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Acute effects of resistance exercise on arterial

compliance

Allison E. DeVan, Maria M. Anton, Jill N. Cook, Daria B. Neidre, Miriam Y.


Cortez-Cooper and Hirofumi Tanaka
J Appl Physiol 98:2287-2291, 2005. First published Feb 17, 2005; doi:10.1152/japplphysiol.00002.2005
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J Appl Physiol 98: 22872291, 2005.


First published February 17, 2005; doi:10.1152/japplphysiol.00002.2005.

Acute effects of resistance exercise on arterial compliance


Allison E. DeVan, Maria M. Anton, Jill N. Cook, Daria B. Neidre,
Miriam Y. Cortez-Cooper, and Hirofumi Tanaka
Department of Kinesiology and Health Education, The University of Texas at Austin, Austin, Texas
Submitted 3 January 2005; accepted in final form 10 February 2005

matched controls (3, 14). Similarly, central arterial compliance


decreases after 4 mo of resistance training in young and
middle-aged adults (15). Interestingly, in this study, a reduction in arterial compliance was achieved in the initial 2 mo of
resistance training, and no further changes were observed
between month 2 and month 4 of the exercise intervention (15).
The ability to modify arterial compliance over such a short
period of time is thought to be due to the modulation of the
contractile states of the vascular smooth muscle cells in the
arterial wall (4). If such mechanisms are involved in modulating the chronic effects of resistance exercise on arterial compliance, it is plausible to hypothesize that an acute bout of
resistance exercise would alter arterial compliance as well. In
fact, plasma norepinephrine levels are elevated after an acute
bout of resistance exercise, giving rise to the possibility that
sympathetic vasoconstrictor tone may also be elevated after
exercise (17). However, it is currently unknown whether arterial compliance is reduced after one bout of resistance exercise
and, if so, how long the acute effects of a resistance exercise
bout persist.
Accordingly, the primary aim of this investigation was to
determine the acute effects of one bout of resistance exercise
on central arterial compliance. We hypothesized that acute
resistance exercise would decrease central arterial compliance
and that the postulated decrease in arterial compliance would
gradually return to baseline levels after the completion of
resistance exercise.

arterial stiffness; carotid artery; weight training


METHODS

the leading cause of death in the


United States and most industrialized countries, and the stiffening of central or cardiothoracic arteries is an emerging risk
factor for cardiovascular disease (5, 12). Decreases in the
elastic properties of the arteries reduce the buffering capacity
of the arteries, leading to increased pulse pressure, aortic
impedance, and left ventricular wall tension (11, 19, 25, 27,
29), all of which augment the workload of the heart. In
addition, the vascular structure of the carotid sinus determines
the deformation and strain on arterial baroreceptor endings
during changes in arterial blood pressure. Because of this,
reduced arterial compliance is associated with impaired arterial
baroreflex regulation of heart rate (16).
Our laboratory has previously demonstrated that aerobic
exercise training increases the elastic properties of central
arteries (26, 28). In contrast, recent studies indicate that central
arterial compliance in young and middle-aged resistancetrained men is decreased compared with sedentary age-

Subjects. Sixteen apparently healthy sedentary or recreationally


active adults (11 men and 5 women) aged 2335 yr were studied
(Table 1). All subjects were nonsmokers, nonobese, and free of overt
cardiovascular or other chronic diseases as assessed by medical
history. None of the subjects were taking cardiovascular-acting medications. Activity status was documented by the Godin physical
activity questionnaire (7), and subjects had not performed resistance
exercise in the past 6 mo. The Human Research Committee reviewed
and approved all procedures, and written, informed consents were
obtained from all subjects.
Procedures. At least 1 wk before the main experimental sessions,
body composition was measured by dual-energy X-ray absorptiometry (Lunar DPX, General Electric Medical Systems, Fairfield, CT),
one repetition maximums were obtained for nine resistance exercises
(1), and upright seated brachial blood pressure measurements were
taken after 510 min of seated rest.
The order of the two testing sessions, resistance exercise and sham
control (quiet seated rest in the exercise room), were randomized.
Before each testing session, subjects were at least 4-h fasted, and
female subjects were in the early-follicular phase of their menstrual

Address for reprint requests and other correspondence: H. Tanaka, Dept. of


Kinesiology, Univ. of Wisconsin-Madison, 2000 Observatory Dr., Madison,
WI 53706 (E-mail: tanaka1@wisc.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.

