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Vol. 83, Issue 5, 1660-1665, 1997
-blockade before and after 10 days of exercise training in men and women
Human Performance Laboratory, Department of Kinesiology and Health Education, The University of Texas at Austin, Austin, Texas 78712
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
ACKNOWLEDGEMENTS
FOOTNOTES
REFERENCES
ABSTRACT 
Mier, Constance M., Melissa A. Domenick, and Jack H. Wilmore. Changes in stroke volume with 
-blockade before and
after 10 days of exercise training in men and women.
J. Appl. Physiol. 83(5):
1660-1665, 1997. We sought to determine whether 10 days of
training would be a sufficient stimulus for cardiac adaptations that
would allow a greater compensatory stroke volume during -blockade. We also sought to determine whether men and women had a similar cardiac
reserve capacity for increasing stroke volume with -blockade during
submaximal exercise. Eight men (age 29 ± 2 yr, mean ± SE) and
eight women (25 ± 2 yr) cycled at 65% of peak
O2 consumption (unblocked) under
placebo-control and -blockade (100 mg atenolol) conditions performed
on separate days. These tests were repeated at the same power output
after training (10 consecutive days, 1 h of cycling per day). Before
training, -blockade significantly (P < 0.05) decreased heart
rate (HR) and cardiac output and increased stroke volume in both men
and women. After training, the increase in stroke volume and decrease
in HR with -blockade was significantly less while cardiac output was
reduced more. There were no gender differences in the effects of
-blockade on HR, stroke volume, or cardiac output. These data
indicate that, during exercise with -blockade, exercise training for
10 days does not enhance the compensatory increase in stroke volume and
that men and women have a similar cardiac reserve capacity for
increasing stroke volume.
short-term training; atenolol; cardiac output; blood pressure
INTRODUCTION Studies in which stroke volume responses to endurance exercise training
in women have been investigated are few, and their results conflicting
(4, 5, 17, 24, 25). Although increases in stroke volume during
submaximal (4) and maximal (17, 25) exercise have been reported in
women after training, others have failed to show these increases (5,
24). Furthermore, gender differences in left ventricular function
during acute exercise appear to exist in that the increase in ejection
fraction and stroke volume from rest to exercise is less in women (1,
12, 14). In light of these data, it is possible that women do not hold
a similar cardiac reserve capacity for increasing stroke volume
compared with men. This could place women at a disadvantage during
exercise with The purpose of this study was twofold:
1) to determine whether, because of
an enhanced compensatory increase in stroke volume, 10 days of
endurance exercise training would attenuate the reduction in cardiac
output with METHODS
-BLOCKADE markedly decreases heart rate (HR) during
exercise. Despite this large reduction in HR, cardiac output is reduced only 5-14% because of the compensatory increase in stroke volume (16, 21, 22, 27). Because both endurance exercise training and
-blockade independently increase stroke volume in untrained men, and
because -blockade increases stroke volume in endurance-trained men
who have a relatively large blood volume (16), it is possible that the
combined effects of training and -blockade on stroke volume would be
greater than the single effect of -blockade if the untrained subject
has a sufficient cardiac reserve capacity. Because significant cardiac
adaptations occur within several days of endurance exercise training
(6), 10 days of training may be a sufficient stimulus for cardiac
adaptations that would allow a greater compensatory stroke volume
during exercise with -blockade.
-blockade if stroke volume cannot adequately compensate for a reduction in HR.
-blockade during submaximal exercise in young, sedentary
men and women and 2) to
determine possible gender differences in the cardiac output and stroke
volume responses to -blockade during submaximal exercise. In
addition, the study design allowed us to examine possible interactive
effects of gender, training, and -blockade on the hemodynamic
responses to submaximal exercise. We hypothesized that 10 days of
endurance exercise training would result in a greater compensatory
increase in stroke volume during submaximal exercise with -blockade.
Second, we hypothesized that women would demonstrate less increase in
stroke volume during submaximal exercise with -blockade, resulting
in a greater decrease in cardiac output compared with men.
O2 peak). Several
days after the first visit, single-blinded and randomly ordered tests
were performed under placebo-control or -blockade conditions on 2 separate days. These tests were separated by at least 3 nontest days to
allow sufficient washout time for the -blocker. During these visits,
a submaximal test (upright cycling) was performed at 65% of cycle
O2 peak
that lasted ~20 min. O2 uptake
(O2), HR, blood pressure,
cardiac output, and blood hemoglobin (Hb) concentration were determined during the submaximal exercise test.
