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Vol. 83, Issue 6, 1900-1906, December 1997
Section of Applied Physiology, Department of Internal Medicine, Washington University School of Medicine, St. Louis, Missouri 63110
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
ACKNOWLEDGEMENTS
FOOTNOTES
REFERENCES
ABSTRACT 
Mier, Constance M., Michael J. Turner, Ali A. Ehsani, and
Robert J. Spina. Cardiovascular adaptations to 10 days of cycle
exercise. J. Appl. Physiol. 83(6):
1900-1906, 1997.
We hypothesized that 10 days of training would
enhance cardiac output (CO) and stroke volume (SV) during peak exercise
and increase the inotropic response to 
-adrenergic stimulation. Ten
subjects [age 26 ± 2 (SE) yr] trained on a cycle
ergometer for 10 days. At peak exercise, training increased
O2 uptake, CO, and SV
(P < 0.001). Left ventricular (LV)
size and function at rest were assessed with two-dimensional echocardiography before (baseline) and after atropine injection (1.0 mg) and during four graded doses of dobutamine. LV end-diastolic diameter increased with training (P < 0.02), whereas LV wall thickness was unchanged. LV contractile
performance was assessed by relating fractional shortening (FS) to the
estimated end-systolic wall stress
(
ES). Training increased the
slope of the FS-ES relationship (P < 0.05), indicating enhanced
systolic function. The increase in slope correlated with increases in
CO (r = 
0.71,
P < 0.05) and SV
(r = 0.70,
P < 0.05). The increase in blood
volume also correlated with increases in CO
(r = 0.80, P < 0.01) and SV (r = 0.85, P < 0.004). These data
show that 10 days of training enhance the inotropic response to
-adrenergic stimulation, associated with increases in CO and SV
during peak exercise.
short-term training; left ventricular function; cardiac output; stroke volume
INTRODUCTION ENDURANCE EXERCISE TRAINING lasting several weeks
increases heart size and improves cardiac reserve capacity manifested
as increases in cardiac output and stroke volume during maximal
exercise (18, 20). This adaptive increase in pump performance of the heart contributes to the increase in maximal
O2 uptake
( Although these adaptations occur with endurance exercise training
lasting several weeks, it is not known whether short-term endurance
exercise training (7-10 consecutive days of training) can elicit
comparable improvements. Similar to endurance exercise training of
several weeks' duration, short-term training induces a significant
increase in stroke volume both at rest and during submaximal-intensity
exercise, as well as significant increases in
Given the significant cardiac adaptations to short-term endurance
exercise training (6), we hypothesized that 10 days of training would
induce cardiovascular adaptations with increases in cardiac output and
stroke volume during peak exercise and enhance the inotropic response
to a METHODS
O2 max) in the trained state (1, 8, 18, 20, 23). The increase in stroke volume
in response to training is mediated by increases in left ventricular
end-diastolic volume and diastolic filling (6, 13), which may likely be
associated with a greater plasma volume (4), and an augmented
contractile response to -adrenergic stimulation (12, 22).
O2 max or peak
O2 uptake
(O2 peak), blood
volume, and left ventricular end-diastolic diameter (4, 6, 15, 21).
Surprisingly, however, it is not known to what degree stroke volume and
cardiac output increase with short-term training during maximal or peak exercise. Furthermore, it is not known whether short-term training enhances the inotropic response to -adrenergic stimulation and whether the changes in -adrenergic-mediated contractile function are
associated with increases in stroke volume and cardiac output during
maximal or peak exercise.
-adrenergic agonist. Furthermore, we sought to determine
whether the increased inotropic response to -adrenergic stimulation
would be related to the increases in cardiac output and stroke volume
during peak exercise.
O2 peak.
O2 peak was
determined on an electrically braked cycle ergometer (Bosch) before and
after training by using a continuous exercise protocol, in which power
output was increased 25-50 W every 2 min.