CARDIOVASCULAR DISEASE IS

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DeVan, Allison E., Maria M. Anton, Jill N. Cook, Daria B.


Neidre, Miriam Y. Cortez-Cooper, and Hirofumi Tanaka.
Acute effects of resistance exercise on arterial compliance. J Appl
Physiol 98: 22872291, 2005. First published February 17, 2005;
doi:10.1152/japplphysiol.00002.2005.Decreased central arterial
compliance is an emerging risk factor for cardiovascular disease.
Resistance training is associated with reductions in the elastic
properties of central arteries. Currently, it is not known whether
this reduction is from one bout of resistance exercise or from an
adaptation to multiple bouts of resistance training. Sixteen healthy
sedentary or recreationally active adults (11 men and 5 women, age
27 1 yr) were studied under parallel experimental conditions on
2 separate days. The order of experiments was randomized between resistance exercise (9 resistance exercises at 75% of 1
repetition maximum) and sham control (seated rest in the exercise
room). Baseline hemodynamic values were not different between
the two experimental conditions. Carotid arterial compliance (via
simultaneous B-mode ultrasound and applanation tonometry) decreased and -stiffness index increased (P 0.01) immediately
and 30 min after resistance exercise. Immediately after resistance
exercise, carotid systolic blood pressure increased (P 0.01),
although no changes were observed in brachial systolic blood
pressure at any time points. These measures returned to baseline
values within 60 min after the completion of resistance exercise.
No significant changes in these variables were observed during the
sham control condition. These results indicate that one bout of
resistance exercise acutely decreases central arterial compliance,
but this effect is sustained for 60 min after the completion of
resistance exercise.

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RESISTANCE EXERCISE AND ARTERIAL COMPLIANCE

and minimum carotid diameters measured from intima to intima, and


P1 and P0 are the highest and lowest blood pressure at the carotid
artery after adjusting for hold-down force. To eliminate interinvestigator variability, one investigator analyzed all arterial images and
blood pressure waveforms. At each time point, an average of 15 heart
cycles were analyzed.
Statistics. ANOVA with repeated measures (condition and time as
within-subjects factors) was used for statistical analyses, and Newman-Keuls post hoc tests were used to identify significant data points
(P 0.05). All data are expressed as means SE.

Table 1. Selected subject characteristics


Variable

Mean SE

Men/women
Age, yr
Height, cm
Body mass, kg
Body fat, %
Physical activity score, units
Brachial systolic BP, mmHg
Brachial diastolic BP, mmHg
Heart rate, beats/min

11/5
271
1723
714
271
123
1182
732
673

RESULTS

BP, blood pressure.

J Appl Physiol VOL

DISCUSSION

The primary findings of this study are as follows. First,


central arterial compliance was decreased immediately and 30
min after resistance exercise. These measures returned to

Fig. 1. Carotid arterial compliance and -stiffness index for sham control
(seated rest) and resistance exercise. Values are means SE. Post, postexercise of post-sham control. *P 0.005 vs. baseline.

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cycle. In an attempt to control for dietary intake and the associated


