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1 Section of Applied Physiology, Division of Geriatrics and Gerontology, and Claude D. Pepper Older Americans Independence Center, and 2 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 strength-trained individuals with physiological concentric left ventricular (LV) hypertrophy exhibit enhanced inotropic responses to catecholamines, we studied 11 bodybuilders, aged 33.0 ± 2 (SE) yr old, and 10 sedentary healthy subjects, aged 31.3 ± 2.4 yr old, at baseline and during infusion of incremental doses of dobutamine after atropine. The bodybuilders had larger LV mass, posterior wall and septal wall thicknesses, and wall thickness-to-radius ratio, assessed with two-dimensional echocardiography, than did the sedentary subjects. There was a significant correlation between LV mass and lean body mass irrespective of training status. Baseline LV fractional shortening was similar in the two groups. There was a greater inotropic response to dobutamine in the strength-trained individuals, as evidenced by a steeper slope of the fractional shortening-end-systolic wall stress relationship with a higher y-axis intercept and by a shallower end-systolic wall stress-end systolic diameter relationship without changes in end-diastolic diameter. The heart rate response to dobutamine was attenuated in the strength-trained athletes. There was a significant correlation (r = 0.604, P < 0.05) between the inotropic sensitivity to dobutamine and LV mass normalized for lean body mass in the bodybuilders. The data suggest that concentric LV physiological hypertrophy in the resistance-trained individuals is associated with enhanced inotropic but not chronotropic responses to catecholamines.
inotropic sensitivity; cardiac function; physiological cardiac concentric hypertrophy
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INTRODUCTION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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ENDURANCE-TRAINED ATHLETES exhibit major adaptations in
the cardiovascular system that result in increases in O2
uptake (
O2) [maximal
O2
(O2 max)], stroke
volume, and cardiac output during maximal exercise (13, 14,
16). These adaptive responses are mediated not only by
left ventricular (LV) eccentric hypertrophy with a greater LV filling,
in part due to a larger blood volume, but also by an increase in the
inotropic sensitivity to 
-adrenergic agonists in both young athletes
and older endurance-trained men (5, 13, 17, 18).
Strength-trained athletes show adaptive changes in the cardiovascular
system that are different from those seen in the endurance-trained
athletes, as reflected in no increase in
O2 max, and an increase
in LV wall thickness (h) without a significant chamber
enlargement resulting in a large increase in the h-to-radius
ratio (h/r) (concentric remodeling) (6, 10, 11). This adaptive
response qualitatively resembles the pressure-overload LV hypertrophy
(concentric remodeling and concentric hypertrophy). Baseline LV
systolic performance in strength-trained subjects with LV concentric
hypertrophy is not different from that observed in endurance-trained
athletes or sedentary subjects (10). However, it is not known whether
physiological concentric hypertrophy in strength-trained individuals is
associated with alterations in inotropic and chronotropic responses to
-adrenergic stimulation, similar to those observed in
endurance-trained athletes or in response to endurance exercise
training (5, 13, 18). Therefore, the aim of the present study was to
determine whether the -adrenergic-stimulated increase in cardiac
inotropic response is enhanced in strength-trained subjects with
physiological concentric LV remodeling and hypertrophy.
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METHODS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Subjects
We studied 11 bodybuilders, aged 33.0 ± 2.0 yr, and 10 sedentary controls, aged 31.3 ± 2.4 yr. There were eight men and three women in the trained group, and there were eight men and two women in the sedentary group. The bodybuilders had been weight training on a regular basis, 3-5 days/wk, for at least 5 yr. None of the subjects was engaged in endurance exercise training. We did not include the subjects who engaged in both strength training and endurance exercise training because our objective was to assess adaptive changes in-adrenergic
responses in concentric physiological LV hypertrophy. All subjects were
normotensive, healthy, and free of cardiopulmonary symptoms. They had
normal cardiovascular examinations and 12-lead resting and exercise
electrocardiogram (ECG). None of the subjects was taking any cardiac
medications or anabolic steroids. All subjects were nonsmokers.