O2 uptake
(O2) was measured
continuously by open-circuit spirometry and was averaged every 30 s
with the use of an automated on-line system. Inspiratory volume was
measured with a Parkinson-Cowan CD-4 dry-gas meter. Fractional
concentrations of O2 and
CO2 were sampled from a mixing
chamber and quantified with the use of electronic O2 (Applied Electrochemistry S3-A)
and CO2 (Beckman LB-2) analyzers. O2 peak was defined
as the mean of the two highest consecutive 30-s
O2 measurements,
corresponding with a respiratory exchange ratio value 
1.10 and a
heart rate within 10 beats of predicted maximum heart rate.
Plasma volume.
Plasma volume was determined before and after training with the Evans
blue dye technique, as previously described (9, 15). Subjects rested
supine 30 min before a known volume (4-5 ml) of a sterile dye
solution (New World Trading, DeBary, FL) was injected into an
antecubital vein via a Teflon catheter. Ten minutes later, a blood
sample was taken for subsequent determination of plasma dye
concentration by using spectrophotometry at 615 nm. Samples were
measured in triplicate, and the average coefficient of variance was
2.2%. Plasma volume was calculated from the plasma dye concentration and a known standard dye concentration. Blood volume was calculated by
dividing plasma volume by (1 hematocrit). Hematocrit was measured in quadruplicate and corrected for trapped plasma and venous
sampling.
Cardiac output.
Cardiac output was measured during peak cycle exercise before and after
training on separate days from the
O2 peak tests by
using the acetylene
(C2H2)
rebreathing method (26). For cardiac output measurements, subjects
rebreathed a mixture of 10% He-45% O2-0.5%
C2H2-44.5%
N2 from a closed-system anesthesia
bag. Concentrations of
C2H2
and He were continuously monitored by a Perkin-Elmer mass spectrometer
(MGA-1100) interfaced with a PDP-11 computer for storage and processing
of the data. Cardiac output was calculated from the exponential
disappearance rate of
C2H2
relative to He in several sequential end expirations. Reproducibility
of this method performed during maximal exercise has been reported
previously by this laboratory (12, 23). The intraclass correlation
coefficient for repeated measures of cardiac output was calculated to
be r = 0.86. Heart rate and blood
pressure (sphygmomanometer) were measured during the test. Blood
pressure was measured at least twice during exercise by the same person
before and after training.
Mean blood pressure (MBP) was calculated as [systolic blood
pressure (SBP) + diastolic blood pressure (DBP) × 2]/3
(mmHg). The arterial and mixed venous
O2 content difference
[(a-
)O2] at peak exercise was calculated as
O2 peak/peak cardiac
output × 100 (ml/100 ml). Total peripheral resistance (TPR) was
estimated as (MBP/cardiac output) × 80 (dyn · s · cm
5).
Left ventricular size and performance.
Left ventricular size and systolic function were evaluated before and
after training by using two-dimensional guided M-mode echocardiography
with a 2.5-MHz transducer (model 77020A, Hewlett-Packard). Left
ventricular end-diastolic dimension (LVEDD), end-systolic dimension
(LVESD), posterior wall thickness (LVPWT), and septal wall thickness
(LVSWT) were measured by using standard guidelines recommended by The
American Society of Echocardiography (19). Fractional shortening (FS)
was estimated as (LVEDD LVESD)/LVEDD × 100. Left
ventricular end-systolic wall stress
(ES) was estimated as
described by Grossman et al. (10),
ES = Pr
/[2h × (1 + h /2r)], where P is SBP,
expressed as grams per square centimeter, r is end-systolic radius (ESD/2), and
h is posterior wall thickness at end
systole. Diastolic-filling dynamics were evaluated by using the pulsed
Doppler transmitral diastolic flow-velocity profile. Early (E), late
(A), and the ratio of early-to-late (E/A) diastolic flow velocities
were used as measurements of left ventricular filling (17).
Reproducibility of echocardiographic measurements from this laboratory
have been reported previously (7, 14). Calculated from repeated
measures, intraclass correlation coefficients were
r = 0.85, 0.80, and 0.87, and
coefficients of variation were 3.6, 5.5, and 5.9% for LVEDD, LVESD,
and LVPWT, respectively.