Three hours before each of the submaximal cycle tests, the subject
ingested either a placebo tablet or a 100-mg atenolol tablet (1-blocker). The dose and time
of ingestion relative to the test were chosen to ensure a maximum
-blockade effect on HR (2a). The drug atenolol was chosen because,
on the basis of previous observations made from this laboratory, less
discomfort (i.e., shortness of breath, general fatigue, nausea) would
be experienced compared with the use of a nonselective -blocker such
as propranolol.
After completing the tests described above, the subjects began
endurance exercise training on a cycle ergometer for 1 h/day on 10 consecutive days. After the training period, the single-blinded, randomly ordered placebo and -blockade tests were repeated. The power output (watts) during these posttraining submaximal cycle tests
was identical to the pretraining power output. Because these tests were
separated by 3 nontest days, subjects performed 1 h of training on 1 of
the nontest days to maintain the training effects.
Exercise tests.
All exercise tests were performed under controlled environmental
conditions (21°C, 50% relative humidity). Expired ventilatory volume and concentrations of O2
and CO2 gas were measured
continuously during both submaximal and maximal tests by a SensorMedics
2900 metabolic cart, an automated computerized analysis system. During the cycle O2 peak
test, subjects warmed up at a low intensity for 2 min. This was
followed by progressive increases in work rate of 25 W each minute
until voluntary exhaustion. The criteria for achieving cycle
O2 peak were a
respiratory exchange ratio value >1.10 and a HR within 10% of the
age-predicted maximum HR. HR was monitored by using a HR monitor (model
XL; Polar USA, Montvale, NJ).
During the submaximal tests, steady-state
O2 was measured
after 5-7 min, immediately before initiation of
noninvasive CO2 rebreathing
maneuvers for determination of cardiac output. The Collier rebreathing
method was used to determine CO2
equilibrium (3) from which cardiac output was estimated by using the
indirect Fick equation corrected for Hb (15). Three
CO2-rebreathing maneuvers were
performed within a 15-min period, and the average cardiac output was
calculated from these measures. HR was recorded every minute, and
before each CO2-rebreathing
maneuver, systolic (SBP) and diastolic (DBP) blood pressures were
measured by using an auscultatory cuff attached to a fully automated
blood pressure monitor (model STBP-680, Colin Medical Instruments, San
Antonio, TX). A 0.5-ml blood sample was drawn without stasis for Hb
measures after the last
CO2-rebreathing maneuver. Hb was
measured in quadruplicate by using the cyanmethemoglobin method.
The three cardiac output measures taken during the placebo-control and
-blockade tests yielded an average coefficient of variation of 4.1 and 3.9%, respectively. SBP and DBP yielded an average coefficient of
variation of 3.0 and 5.7%, respectively, for the placebo-control tests
and 2.7 and 4.6%, respectively, for the -blockade tests. The
day-to-day reproducibility for cardiac output, SBP, and DBP determined
at 60% of O2 peak
has been previously reported from this laboratory (28). For cardiac
output, SBP, and DBP, the coefficient of variation was 5.9, 5.7 and
8.3%, respectively, and the intraclass correlation coefficients were
0.93, 0.82, and 0.77, respectively.
Cardiac output and HR were used to calculate stroke volume. Mean blood
pressure (MBP) was calculated as [(2 × DBP) + SBP]/3. Using a correction factor of 80 (converting
mmHg · min · l
1 to
dyn · s · cm5),
total peripheral resistance (TPR) was calculated from MBP and cardiac
output.
Training.
Training consisted of 1-h cycling bouts performed daily on 10 consecutive days. During each bout, subjects cycled for 30 min at a
power output that elicited ~80% of peak HR. During the second 30-min
period, subjects cycled at a power output that elicited ~95% of peak
HR for 2 min, followed by 1 min of low-intensity pedaling, for a total
of 10 intervals. Power output was increased on a daily basis to achieve
the appropriate training HR within a range of 5 beats/min.
Statistical analyses.
A three-way repeated-measures analysis of variance (1 between, 2 within) was performed to determine the effects of -blockade, gender,
and training on the physiological responses to submaximal exercise.
Where a significant interactive effect occurred, a Duncan's multiple-range test was performed to determine significant differences among groups. Significant differences were established at
P < 0.05, and data were expressed as
means ± SE.
RESULTS
-blockade.