Informed consent was obtained from each subject, and the study was
approved by the Human Studies Committee of Washington University.
O2 max
O2 was determined
with the use of a treadmill-running protocol, as previously reported
(5). Briefly, after 5-min warm-up during which the subjects exercised
at an intensity equal to ~75% of their age-predicted maximal heart
rate at 0 level, the grade was increased by 2% every 2 min while
constant speed until exhaustion was maintained.
O2 was measured by standard
open-circuit spirometry that incorporated a computer for calculation of
O2 every 30 s during
exercise (5). Inspiratory volume was measured by a Parkinson-Cowan CD-4
dry-gas meter. Fractional concentrations of expired O2 and
CO2 were measured from a mixing chamber by electronic O2 (model S3-A, Applied Electrochemistry) and
CO2 (model LB-2, Beckman) analyzers.
Attainment of O2 max
was documented if two of the following criteria were met: 1) a
plateau of O2, defined as
no further rise in O2 with
increasing exercise intensity; 2) a respiratory exchange ratio
>1.10; 3) maximal attainable heart rate within 10 beats/min
of the age-predicted heart rate; and 4) a highest measured
O2 below the estimated
level of O2 required to
perform the work.
Body Composition
Hydrostatic weighing was used to measure lean body mass. We used a partial-expiration technique that has been validated and reported previously (8). Data from four to five trials were collected from each subject and averaged.Assessment of LV Size, Geometry, and Function
We used two-dimensional and two-dimensional guided M-mode echocardiography (Hewlett-Packard ultrasonograph 2000) with a 2.5-MHz transducer to assess LV structure and performance at baseline and during-adrenergic stimulation with dobutamine.
Recordings were obtained by using the standard views according to the
guidelines recommended by the American Society of Echocardiography
(15). The end-diastolic diameter (EDD) and end-systolic diameter (ESD) were measured by using the standard guidelines (15). The
reproducibility of these measurements has been previously reported from
our laboratory (12). At least six cardiac cycles were used for data
analysis. Fractional shortening (FS) was calculated as FS = (EDD 
ESD)100/EDD. LV end-systolic wall stress (
es)
was estimated as described by Grossman et al. (3): es = Pr/2h (1 + h/2r), where P is
end-systolic blood pressure (BP) expressed as grams per square
centimeter (mmHg × 1.36), r is end-systolic radius
(ESD/2), and h is posterior wall thickness at end
systole. End-systolic pressure (ESP) was estimated from
the equation ESP = [2 · systolic blood pressure (SBP) + diastolic blood pressure (DBP)]/3, which has been shown to correlate with ESP (7). LV contractile performance was assessed by
using the FS-es and es-ESD relationships
by plotting FS as a function of es, and
es as a function of ESD, respectively, at baseline,
after intravenous administration of atropine, and during incremental
doses of dobutamine infusion. Echocardiographic data were recorded
simultaneously with measurement of BP with the use of a mercury sphygmomanometer.
Baseline studies. The subjects rested in the laboratory in the supine position for 30 min after an intravenous catheter was placed in the forearm vein. Echocardiographic recordings were then made simultaneously with measurement of BP with the use of a mercury sphygmomanometer.
-Adrenergic stimulation.
After acquisition of baseline resting images, each subject was given
1.0 mg of atropine intravenously in an attempt to lessen differences in
vagal tone that might have existed between the two groups.
Echocardiographic images were recorded 2 min after administration of
atropine. Infusion of dobutamine was commenced with 3.0 µg · kg
1 · min1
and increased sequentially to 6.0, 9.0, and 12.0 µg · kg1 · min1.
Each infusion trial lasted for 5 min, and echocardiographic images were
recorded in the last 2 min of the infusion. BP was recorded
simultaneously with all of the echocardiographic
examinations. ECG was monitored throughout the infusion. After
completion of dobutamine infusion, the subjects were monitored for 10 min with ECG and frequent BP recordings.
Statistics
The differences in the baseline variables between the two groups were compared with the use of the unpaired Student's t-test when appropriate. Furthermore, two-way analysis of variance was used to examine the differences in the physiological variables during dobutamine infusion. The data that were not normally distributed were analyzed with the use of the rank-sum test analysis of variance. The data are presented as means ± SE. The probability level of P
0.05 was considered significant.