Response to a -adrenoreceptor agonist.
After acquisition of baseline echocardiographic, Doppler, and blood
pressure data, 1.0 mg of atropine was administered intravenously. The
rationale for the use of atropine was to facilitate detection of
enhanced -adrenergic-mediated left ventricular contractile function
that might otherwise have been blunted by increased vagal tone after
training (25). Echocardiographic, Doppler, and blood pressure
measurements were repeated 2 min after atropine injection. Dobutamine
was then continuously infused at successive doses of 3.0, 6.0, 9.0, and
12.0 µg · kg1 · min1
by using an infusion pump (model 122, Harvard Apparatus, South Natick,
MA). Echocardiographic, Doppler, and blood pressure measurements were
taken beginning at 2 min after each dose. Blood pressure was measured
three times at baseline, after atropine injection, and during each dose
of dobutamine. Each dose lasted ~5-6 min. Left ventricular
contractile performance was assessed by using the
FS-ES relationship by plotting
FS as a function of ES, with a
steeper slope being suggestive of enhanced contractile function (2).
Measurement of plasma catecholamine concentrations.
A 1-ml blood sample was taken at baseline, after atropine injection,
and during each dose of dobutamine. In addition, blood samples were
obtained during the cycle ergometer test for peak cardiac output. The
plasma was separated and stored at 80°C for later analysis.
Plasma catecholamines were assayed by using a single-isotope derivative
method (5).
Exercise training.
Exercise training consisted of 1-h cycling bouts performed daily on 10 consecutive days. During each bout, subjects initially cycled for 10 min at 65% O2 peak
followed by 25 min at 75%
O2 peak. During the
last 25 min of each bout, subjects cycled for 3 min at 95%
O2 peak followed by 2 min of low-intensity pedaling, a pattern that was repeated for a total
of five intervals. Work rates were increased daily to
maintain the established target heart rate. Target heart rates at each
intensity were established on day 1 concurrently with O2
measurements.
Statistics.
Physiological variables during peak exercise and -adrenergic
stimulation were compared with a repeated-measures analysis of variance
design. Differences among responses during the dobutamine infusion were
determined by using Duncan's multiple-range post hoc test when a
significant training or dobutamine effect, or a significant interaction
between training and dobutamine, was evident. Linear regression was
used to determine the slope and intercept of the
FS-ES relationship and the
ES-ESD relationship for each
individual, and a paired Student's
t-test was used to compare the mean of
the individual slopes and intercepts before and after training. Linear
regression was used to determine independent variables relating to the
training-induced changes in stroke volume, cardiac output, and
O2 peak during peak
cycle exercise. Significant differences and significant linear
relationships were established at P 
0.05, and all data were expressed as means ± SE.
RESULTS
O2 peak.
All subjects completed the 10 days of training. Body weight did not
change significantly with training (70.4 ± 4.5 vs. 70.9 ± 4.7 kg after training) in either men (78.5 ± 7.1 vs. 79.4 ± 7.3 kg)
or women (62.3 ± 3.1 vs. 62.5 ± 3.1 kg). Cycle
ergometer O2 peak
increased 10% from 2.54 ± 0.29 l/min (35.4 ± 2.5 ml · kg1 · min1)
to 2.80 ± 0.32 l/min (38.9 ± 2.9 ml · kg1 · min1)
(P < 0.0001). In men,
O2 peak increased
from 3.32 ± 0.27 to 3.64 ± 0.30 l/min (42.6 ± 1.5 to 46.2 ± 1.5 ml · kg1 · min1),
and in women it increased from 1.75 ± 0.09 to 1.96 ± 0.11 l/min (28.2 ± 1.0 to 31.5 ± 1.9 ml · kg1 · min1).
There was no difference between men and women in the
O2 peak response to
training.
Hemodynamic and hormonal responses to peak exercise (Table
1).
