J Appl Physiol 112: 1891–1896, 2012.
First published March 15, 2012; doi:10.1152/japplphysiol.01460.2011.
Impact of chronic exercise training on the blood pressure response
to orthostatic stimulation
Jun Sugawara,1 Hidehiko Komine,1 Taiki Miyazawa,2 Tomoko Imai,3 James P. Fisher,4
and Shigehiko Ogoh2
1
Human Technology Research Institute, National Institute of Advanced Industrial Science and Technology, Tsukuba, Ibaraki,
Japan; 2Department of Biomedical Engineering, Toyo University, Kawagoe, Saitama, Japan; 3Graduate School of
Comprehensive Human Sciences, University of Tsukuba, Tsukuba, Ibaraki, Japan; and 4School of Sport and Exercise
Sciences, University of Birmingham, Edgbaston, Birmingham, United Kingdom
Submitted 28 November 2011; accepted in final form 12 March 2012
cardiovascular adaptation; endurance training; resistance training;
head-up tilt
(BP) is typically well regulated during
short-term central hypovolemia (e.g., orthostatic stress, hemorrhage) as the unloading of the arterial and cardiopulmonary
baroreceptors compensates for the decrease in stroke volume
(SV) by evoking neurally and hormonally mediated increases
in heart rate (HR) and peripheral vascular resistance (12, 20).
ARTERIAL BLOOD PRESSURE
Address for reprint requests and other correspondence: J. Sugawara, Human
Technology Research Institute, National Institute of Advanced Industrial
Science and Technology (AIST), Tsukuba Central 6, Tsukuba, Ibaraki, 3058566 Japan (e-mail: [email protected]).
http://www.jappl.org
However, exercise training-induced adaptations in cardiovascular structure may modify the functional regulation of BP. It
is well known that there is a high prevalence of orthostatic
hypotension in elite endurance athletes (2, 5, 6, 15). Highintensity endurance training, which is characterized by volume
overload associated with the high cardiac output during exercise, induces an increase in left ventricle (LV) volume with a
proportional increase in wall thickness (i.e., eccentric hypertrophy) (14), increases LV compliance (6), and reduces the
stiffness of large-conduit arteries (13). These cardiovascular
adaptations are favorable for achieving the high rates of oxygen consumption required for elite endurance exercise performance. However, the structural adaptations of the LV that
occur with endurance training also result in a steeper FrankStaring cardiac function curve (6). This is associated with a
substantial drop in SV during orthostatic stress and likely
contributes to the increased incidence of orthostatic hypotension and syncope in well-trained endurance athletes (6).
In contrast, there is a lack of information regarding the
impact of regular resistance training on the hemodynamic
response to the orthostatic stress. Although a few studies have
suggested that resistance training is associated with superior
orthostatic tolerance (8, 17), the precise etiology is unknown.
The marked and repetitive increase in BP with high-intensity
resistance training may elicit a thickening of the LV wall with
unchanged LV chamber size (i.e., concentric hypertrophy) (14)
and stiffening of the large-conduit arteries (10, 13). Such LV
concentric hypertrophy may limit the distension of the LV
chamber and attenuate the reduction in SV during orthostatic
stimulation. On the other hand, baroreceptor sensitivity may be
blunted by a stiffening of the central conduit arteries in which
these mechanoreceptors are embedded (e.g., ascending aorta
and carotid artery), thus leading to impaired BP regulation
during orthostatic stress. Such a mechanism is suggested to
contribute to age-related alterations in BP control (9). However, the influence of large-artery stiffening caused by vigorous
resistance training on the BP response to orthostatic stimulation remains unknown.
We aimed to investigate the influence of habitual training
modality on the BP responses to the orthostatic stimulation and
to examine the underlying mechanism(s). We hypothesized
that endurance-trained and resistance-trained individuals exhibit distinct BP responses to the orthostatic stimulation and
that such divergent BP responses would be associated with
exercise training-induced morphological adaptations of LV and
large-conduit vessels.