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RESULTS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Subjects' Characteristics and
O2 max
O2 max,
expressed in absolute terms (3.26 ± 0.26 vs. 3.14 ± 0.26 l/min;
P = 0.74) or when normalized for either body weight or lean
body mass (Table 1). The respiratory exchange ratio was 1.23 ± 0.02 in the bodybuilders and 1.19 ± 0.03 in the controls
(P = 0.11). Maximal heart rate was also similar in the two
groups (Table 1).
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Body Composition
The bodybuilders' average body weight was 7 kg greater than that of the controls. This difference was not statistically significant because of the considerable variability in the body size (Table 1). The lean body mass was slightly higher in the athletes, but the difference was not statistically significant (Table 1).Baseline LV Structure, Geometry, and Function
The bodybuilders had greater LV septal and posterior wall thicknesses than did the sedentary controls (Table 1). The LV EDD and ESD were not different between the two groups (Table 2). The LV h/r and mass were markedly larger in the resistance-trained athletes than in the sedentary controls, suggestive of LV concentric hypertrophy and remodeling (Table 1). However, when LV mass was normalized for lean body mass or body weight, the differences between the two groups were small and insignificant (Table 1). There was a significant correlation (r = 0.66, P = 0.001; Fig. 1) between lean body mass and LV mass in the entire study population (trained and untrained subjects) with the subjects with a larger lean body mass (i.e., the bodybuilders) tending to have a larger LV mass (Fig. 1). Thus it appears that cardiac hypertrophy is proportional to skeletal muscle hypertrophy in the bodybuilders. SBP and DBP at baseline were similar in the two groups (Table 2). LV FS was not different between the trained and untrained subjects. LVes was significantly lower in the
bodybuilders than in the controls (51.2 ± 3 vs. 39.5 ± 4 g;
P < 0.05; Table 2).
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Cardiovascular Responses to Partial Cardiac Muscarinic Receptor Blockade
Atropine had no significant effect on SBP, LV systolic shortening, EDD and ESD, or LVes in either group (Table 2). Heart rate
increased with atropine in both groups, but was slightly higher in the
controls than the bodybuilders (Table 2). When normalized for body
weight, the dosage of atropine was similar in the bodybuilders and
sedentary controls (bodybuilders: 13.8 ± 0.9 vs. controls:
14.4 ± 1.0 µg · kg1 · min1;
P = 0.7).
Cardiovascular Responses to Dobutamine
LV FS increased significantly (P < 0.001) in response to dobutamine in both groups (Table 2). However, the increase in FS was significantly greater in the bodybuilders than in the sedentary controls (P = 0.001; Fig. 2, Table 2). LVes decreased in response to dobutamine in both
groups (P < 0.001; Table 2). Furthermore, es
was significantly lower in the bodybuilders than in the sedentary controls (P < 0.001; Table 2). However, when the values were adjusted for the baseline differences in es, the
observed differences in the es during dobutamine
infusion were abolished (P = 0.53; data not shown). LV ESD
decreased in response to dobutamine in both groups (P < 0.001, Table 2), with the bodybuilders exhibiting a greater decrease
(P = 0.001) in ESD than the sedentary controls (Table 2). There
were no significant changes in EDD induced by dobutamine in either
group (Table 2) nor were there any differences in EDD responses between
the two groups (Table 2).
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SBP increased significantly in response to dobutamine in both groups (P < 0.001), but the resistance-trained subjects showed a smaller rise in SBP (P = 0.003) than did the sedentary subjects (Table 2). There were no significant differences, however, in DBP (Table 2). Dobutamine-induced increases in heart rate in both groups (P < 0.001; Table 2). However, the bodybuilders exhibited a diminished chronotropic response to dobutamine compared with the sedentary controls (P = 0.026; Table 2).