The 10% increase in cycle
O2 peak was associated
with a 12% increase in cardiac output during peak exercise
(P < 0.001). This increase in
cardiac output was solely the result of an increase in stroke volume,
which was 15% higher after training
(P < 0.001) because peak heart rate
did not change, although there was a tendency for it to be lower after
training (P < 0.060). The change in
cardiac output was greater in men (3.3 vs. 1.2 l/min in women,
P < 0.03). Similarly, the absolute
increase in stroke volume was greater in men (22.3 vs. 8.3 ml/beat in
women, P < 0.02). Training did not
affect peak exercise SBP
or(a-)O2
but reduced DBP (P < 0.01), MBP
(P < 0.005), and TPR
(P < 0.0001). The effect of training on heart rate, SBP, DBP, MBP,
(a-)O2,
or TPR did not differ between men and women. Plasma epinephrine
concentrations during peak exercise did not change significantly with
training. However, there was a tendency for norepinephrine
concentrations to be higher after training
(P < 0.055). Catecholamine responses
did not differ between men and women.
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ES changed significantly with
training. Neither plasma norepinephrine (pretraining: 255 ± 55 pg/ml; posttraining: 186 ± 10 pg/ml) nor
epinephrine (pretraining: 16.7 ± 3.6 pg/ml; posttraining: 18.2 ± 2.7 pg/ml) concentrations changed
significantly with training at baseline.
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ES
increased with atropine both before and after training
(P < 0.03). Neither plasma
norepinephrine nor epinephrine concentrations were changed by atropine.
There were no differences between men and women in response to
atropine.
Effects of -adrenergic stimulation (Table
3).
Throughout the infusion of dobutamine, LVEDD was greater after training
(P < 0.004). However, the increasing
doses of dobutamine had no effect on LVEDD from postatropine values
either before or after training. In contrast, LVESD decreased during
dobutamine infusion (P < 0.0001),
reaching a plateau at 9.0 µg · kg1 · min1
both before and after training. LVESD was greater in response to
training after atropine and during dobutamine infusion (except at 3.0 µg · kg1 · min1;
P < 0.05). SBP increased in response
to dobutamine both before and after training
(P < 0.0001), reaching a plateau at
9.0 µg · kg1 · min1.
Training, however, had no effect on SBP response to dobutamine. DBP was
not affected significantly by either dobutamine or training. The
changes in plasma epinephrine and norepinephrine concentrations during
dobutamine infusion were not significant, nor did training affect
catecholamine concentrations significantly.
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1 · min1)
was less after than before training (P < 0.01). Heart rate was lower after training at each dose of
dobutamine (P < 0.004),
even though postatropine heart rate values were similar. FS increased during dobutamine infusion (P < 0.0001), reaching a plateau at 9.0 µg · kg1 · min1,
both before and after training (Fig.
1B). Training, however, did not
influence FS responses to -adrenergic stimulation. Estimated ES decreased progressively in
response to dobutamine before training (P < 0.0001) (Fig.
1C). After training, however,
ES decreased initially and then
reached a plateau at the dobutamine dose of 6.0 µg · kg1 · min1
with no further decrease. At the highest dobutamine dose (12.0 µg · kg1 · min1),
ES was higher after training
(P < 0.004). There were no
differences in left ventricular function between men and women in
response to dobutamine.
P < 0.05 interactive effect between training and dobutamine. Post,
posttraining.
The slope of the FS-
ES
relationship increased for each subject, and the mean of the individual
slopes was significantly steeper with training (0.55 ± 0.09 vs. 0.89 ± 0.14, P < 0.03), indicating enhanced contractile response to -adrenergic
stimulation (Fig. 2A). The
intercept of the FS-ES
relationship increased for each subject, and the mean of the individual
intercepts was significantly greater with training (65.2 ± 2.9 vs.
84.7 ± 9.0, P < 0.05).
The correlation coefficients for the individual
FS-ES relationships ranged from
0.70 to 0.98 before training and from 0.88 to
0.99 after training.