differences in hormonal milieu, diet before the second testing session
was reproduced the 3 days before the last testing session. Both
sessions were initiated around the same time of day to minimize
possible diurnal changes in the dependent variables.
Brachial blood pressure was measured two to three times using the
oscillometric pressure sensor method after subjects had rested in the
supine position at least 10 min in a quiet, dimly lit, temperaturecontrolled room. Oscillometric blood pressure measurements have
been found to be valid (13), and reproducibility of resting blood
pressure measurements using this procedure in our laboratory is
excellent. The coefficient of variation for two trials performed 1 wk
apart is 1% for systolic blood pressure. The correlation coefficient
between the trial one and trial two values is r 0.98. Arterial
stiffness and arterial compliance were measured as previously described (15). Briefly, while imaging subjects left common carotid
artery by B-mode ultrasound (HDI 5000CV, ATL Instruments,
Bothel, WA), blood pressure was obtained by applanation tonometry
(Millar TCB-500, Millar Instruments, Houston, TX) secured by the
neck collar in the right common carotid artery. Because baseline
levels of carotid blood pressure are subjected to hold-down force, the
pressure signal obtained by the tonometry was calibrated by equating
the carotid mean arterial and diastolic blood pressure to the brachial
artery value as previously described (2). These calibrations were
performed at each measurement time point. After these preexercise
measures, subjects either sat quietly in the exercise room for 30 45
min or performed a weight training session consisting of one warm-up
set of 8 12 repetitions at 50% of one repetition maximum and one set
to exhaustion at 75% of one repetition maximum for nine exercises in
the following order: seated row, seated chest press, leg press, seated
overhead press, seated biceps curl, leg extension, seated leg curl,
standing triceps extension, and seated calf raise. After this, the
preexercise measurements described above were repeated immediately after (510 min post-sham control or postexercise) and 30, 60,
90, 120, and 150 min post-sham control or postexercise.
Ultrasound images were transferred to digital viewing software
(Access Point 2000, Freeland, Westfield, IN) where pulsatile changes
in carotid artery diameters were analyzed 12 cm past the carotid bulb
as described previously (15). Carotid artery blood pressure waveforms
were analyzed at each time point by waveform browsing software
(WinDaq Waveform Browser Software, 2000, Dataq Instruments,
Akron, OH). A combination of ultrasound imaging at the common
carotid artery with simultaneous applanation of tonometrically obtained arterial pressures from the contralateral carotid artery permitted
noninvasive determinations of arterial compliance. In addition to
arterial compliance, we also calculated -stiffness index, which provides an index of arterial compliance adjusted for distending pressure
(9, 30). Arterial compliance and -stiffness index were calculated
using the following equations: [(D1 D0)/D0]/[2(P1 P0)] D02
and (lnP1/P0)/[(D1 D0)/D0], where D1 and D0 are the maximum

Baseline hemodynamic values were not different between


the two conditions. Carotid arterial compliance and -stiffness
index (Fig. 1) after resistance exercise were both different from
baseline measures immediately and 30 min post-sham control
or postexercise (P 0.005). These values returned to baseline
by 60 min after resistance exercise. Mean arterial blood pressure was not significantly different from baseline values at any
time point (Table 2). Heart rate increased (from 8 to 16
beats/min), and diastolic blood pressure decreased immediately
and 30 min postexercise. Brachial systolic blood pressure did
not change significantly (Fig. 2), whereas carotid artery systolic blood pressure increased (P 0.001) immediately after
resistance exercise. No significant changes were observed in
any variables in the sham control condition except for a
decrease in heart rate immediately, 30, 60, and 90 min postsham control or postexercise.

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RESISTANCE EXERCISE AND ARTERIAL COMPLIANCE

Table 2. Hemodynamic variables for sham control and resistance exercise


Time Point
Condition

Immediately
Post

30 min
Post

60 min
Post

90 min
Post

120 min
Post

150 min
Post

1122
821
651
471
1053
403
622
0.70.05

1122
832
672
452
1023
352
572*
0.69.05

1122
822
672
451
1012
342
582*
0.67.05

1112
812
662
451
993
323
572*
0.69.04

1122
832
672
451
1013
332
582*
0.67.04

1132
852
692*
451
1044
364
592
0.66.04

1143
842
682
461
1022
342
592
0.67.04

1122
822
652
471
1033
383
612
0.66.05

1122
852
612*
511*
1154*
544*
773*
0.63.06

1112
832
622*
492*
1104
484*
693*
0.63.05

1112
822
632
482
1063
443
652
0.68.05

1122
822
642
481
1063
412
632
0.66.04

1123
822
652
472
1023
373
612
0.67.04

1142
842
672
471
1074
404
632
0.66.04

Values are means SE. Post, post-sham control or postexercise; SBP, systolic blood pressure; MAP, mean BP; DBP, diastolic BP; PP, pulse pressure;
, distention. *P 0.005 vs. baseline.

baseline levels within 60 min after resistance exercise. These


results suggest that the increased central arterial stiffness and
reduced central arterial compliance previously observed in
resistance-trained adults may be due to the chronic effects of
resistance exercise training. Second, one bout of resistance
exercise was associated with elevations in carotid systolic
blood pressure, although there were no significant changes in
brachial systolic blood pressure. These results suggest that
measurements of central blood pressure may reveal the vascu-