Inotropic Responses to -Adrenergic Stimulation
es relationships in the trained subjects was also
significantly steeper than those in the sedentary group (1.10 ± 0.08 vs. 0.626 ± 0.10; P = 0.002), showing that,
for a given decrease in es, there was a greater increase
in LV FS (Fig. 4). The y-axis
intercept of the FS-es relationship was 77.3 ± 3.2%
in the bodybuilders and 67.1 ± 3.6% in the sedentary controls
(P = 0.048; Fig 4). The correlation coefficients of the
FS-es relationships were r = 0.93 ± 0.02 for
the bodybuilders and r = 0.84 ± 0.04 for the sedentary
subjects. The mean of the individual slopes of the
es-ESD relationships was 1.66 ± 0.10 in the
bodybuilders and 2.15 ± 0.20 in the sedentary subjects (P = 0.05), showing that, for a given reduction in ESD, the bodybuilders
exhibited a smaller decrease in es than did the
sedentary subjects, consistent with enhanced LV systolic function. The
differences in the y-axis intercepts of this relationship were
not statistically significant. The correlation coefficient of the
es-ESD relationships was r = 0.96 ± 0.01 for
the strength-trained subjects and r = 0.88 ± 0.03 for the sedentary controls.
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There was a modest but significant correlation between the inotropic
sensitivity to -adrenergic stimulation (slope of the increase in
systolic shortening in response to dobutamine) and LV mass normalized
for lean body mass (r = 0.604, P < 0.05; Fig. 5), showing that those bodybuilders who had
a larger LV mass were likely to have a greater increase in LV systolic
shortening in response to dobutamine.
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DISCUSSION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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The findings of this investigation suggest that physiological LV
concentric hypertrophy and remodeling in the strength-trained young
subjects is associated with an enhancement of LV systolic performance
in response to dobutamine, similar to that in endurance-trained athletes with eccentric LV hypertrophy, even though the adaptive changes in LV morphology and geometry differ between these two groups
(5, 18). The greater -adrenergic-stimulated enhancement of LV
contractile function in the bodybuilders is evidenced by a steeper
slope and a higher y-axis intercept of the systolic shortening-es relationship. Because acute changes in LV
systolic (fractional) shortening are highly sensitive to alterations in LV es (afterload), this relationship is a reliable and
useful measure of contractile state providing there is no increase in either EDD (preload) or heart rate. In this study the heart rate was
lower and the changes in LV EDD were too small to account for the
enhancement of LV systolic function. The shallower slope of the
es-ESD relationship, showing that for a given decrease in ESD there was a smaller reduction in es, provides
additional evidence suggestive of an augmented contractile response to
dobutamine in the strength-trained subjects. These -adrenergic
adaptive responses were associated with concentric LV hypertrophy and
remodeling, as evidenced by larger LV mass, LV h, septal wall
thickness, and LV h/r. The significant correlation between LV
mass and inotropic sensitivity to dobutamine in the bodybuilders
suggest that, unlike pathological concentric LV hypertrophy, which is
associated with diminished inotropic responsiveness to -agonists and
reduced LV -adrenoceptor density (1, 2), physiological concentric hypertrophy and remodeling is associated with enhanced inotropic responsiveness to -adrenergic stimulation.
Although modest in magnitude, the morphological cardiac changes in our strength-trained subjects are similar to those in previous studies (10, 11). The larger LV mass was proportional to the greater lean body mass in these athletes because the differences in LV mass between the bodybuilders and sedentary subjects were virtually abolished when the values were normalized for lean body mass. This observation is one of the characteristic features of physiological concentric LV hypertrophy, as reported earlier by Longhurst et al. (10), and is useful in distinguishing physiological hypertrophy from pathological hypertrophy.