-adrenergic stimulation, i.e., for a given
decrease in LVES wall stress there is a larger increase in fractional
shortening and a greater decrease in LVESD after training.
To control for the effect of preload (2, 3), we compared FS responses during
-adrenergic stimulation in those subjects (n = 6) whose LVEDD either decreased
or changed little (<0.25 mm). At a similar change in LVEDD
(pretraining: 0.3 ± 0.3 mm; posttraining: 0.3 ± 0.4 mm), the
increase in FS with dobutamine was greater after training in four of
these subjects (14.1 ± 1.5 vs. 9.6 ± 2.7%,
P < 0.05). Furthermore, the change
in LVEDD did not correlate significantly with the change in FS
(r = 0.23, P = 0.24). Because the relationship
between estimated ES and ESD is
probably less dependent on preload, we also compared the
slopes and intercepts of the
ES-ESD relationship before and
after training. The slope of the
ES-ESD relationship decreased
for each subject, and the mean of the individual slopes was
significantly less steep with training (3.38 ± 0.55 vs. 2.11 ± 0.40, P < 0.005), indicating a
greater decrease in ESD for a given decrease in estimated
ES (Fig.
2B). The
ES-ESD relationship shifted
upward for each subject, as evidenced by higher individual intercepts
after training (45.4 ± 14.5 vs. 10.6 ± 11.9, mean ± SE, P < 0.002). The
correlation coefficients for the individual
ES-ESD relationships ranged
from 0.79 to 0.99 before training and from 0.70 to 0.99 after training.
Left ventricular filling dynamics.
To evaluate the effects of training on left ventricular filling
dynamics, comparisons were made at comparable heart rates before and
after training during dobutamine infusion. Six subjects whose heart
rates were similar before and after training (92 ± 8 beats/min both
pre- and posttraining) were included in this comparison. Although there
was a trend for the early (E) transmitral flow velocity to increase
from 80.8 ± 11.0 to 96.0 ± 11.1 cm/s (P < 0.07), neither the late (A)
transmitral flow velocity (pretraining: 55.5 ± 8.6 cm/s;
posttraining: 57.5 ± 4.5 cm/s) nor the E/A (pretraining: 1.50 ± 0.13; posttraining: 1.66 ± 0.10) was changed significantly with
training.
Relationships between physiological variables.
The training-induced increase in blood volume correlated with
training-induced increases in cardiac output
(r = 0.80, P < 0.01) and stroke volume
(r = 0.85, P < 0.004) during peak exercise. The
increase in blood volume with training also tended to correlate with
the increase in O2 peak
(r = 0.65, P < 0.08). The change in the slope
of the FS-ES relationship with
training correlated significantly with the training-induced increases
in cardiac output (r = 0.71,
P < 0.05) and stroke volume
(r = 0.70,
P < 0.05) but not with the increase
in O2 peak
(r = 0.50,
P = 0.20). Both before and after
training, resting baseline LVEDD correlated significantly with stroke
volume (pretraining: r = 0.79, P < 0.01; posttraining:
r = 0.83, P < 0.005) and blood volume
(pretraining: r = 0.85, P < 0.003; posttraining:
r = 0.85, P < 0.004). However, the change in
resting baseline LVEDD induced by training did not correlate with the
change in either stroke volume (r = 0.36, P = 0.37) or blood volume
(r = 0.47,
P = 0.24).
DISCUSSION
The results of this study show that 10 days of training induces
adaptations suggestive of an increased inotropic response to
-adrenergic stimulation, and these adaptations are associated with
increases in cardiac output and stroke volume during peak exercise. The
adaptive enhancement of the inotropic response to -adrenoreceptor
stimulation appears to be similar to those attained with long-term
training (12, 22). In the present study, the training-induced
improvement in the inotropic response to -adrenergic stimulation was
reflected by a steeper slope of the
FS-ES relationship such that,
for a given -adrenergic-mediated decrease in
ES, there was a greater
increase in FS observed at similar plasma catecholamine concentrations
and without a higher heart rate response.