8750-7587/12 Copyright © 2012 the American Physiological Society
1891
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Sugawara J, Komine H, Miyazawa T, Imai T, Fisher JP, Ogoh
S. Impact of chronic exercise training on the blood pressure response
to orthostatic stimulation. J Appl Physiol 112: 1891–1896, 2012. First
published March 15, 2012; doi:10.1152/japplphysiol.01460.2011.—
Exercise training elicits morphological adaptations in the left ventricle
(LV) and large-conduit arteries that are specific to the type of training
performed (i.e., endurance vs. resistance exercise). We investigated
whether the mode of chronic exercise training, and the associated
cardiovascular adaptations, influence the blood pressure responses to
orthostatic stimulation in 30 young healthy men (10 sedentary, 10
endurance trained, and 10 resistance trained). The endurance-trained
group had a significantly larger LV end-diastolic volume normalized
by body surface area (vs. sedentary and resistance-trained groups),
whereas the resistance-trained group had a significantly higher LV
wall thickness and aortic pulse wave velocity (PWV) compared with
the endurance-trained group. In response to 60° head-up tilt (HUT),
mean arterial pressure (MAP) rose in the resistance-trained group
(⫹6.5 ⫾ 1.6 mmHg, P ⬍ 0.05) but did not change significantly in
sedentary and the endurance-trained groups. Systolic blood pressure
(SBP) decreased in endurance-trained group (⫺8.3 ⫾ 2.4 mmHg, P ⬍
0.05) but did not significantly change in sedentary and resistancetrained groups. A forward stepwise multiple regression analysis revealed that LV wall thickness and aortic PWV were significantly and
independently associated with the MAP response to HUT, explaining
⬃41% of its variability (R2 ⫽0.414, P ⬍ 0.001). Likewise, aortic
PWV and the corresponding HUT-mediated change in stroke volume
were significantly and independently associated with the SBP response to HUT, explaining ⬃52% of its variability (R2 ⫽ 0.519, P ⬍
0.0001). Furthermore, the change in stroke volume significantly correlated with LV wall thickness (r ⫽ 0.39, P ⬍ 0.01). These results
indicate that chronic resistance and endurance exercise training differentially affect the BP response to HUT, and that this appears to be
associated with training-induced morphological adaptations of the LV
and large-conduit arteries.
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Exercise Training, Cardiovascular Adaptation, and Blood Pressure Regulation
METHODS
Subjects
Experimental Protocol
Subjects were instructed to avoid regular exercise training at least
24 h before the experimental visit to minimize the acute impact of
exercise on the studied variables. All measurements were performed
in a quiet, temperature-controlled room (24 –26 C°) after at least 4 h
of fasting and abstinence from caffeinated beverage. However, subjects were instructed to consume a little water prior to the measurements to maintain adequate hydration. After the physical characteristics measurements, cardiovascular measurements were conducted in a
quiet room, and following ⬎10 min of supine rest, subjects underwent
a Doppler-echocardiography examination. Following this hemodynamic variables were continuously monitored during supine rest and
60° head-up tilt (HUT) (5 min each). Aortic pulse wave velocity was
evaluated during supine rest only. During HUT, subjects stood on the
foot rest of a tilt bed and were instructed not to move or voluntarily
contract muscles in lower limbs.
Measurements
Sugawara J et al.
the aortic annulus immediately proximal to the aortic valve leaflets
from the apical five-chamber view [e.g., LV outflow method (7);
average of five cardiac cycles]. Echocardiographically determined
measures of SV were used to calibrate Modelflow measures of SV as
described below.
Aortic pulse wave velocity. To quantify aortic arterial stiffness,
aortic (i.e., carotid-femoral) pulse wave velocity (PWV) was measured as previously described (18). Carotid and femoral arterial pulse
waveforms were simultaneously measured throughout the BP measurement in supine position with a vascular testing device (Form
PWV/ABI, Colin Medical Technology, Komaki, Japan). PWV was
calculated from the distance between two arterial recording sites
divided by the transit time. Carotid and femoral artery pulse waves
were measured with arterial applanation tonometry incorporating an
array of 15 micropiezoresistive transducers attached on the left common carotid and left common femoral arteries. The transit time
between carotid and femoral arterial pressure waveforms was acquired using the foot-to-foot method. Arterial path length was assumed as the straight distance between carotid and femoral recording
sites.
Hemodynamic variables. Heart rate was recorded with ECG (ML
132 Bio Amp, ADInstruments, Colorado Springs, CO). Finger arterial
pressure wave forms were continuously recorded at right index finger
fixed at the heart level by a noninvasive beat-to-beat blood pressure
monitoring system (Finometer, TNO TPD Biomedical Instruments,
Amsterdam, The Netherlands). Brachial systolic (SBP), diastolic
(DBP), and mean arterial BP (MAP) were estimated by a filtering of
the finger arterial pressure waveform (BeatScope 1.1, TNO TPD
Biomedical Instruments, Amsterdam, The Netherlands). SV and cardiac output (Q) were computed from the blood pressure waveform
using the validated Modelflow method, incorporating age, sex, height,
and weight (19, 21), and then calibrated by a constant, the ratio of
mean Modelflow SV to baseline (before HUT) SV by echocardiography. Total peripheral resistance (TPR) was calculated as MAP/Q.