The strength training-stimulated increase in LV h, by reducing
LV es, is one mechanism that contributed to the greater
LV systolic shortening in response to dobutamine. However, the steeper slope and the higher y-axis intercept of the
FS-es relationship, in the absence of increases in
preload (i.e., EDD) and heart rate, suggest that, in addition to a
lower afterload, the greater LV systolic shortening in response to
dobutamine is also due to an enhancement of contractile function in
these trained subjects because at any given reduction in LV
es there was a greater increase in LV systolic
shortening. Therefore, it seems that, in the strength-trained subjects
with physiological concentric remodeling and hypertrophy, the greater
LV systolic shortening in response to catecholamines is mediated by two
different but complementary mechanisms. One is a lower LV
es due to a larger LV h and a smaller increase in SBP, and the other is a greater inotropic response to -adrenergic stimulation, both contributing to a more effective systolic shortening and enhancement of LV systolic function. This adaptation is, to some
extent, different from that seen in endurance-trained athletes whose
increased LV shortening is due to a greater preload and a higher
catecholamine-stimulated inotropic response (5).
In contrast to enhanced inotropic sensitivity, the chronotropic
responses to dobutamine were significantly blunted in the resistance-trained subjects. The reason for this dissociation is not
clear. However, similar findings have been observed in endurance-trained athletes (5). In endurance-trained pigs, the
diminished chronotropic response was associated with selective downregulation of the -adrenergic receptors in the right atrium (4).
It is not known, however, whether a similar selective adaptation can
occur with strength training.
The absence of differences in aerobic power between the
strength-trained and sedentary subjects in our study is consistent with
an earlier report showing that resistance training does not increase
aerobic power and functional capacity (6). Nevertheless, cardiac
adaptations in the strength-trained subjects can provide a useful
mechanism, making it possible for them to maintain stroke volume and
cardiac output during high-intensity isometric effort by a greater
catecholamine-mediated inotropic response as well as a smaller increase
in LV es.
Potential limitations of our study include the use of the noninvasive
cuff pressure technique to calculate end-systolic pressure. Therefore,
the values for LV es should be considered as only an
estimate in our study. Because of the cross-sectional study design, the
influence of genetic factors cannot be excluded. Furthermore, it is
likely that the extent of vagal blockade may have been different between the two groups even though the doses of atropine relative to
body weight were similar. However, judging from the heart rate, FS, and
BP responses, we believe that any differences in vagal blockade were
small. In addition, if there were a difference in the extent of vagal
blockade between the two groups, a relatively higher vagal tone that is
likely to exist in these trained subjects should have resulted in
underestimation of inotropic sensitivity to dobutamine because a
greater vagal tone can, in fact, attenuate the increase in contractile
function in response to catecholamines (9).
In summary, our data suggest that, similar to endurance-trained
athletes, the strength-trained individuals exhibit an enhanced inotropic response to catecholamines without an increase in
chronotropic sensitivity. Furthermore, it is likely that physiological
LV concentric hypertrophy, unlike pathological concentric hypertrophy,
is a useful adaptation that is associated with enhanced
-adrenergic-mediated LV contractile function.
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ACKNOWLEDGEMENTS |
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This work was supported by National Institutes of Health (NIH) Claude D. Pepper Older Americans Independence Center Grants AG-13629 and R01 AG-12822 and General Clinical Research Center Grant MO1-RR-00036. O. E. Suman was supported by NIH Institutional National Service Award AG-00078. D. Hasten was supported by NIH Grant DK-49393 and National Research Service Award AG-05771-02. M. J. Turner was supported by Individual National Research Service Award 1-F32-AG05756-01. M. R. Rinder was supported by NIH Institutional Training Grant T-32 HL-07081-22.
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FOOTNOTES |
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Present addresses: O. E. Suman: Dept. of Pulmonary and Critical Care Medicine, Mayo Clinic, Alfred Bldg., Rm. 4-411, Rochester, MN 55905; M. J. Turner: Dept. of Health Promotion and Kinesiology, University of North Carolina at Charlotte, 9201 University City Blvd., Charlotte, NC 28223-0001; and R. J. Spina: Dept. of Kinesiology and Health Education, The University of Texas at Austin, Bellmont Hall 222, Austin, TX 78712.
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: A. A. Ehsani, Dept. of Medicine, Washington Univ. School of Medicine, 4566 Scott Ave., Box 8113, St. Louis, MO 63110 (E-mail: aehsani{at}imgate.wustl.edu).
Received 22 February 1999; accepted in final form 29 October 1999.
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
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