Improved contractile function in response to -adrenergic activation
after several weeks of training has been demonstrated in isolated
ventricular papillary muscle in animals (16, 27). In these animal
models, training enhanced the contractile response to -adrenergic
stimulation by increasing the maximum rate of tension development and
decreasing the time to peak tension in isolated heart muscle
preparations. In humans, 12 wk of training resulted in an increase in
the inotropic response to -adrenergic stimulation at comparable
changes in preload, reflected by a greater FS response (22). In
addition, in a cross-sectional study, a steeper slope in the
FS-ES relationship was
demonstrated in response to dobutamine in endurance-trained athletes
compared with untrained individuals (12).
In this study, the training-induced larger preload after 10 days of
training was evidenced by an increase in LVEDD, associated with a
larger blood volume, even though the training-induced changes in LVEDD
did not correlate with those in blood volume. The trend observed for
enhanced early diastolic-filling velocity was probably due to a larger
LVEDD and also to increased sensitivity to catecholamines. The increase
in stroke volume during peak exercise can result from increased
preload, reduced afterload, and/or enhanced inotropic response
to -adrenergic stimulation (1). Our data suggest that both a larger
preload and increased inotropic response to -adrenergic stimulation
are associated with the greater stroke volume during peak exercise
after 10 days of training.
In contrast to an enhanced inotropic response, the chronotropic
response to -adrenergic stimulation was significantly reduced in
response to training. Similar results have also been observed in
animals (11) and in humans (12, 24) after training. Evidence for this
uncoupling of inotropic and chronotropic responses comes from a
previous animal study that reported a selective downregulation in
-adrenergic receptors located in the right atrium, associated with a
lower chronotropic response to -adrenergic stimulation, whereas no
change in -receptor number was observed in the left ventricle of
pigs (11). In the present study, the attenuated heart rate response
after training was not accompanied by a smaller increase in plasma
catecholamine concentrations during dobutamine infusion. This suggests
that the increase in sympathetic activity in response to dobutamine was
probably similar before and after training. The attenuated heart rate
response suggests that enhanced LV systolic function was due to a
direct effect of dobutamine on -adrenergic receptors rather than to
enhancement of the force-frequency relationship (11).
Although the purpose of this study was not to study gender differences,
the fact that both men and women were included in this study warranted
attention. There were no differences between men and women in the
response to -adrenergic stimulation, and each subject demonstrated
an increase in the FS-ES
relationship, indicating that both men and women responded to training
with an increased contractile response to -adrenergic stimulation. Furthermore, there were no gender differences in
O2 peak response to
training. However, training increased peak exercise cardiac output and
stroke volume and also increased blood volume more in men. Given the
small number of men and women in the present study, these data should
be interpreted with caution.
A limitation of this study is that measurement of
ES is only an estimate. Second,
the FS-ES relationship is not
totally independent of preload because preload is known to increase FS (2, 3). However, our data suggest that the observed increase in FS in
the trained state was at least partially independent of an increase in
LVEDD. First, the changes in LVEDD during dobutamine infusion were
similar before and after training. Second, there was no significant
correlation between the change in FS and the change in LVEDD
(r = 0.23). Furthermore, in those
subjects whose LVEDD were decreased or had changed insignificantly
after training (n = 6), we found that
FS response to dobutamine was greater after training in four of these
subjects during the dobutamine infusion. We also evaluated the
ES-ESD relationship, which is
probably less dependent on preload, and found a greater decrease in ESD for a given decrease in ES
after training during the dobutamine infusion.
In conclusion, our findings suggest that 10 days of training, similar
to training lasting several weeks, can result in increases in cardiac
output and stroke volume during peak exercise in the trained state in
young subjects. Furthermore, both a training-induced enhancement of
inotropic response to -adrenergic stimulation and a greater blood
volume at rest are associated with increases in cardiac output and
stroke volume during peak exercise. These results indicate that
significant cardiac adaptations can occur in response to short-term
exercise training and provide insight into the mechanisms for cardiac
adaptations associated with increased exercise capacity after
short-term training.
