic shortening
in response to isoproterenol was actually slightly less in the trained
state. Furthermore, the changes in the slopes of the LV systolic
shortening-end systolic wall stress relationship attributable to
training were very small so that, even with an attainment of a
statistical significance, the differences would still be
physiologically insignificant. 2) The other potential limitation is lack of a control group. However, because there were only
small and insignificant cardiac adaptations to 11 mo of training,
inclusion of a control group would have been essential only if there
were any expectations of a substantial reduction in the
-adrenergic inotropic sensitivity over a 1-yr interval in these
women. Recent data, however, suggest that women exhibit only a
small attenuation of cardiac -adrenergic sensitivity over a
several-decade interval (25). Therefore, it is improbable that training could have prevented a marked age-associated decline in
inotropic sensitivity to catecholamines in these older women. 3) Another limitation of our study is an insufficient dose
of atropine to induce complete cardiac muscarinic blockade,
particularly in the trained state, in which, because of enhanced vagal
tone, cardiac muscarinic blockade might have been less complete. It can
therefore be argued that this inconsistency in the extent of vagal
blockade was responsible for our findings. Although we cannot rule out
this possibility entirely, we should point out that because of weight
loss, the weight-adjusted dose of atropine was actually higher after
training, which may partially offset the effect of enhanced vagal tone
in the trained state. Furthermore, judging from the values for resting
heart rate, which were similar, it appears that increased vagal tone in
the trained state may not have been substantial in these older women.
4) Despite the known variability of the echocardiographic
measurements, the reproducibility of our echocardiographic data was
good. Furthermore, E/A, used here as an index of LV diastolic filling,
is sensitive to several variables, including heart rate and cardiac
loading conditions. We attempted to minimize this potential limitation
by normalizing E/A for heart rate and preload (EDD). We also recognize
that cardiac responses to several years of training may be different
from those we reported in these women. Therefore, our conclusions may
not be applicable to the older postmenopausal endurance-trained female athletes, and it is possible that, unlike these women, the female master athletes may show increased cardiac function in response to catecholamines.
In summary, our results suggest that older women do not exhibit any
changes in -adrenergic cardiac sensitivity to endurance exercise
training, even though they can attain a sizable increase in their
O2 max. The lack of this adaptation
helps to account, in part, for the absence of higher stroke volume and cardiac output during maximal exercise in response to training in older women.
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ACKNOWLEDGEMENTS |
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This study was supported by National Institutes of Health Grants Claude D. Pepper Older American Independence Center AG-13629, RO1 AG-12822, RO1 AG-12235, and RO1 HL-58878 and by General Clinical Research Center Grant S-M01-RR-00036.
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FOOTNOTES |
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Present address of R. J. Spina: Dept. of Kinesiology and Health Education, The University of Texas at Austin, Bellmont Hall 222, Austin, TX 78712.
Address for reprint requests and other correspondence: A. A. Ehsani, Washington Univ. School of Medicine, 4566 Scott Ave., Campus Box 8113, St. Louis, MO 63110 (E-mail: aehsani{at}im.wustl.edu).
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. Section 1734 solely to indicate this fact.
Received 16 March 2000; accepted in final form 21 July 2000.
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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