Ten days of endurance exercise training significantly increased cycle
O2 peak
similarly in men (3.14 ± 0.13 vs. 3.42 ± 0.13 l/min) and in
women (2.11 ± 0.10 vs. 2.37 ± 0.12 l/min). Peak HR did not
change with training in either men (190 ± 3 vs. 190 ± 3 beats/min) or women (189 ± 3 vs. 189 ± 2 beats/min). When measurements were determined at 65% of pretraining
O2 peak (unblocked), we
found that training significantly decreased HR and increased stroke
volume in both men and women while having no effect on O2, cardiac output, SBP, DBP,
MBP, or TPR (Table 1).
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O2 peak, -blockade
significantly reduced HR, cardiac output, SBP, DBP, and MBP, and
increased stroke volume compared with placebo control (Table
2). After subjects were trained, the effect
of -blockade on HR was attenuated (Table 3, column T × B). However, the
decrease in cardiac output with -blockade was greater after training
because of the lower increase in stroke volume. Both DBP and
MBP were reduced more after training with -blockade.
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O2 peak during both the
placebo-control and -blockade tests in men and women. HR was
significantly decreased with training during both the placebo-control
and -blockade tests. Whereas stroke volume was significantly greater
after training during the placebo-control test, there was no difference
in stroke volume before and after training during the -blockade
test. Cardiac output tended to be greater after training during the
placebo-control test (P < 0.053) but
tended to be lower after training during the -blockade test
(P < 0.086).
O2 peak) under placebo-control (no block) and -blockade (-block) conditions before [Pre (
and dashed line)] and after [Post
(
and solid line)] 10 days of endurance exercise training.
* P < 0.05 vs. pretraining.
Interactive effects of training and
-blockade
with gender.
At 65% of pretraining
O2 peak, men had
significantly greater O2,
stroke volume, cardiac output, SBP, DBP, and MBP. Neither HR nor TPR
differed between men and women. There were no significant interactive
effects of training and gender or -blockade and gender (Table 3,
columns T × G and B × G). There was a tendency for cardiac
output to be reduced more in men with -blockade
(P < 0.053); however, the effect of
-blockade was significant in both men and women. Although SBP and
MBP were both significantly reduced with -blockade before and after
training, the effect after training was greater in women compared with
men and compared with women's pretraining responses (Table 3, column T × B × G). In women, there was a tendency for -blockade
to increase TPR before training and to decrease it after training
(P < 0.61). In men, the effects of -blockade on SBP,
DBP, MBP, and TPR were similar before and after training.
Figure 2 illustrates the effects of
training on MBP and TPR during both the placebo-control and
-blockade tests. In women, MBP was significantly greater
after training during the placebo-control tests, whereas during the
-blockade test, MBP tended to be lower after training
(P < 0.057). Similarly, in women,
SBP was significantly greater during the placebo-control tests after
training, whereas during the -blockade test, SBP tended to be lower
after training (P < 0.071). TPR or
DBP did not differ before and after training in women during either the
placebo-control or -blockade test. In men, there were no differences
in SBP, DBP, MBP, and TPR before and after training during either the
placebo-control or -blockade tests.
O2 peak under
placebo-control (no block) and -block conditions before and after 10 days of endurance exercise training. Symbols and lines as in Fig. 1.
* P < 0.05 vs. pretraining.
DISCUSSION
-blockade on cardiac output during submaximal exercise. Instead,
there was a greater attenuation of cardiac output with -blockade
after training because of an inadequate increase in stroke volume.
During submaximal exercise, the increase in stroke volume with
-blockade in both men and women after training was ~50% that of
the increase before training (20 vs. 9%, respectively). Previously,
stroke volume has been shown to increase ~20% with -blockade
during exercise in highly trained men (16); this suggests that the
capacity to raise stroke volume under the effects of -blockade is
not limited by an already large preload in these athletes. Although 10 days of endurance exercise training resulted in an increase in stroke
volume during submaximal exercise under placebo-control conditions,
stroke volume was no different before and after training under
-blockade con- ditions. Furthermore, cardiac output
during -blockade tended to be lower after training because
of a lower HR response during exercise.
Differences in stroke volume response to -blockade between these
subjects, who underwent 10 days of endurance exercise training, and
highly trained athletes suggests that there are some myocardial or
extramyocardial adaptations associated with long-term training that do
not occur within 10 days (13). After 10 days of endurance exercise
training, end-diastolic volume may be at or near maximum capacity by
having reached the limit of the myocardium and/or pericardium
such that preload could increase no further with -blockade. These
data indicate that 10 days of endurance exercise training is not an
adequate training stimulus for cardiac adaptations that would allow a
greater compensatory stroke volume during -blockade, despite there
being a greater stroke volume during placebo control.