ACKNOWLEDGEMENTS
This work was supported by National Institutes of Health Grants Claude D. Pepper OAIC AG-13629, RO1-AG-12235, and General Research Center Grant 5-MO1-RR-00036. C. M. Mier and M. J. Turner are supported by Institutional National Research Service Award AG-00078.
FOOTNOTES
Address for reprint requests: R. J. Spina, Section of Applied Physiology, Washington Univ. School of Medicine, 4566 Scott Ave., Campus Box 8113, St. Louis, MO 63110.
Received 18 November 1996; accepted in final form 23 July 1997.
REFERENCES
| 1. | Blomquist, C. G. Cardiovascular adaptations to physical training. Annu. Rev. Physiol. 45: 169-189, 1983[Medline]. |
| 2. | Borow, K. M., L. H. Green, W. Grossman, and E. Braunwald. Left ventricular end-systolic stress-shortening and stress-length relations in humans. Am. J. Cardiol. 50: 1301-1308, 1982[Medline]. |
| 3. | Colan, S. D., K. M. Borow, and A. Neumann. Left ventricular end-systolic wall stress-velocity of fiber shortening relation: a load-independent index of myocardial contractility. J. Am. Coll. Cardiol. 4: 715-724, 1984[Abstract]. |
| 4. | Convertino, V. A. Blood volume: its adaptation to endurance training. Med. Sci. Sports Exerc. 23: 1338-1348, 1991[Medline]. |
| 5. | Cryer, P. E., R. A. Rizza, M. W. Haymond, and J. E. Gerich. Epinephrine and norepinephrine are cleared through beta-adrenergic, but not alpha-adrenergic, mechanisms in man. Metabolism 29, Suppl. 1: S1114-S1118, 1980. |
| 6. | Ehsani, A. A., J. M. Hagberg, and R. C. Hickson. Rapid changes in left ventricular dimensions and mass in response to physical conditioning and deconditioning. Am. J. Cardiol. 42: 52-56, 1978[Medline]. |
| 7. | Ehsani, A. A., W. H. Martin III, G. W. Heath, and E. F. Coyle. Cardiac effects of prolonged and intense exercise training in patients with coronary artery disease. Am. J. Cardiol. 50: 246-254, 1982[Medline]. |
| 8. |
Ekblom, B,
P.-O. Åstrand,
B. Saltin,
J. Stenberg,
and
B. Wallström.
Effect of training on circulatory response to exercise.
J. Appl. Physiol.
24:
518-528,
1968 |
| 9. |
Greenleaf, J. E.,
V. A. Convertino,
and
G. R. Mangseth.
Plasma volume during stress in man: osmolality and red cell volume.
J. Appl. Physiol.
47:
1031-1038,
1979 |
| 10. | Grossman, W., D. Jones, and L. P. McLaurin. Wall stress and patterns of hypertrophy in the human left ventricle. J. Clin. Invest. 56: 56-64, 1975. |
| 11. |
Hammond, H. K.,
F. C. White,
L. L. Brunton,
and
J. C. Longhurst.
Association of decreased myocardial -receptors and chronotropic response to isoproterenol and exercise in pigs following chronic dynamic exercise.
Circ. Res.
60:
720-726,
1987 |
| 12. |
Hopkins, M. G.,
R. J. Spina,
and
A. A. Ehsani.
Enhanced -adrenergic-mediated cardiovascular responses in endurance athletes.
J. Appl. Physiol.
80:
516-521,
1996 |
| 13. |
Levy, W. C.,
M. D. Cerqueira,
I. B. Abrass,
R. S. Schwartz,
and
J. R. Stratton.
Endurance exercise training augments diastolic filling at rest and during exercise in healthy young and older men.