Fig. 2. Brachial and carotid systolic blood pressure (SBP) for sham control
(seated rest) and resistance exercise. Values are means SE. Post, postexercise or post-sham control. *P 0.0001 vs. baseline.
J Appl Physiol VOL

lar effects of resistance exercise that may not be unmasked by


routine brachial blood pressure assessments.
In the present study, measures of arterial compliance decreased after resistance exercise, but these measures were no
longer different from baseline values 60 150 min after resistance exercise. Thus the acute effects of resistance exercise on
the vasculature appear to be transient in nature, lasting no
longer than 1 h. In previous intervention studies, which found
decreased central arterial compliance after chronic weight
training, arterial stiffness was assessed 24 48 h after the last
bout of resistance exercise (15). Taken together, these results
suggest that the lower arterial compliance or higher arterial
stiffness previously observed in those who habitually engage in
weight training seem to be a result of the chronic effects of
daily resistance exercise.
It is not clear why arterial stiffness is elevated acutely after
resistance exercise. It is possible that the increase in central
arterial stiffness and decrease in central arterial compliance
with one bout of resistance exercise may be due to an epiphenomenon of corresponding blood pressure changes. However,
mean arterial blood pressure, which is used to display the
pressure-compliance relation, did not change significantly, and
there was an 5% reduction in carotid distention following the
resistance exercise bout. Additionally, the decrease in the
elastic properties of the carotid artery was also observed even
when -stiffness index, which provides an index of arterial
compliance adjusted for distending pressure (9, 30), was used
to represent these changes. Other possibilities include increased sympathetic adrenergic vasoconstrictor tone (6, 22, 23)
and/or impaired endothelial function (31), both of which were
not measured in the present study.
In the present study, brachial blood pressure responses after
one bout of resistance exercise are similar to other studies of
sedentary and recreationally active adults (18, 24). Two sets of
8 12 repetitions for 12 resistance exercises had no significant
effect on brachial systolic or mean blood pressure during the

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Sham control
Brachial SBP, mmHg
Brachial MAP, mmHg
Brachial DBP, mmHg
Brachial PP, mmHg
Carotid SBP, mmHg
Carotid PP, mmHg
Heart rate, beats/min
Carotid diameter, mm
Resistance exercise
Brachial SBP, mmHg
Brachial MAP, mmHg
Brachial DBP, mmHg
Brachial PP, mmHg
Carotid SBP, mmHg
Carotid PP, mmHg
Heart Rate, beats/min
Carotid diameter, mm

Baseline

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6.

7.
8.
9.

10.
11.

12.

13.

14.

15.

16.

17.

18.

19.
20.

ACKNOWLEDGMENTS
We thank Rhea Montemayor and Phil Stanforth for technical assistance.

21.

GRANTS
This study was supported in part by National Institutes of Health Awards
AG-20966 and HL-072729 and by the Ministerio de Educacion of the government of Spain.

22.

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24 h after resistance exercise when compared with control


values (24). Our present study is consistent with these previous
observations. A novel finding of the present study is that,
although peripheral systolic blood pressure at the brachial
artery remained constant, central systolic blood pressure was
significantly elevated above baseline levels immediately after
resistance exercise. ORourke (19) argued that the effects of
disease states or drugs on the vasculature may be underappreciated when one relies solely on brachial blood pressure measurements. For example, it has been reported that nitroglycerin
causes substantial reductions in aortic systolic pressure (10
mmHg via direct intra-aortic blood pressure measurements)
without causing any significant alterations in brachial systolic blood pressure (20). Similarly, in response to lower
body negative pressure, carotid blood pressure displayed
twice as much change as brachial blood pressure (21). Our
present study extends this concept to the stimuli of resistance training and suggests that measurements of central
blood pressure may unmask the vascular effects of resistance exercise that an assessment of brachial blood pressure
would not.
In summary, one bout of moderate-intensity full-body resistance exercise increases central arterial stiffness and decreases
central arterial compliance in young, healthy adults, but these
changes persist 60 min. Therefore, the acute effects of
resistance exercise on arterial stiffness are transient in nature,
and the reduced elastic properties of central arteries previously
observed in resistance-trained adults appear to be due to the
chronic effects of resistance exercise training. Further research
into the mechanisms, time course, and severity of the resistance
training-induced decrease in the elastic properties of central
arteries is crucial because many exercise professionals are
prescribing resistance training to increase musculoskeletal
strength (1, 8, 10). In particular, such exercise prescriptions
might be contraindicated for those at risk or who already have
cardiovascular disease. With the increasingly accumulating
knowledge regarding the effects of resistance exercise on the
vasculature, exercise prescriptions can be better tailored to
individuals whose aims are to prevent and treat cardiovascular
disease.

RESISTANCE EXERCISE AND ARTERIAL COMPLIANCE


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