Effects of gender.
The effects of -blockade on HR and stroke volume during submaximal
exercise were similar in men and women. Furthermore, 10 days of
endurance exercise training increased stroke volume similarly in
men and women. A compensatory increase in stroke volume with -blockade results from a greater preload facilitated by enhanced diastolic filling time and from a reduced afterload that accommodates left ventricular emptying (2, 21, 23). Our data indicate that the
compensatory increase in stroke volume previously demonstrated in men
(16, 21, 22, 27) occurs as well in women. This result suggests that
women have a similar cardiac reserve capacity for raising stroke volume
during submaximal exercise under -blockade conditions. Previously,
gender differences in left ventricular function were observed during
acute exercise, possibly mediated by differences in afterload or the
contractile reserve of the left ventricle (1, 12, 14). It
is possible that whatever the mechanisms for gender differences in left
ventricular function are, they may not become apparent at moderate
exercise intensities during -blockade.
An unexpected result was that, after 10 days of training, -blockade
reduced blood pressure more in women than in men, despite having a
similar effect on cardiac output in men and women. Reportedly, men
respond to isometric exercise and postexercise ischemia with greater
muscle sympathetic nervous activity as well as a greater blood pressure
response, independent of muscle mass (7). Furthermore, during
orthostatic challenge, women demonstrate a similar or greater increase
in HR, whereas men demonstrate a greater increase in TPR (8, 10). These
data indicate gender differences in cardiovascular control under
specific conditions. Unlike the men in this study, women did not
increase TPR with -blockade. As a result, blood pressure was more greatly compromised under -blockade conditions in
women after training. Mechanisms for these gender differences are not
known. However, because of the potent vasodilatory effects of estrogen
(9, 18, 26), it is possible that estrogen potentiates the
endothelial-mediated increase in vasodilation that occurs in the
skeletal muscle vasculature during exercise. Under -blockade conditions when cardiac output and HR are compromised, an enhanced vasodilatory response from estrogen may not allow TPR to increase adequately, which would in turn result in a lower blood pressure response.
Limitations.
Our sample size of eight men and eight women may limit
the interpretation of our data. It is possible that significant
differences may arise with a larger sample population. We recognize
that the blood pressure response to -blockade was not the primary
focus of this study. Therefore, not having measured either sympathetic nerve activity or blood levels of catecholamines limits our
interpretation of the blood pressure data. Such measurements might
reveal potential mechanisms for gender differences in blood pressure
regulation during exercise with -blockade.
Each subject ingested 100 mg of atenolol before exercise. Because of
gender differences in body weight, women received a greater dose
relative to their weight; this fact may have resulted in a greater
effect in women. However, this did not appear to be the case, because
-blockade reduced HR similarly in men and women. Because of the
number of tests and the time necessary to allow sufficient -blockade
washout, we were unable to control for the menstrual cycle. The
menstrual cycle may have confounded some of the results, because a
higher HR response during exercise has been reported during the luteal
phase compared with the follicular phase (11, 20). However, in this
study, possible menstrual cycle effects may have been masked by the
training and -blockade effects. Furthermore, there were no
differences in HR response during exercise in men and women.
Conclusions.
Ten days of endurance exercise training did not attenuate the effect of
-blockade on cardiac output during submaximal exercise because of an
inadequate increase in stroke volume. This indicates that
although stroke volume increased during placebo-control phases, 10 days
of training is not an adequate training stimulus to provide a greater
compensatory increase in stroke volume during -blockade. Second,
-blockade had a similar effect on stroke volume in men and women
during submaximal exercise, indicating that men and women have a
similar cardiac reserve capacity for increasing stroke volume during
-blockade. In addition, men better maintained their blood pressure
response to submaximal exercise during -blockade after
endurance exercise training, indicating gender differences in the
mechanisms involved in cardiovascular control during exercise.
ACKNOWLEDGEMENTS
The authors thank Dr. Paul Roach for his generous gift of atenolol. The significant intellectual contribution of Dr. Michael Joyner is greatly appreciated.
FOOTNOTES
Address for reprint requests: C. Mier, Dept. of Sport and Exercise Sciences, Barry University, 11300 Northeast Second Ave., Miami Shores, FL 33161-6695 (E-mail: CMIER{at}BU4090.barry.edu).
Received 15 January 1997; accepted in final form 18 July 1997.
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