Circulation
88:
116-126,
1993 |
| 14. | Martin, W. H., E. F. Coyle, M. A. Bloomfield, and A. A. Ehsani. Effects of physical deconditioning after intense endurance training on left ventricular dimensions and stroke volume. J. Am. Coll. Cardiol. 7: 982-989, 1986[Abstract]. |
| 15. |
Mier, C. M.,
M. A. Domenick,
N. T. Turner,
and
J. H. Wilmore.
Changes in stroke volume and maximal aerobic capacity with increased blood volume in men and women.
J. Appl. Physiol.
80:
1180-1186,
1996 |
| 16. |
Molé, P. A.
Increased contractile potential of papillary muscles from exercise-trained rat hearts.
Am. J. Physiol.
234 ((Heart Circ. Physiol. 3):
H421-H425,
1978 |
| 17. | Nishimura, R. A., M. D. Abel, L. K. Hatle, and A. J. Tajik. Assessment of diastolic function of the heart: background and current applications of Doppler echocardiography. Mayo Clin. Proc. 64: 181-204, 1989[Medline]. |
| 18. |
Ogawa, T. R.,
R. J. Spina,
W. H. Martin III,
W. M. Kohrt,
K. B. Schechtman,
A. A. Ehsani,
and
J. O. Holloszy.
Effects of aging, sex, and physical training on cardiovascular responses to exercise.
Circulation
86:
494-503,
1992 |
| 19. |
Sahn, D. J.,
A. DeMaria,
J. Kisslo,
and
A. Weyman.
Recommendations regarding quantitation in M-mode echocardiography: results of a survey of echocardiographic measurements.
Circulation
58:
1072-1082,
1978 |
| 20. | Saltin, B., C. G. Blomquist, J. H. Mitchell, R. L. Johnson, K. Wildenthal, and C. B. Chapman. Response to exercise after bedrest and after training. Circulation 38 Suppl. VII: S1-S75, 1968. |
| 21. |
Spina, R. J.,
M. M.-Y. Chi,
M. G. Hopkins,
P. M. Nemeth,
O. H. Lowry,
and
J. O. Holloszy.
Mitochondrial enzymes increase in muscle in response to 7-10 days of cycle exercise.
J. Appl. Physiol.
80:
2250-2254,
1996 |
| 22. |
Spina, R. J.,
T. Ogawa,
A. R. Coggan,
J. O. Holloszy,
and
A. A. Ehsani.
Exercise training improves left ventricular contractile response to -adrenergic agonist.
J. Appl. Physiol.
72:
307-311,
1992 |
| 23. |
Spina, R. J.,
T. Ogawa,
W. H. Martin III,
A. R. Coggan,
J. O. Holloszy,
and
A. A. Ehsani.
Exercise training prevents decline in stroke volume during exercise in young healthy subjects.
J. Appl. Physiol.
72:
2458-2462,
1992 |
| 24. |
Stratton, J. R.,
M. D. Cerqueira,
R. S. Schwartz,
W. C. Levy,
R. C. Veith,
S. E. Kahn,
and
I. B. Abrass.
Differences in cardiovascular responses to isoproterenol in relation to age and exercise training in healthy men.
Circulation
86:
504-512,
1992 |
| 25. |
Stratton, J. R.,
M. A. Pfeifer,
and
J. B. Halter.
The hemodynamic effects of sympathetic stimulation combined with parasympathetic blockade in man.
Circulation
75:
922-929,
1987 |
| 26. | Triebwasser, J. H., R. L. Johnson, and R. P. Burpo. Noninvasive determination of cardiac output by a modified acetylene rebreathing procedure using mass spectrometer. Aviat. Space Environ. Med. 48: 203-210, 1977[Medline]. |
| 27. | Wyatt, H. L., L. Chuck, B. Rabinowitz, J. V. Tyberg, and W. W. Parmley. Enhanced cardiac response to catecholamines in physically trained cats. Am. J. Physiol. 234 ((Heart Circ. Physiol. 3): H608-H613, 1978. |
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O2, arterial and
mixed venous O2 content difference calculated from