SV, Q, and TPR were normalized by body surface area and defined as
SV index, cardiac index, and TPR index, respectively. Continuous
data for the last 1 min during each posture (Supine, HUT) were
averaged and reported.
Statistical Analyses
One-way ANOVA was used to determine the effects of habitual
training modality on physiological characteristics. Mixed-design
Table 1. Subject characteristics
Physical characteristics. Height, body mass (via a digital scale,
BWB-200, TANITA, Tokyo, Japan), body mass index, thigh circumference (via a nonelastic tape measure), and leg volume (via water
replacement method with a bathtub) were measured.
Echocardiography. LV dimension, wall thickness, and LV function
were determined using echocardiography according to established
guidelines (1). LV mass (LVM), LV wall thickness (LVWT), and
fractional shortening (FS) were calculated according to following
equation:
LVM 共g兲 ⫽ 1.04[(LVEDD ⫹ PWT ⫹ IVST)3 ⫺ (LVEDD)3] ⫺ 14 (3)
LVWT 共mm兲 ⫽ (IVST⫹PWT)/2
FS (%) ⫽ (LVEDD ⫺ LVESD)/LVEDD*100
where LVEDD is LV end-diastolic internal diameter, PWT is posterior wall thickness, IVST is interventricular septal thickness, and
LVESD is LV end-systolic internal diameter.
SV was calculated as the product of the cross-sectional area of the
aortic annulus and the time-velocity integral. The cross-sectional area
of the aortic annulus was calculated from its diameter during early
systole (M-mode image from parasternal long-axis view). The velocity of LV outflow was measured with the sample volume positioned at
Variables
Sedentary
Endurance Trained
Resistance Trained
Age, yr
Height, cm
Body mass, kg
BMI, kg/m2
Thigh circumference, cm
Leg volume, liters
LVEDV, ml
LVEDV index, ml/m2
LVWT, cm
LVWT index, ratio
LVM, g
LVM index, g/m2
FS, %
Aortic EDD, cm
Aortic PWV, cm/s
24 ⫾ 0.9
173 ⫾ 2.1
66 ⫾ 3.3
22.2 ⫾ 0.8
51.7 ⫾ 1.1
7.3 ⫾ 0.3
94.2 ⫾ 6.9
52.3 ⫾ 3.6
0.91 ⫾ 0.03
0.20 ⫾ 0.01
155 ⫾ 12
86.2 ⫾ 6.1
29.7 ⫾ 1.6
2.4 ⫾ 0.0
900 ⫾ 29
22 ⫾ 1.3
174 ⫾ 1.2
62 ⫾ 1.2
20.8 ⫾ 0.3
51.1 ⫾ 0.5
6.8 ⫾ 0.3
125.5 ⫾ 5.7†
71.5 ⫾ 3.1†
0.85 ⫾ 0.01
0.17 ⫾ 0.01†
177 ⫾ 10
100.4 ⫾ 5.3
34.7 ⫾ 2.5
2.4 ⫾ 0.1
842 ⫾ 21
21 ⫾ 0.4
176 ⫾ 2.0
80 ⫾ 4.1†‡
26.2 ⫾ 1.1†‡
58.3 ⫾ 1.3†‡
9.5 ⫾ 0.8†‡
114.5 ⫾ 7.8†
58.1 ⫾ 4.4‡
1.08 ⫾ 0.05‡
0.22 ⫾ 0.02†‡
234 ⫾ 19†
117.5 ⫾ 9.1†‡
33.5 ⫾ 1.2
2.4 ⫾ 0.1
949 ⫾ 33‡
Data are means ⫾ SE. BMI, body mass index; LVEDV, left ventricular
end-diastolic volume; LVEDV index, LVEDV normalized by body surface
area; LVWT, LV wall thickness; LVWT index, LVWT normalized by LV
end-diastolic internal diameter (EDD); LVM, LV mass; LVM index, LVM
normalized by body surface area; FS, fractional shortening; PWV, pulse wave
velocity. †P ⬍ 0.05 vs. sedentary; ‡P ⬍ 0.05 vs. endurance trained.
J Appl Physiol • doi:10.1152/japplphysiol.01460.2011 • www.jappl.org
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A total of 30 apparently healthy Japanese men (10 sedentary, 10
endurance trained, and 10 resistance trained) were studied. Habitual
physical activity status of each subject was determined upon initial
screening prior to the experiment (via e-mail), then subsequently
verified and explored in detail at the experimental visit (by interview
and questionnaire). All subjects had no apparent cardiovascular disease as assessed by medical history. Subjects who were current
smokers or smoked within the past two years were excluded. None of
the sedentary subjects had engaged in regular physical activity (⬎2
days/wk). The endurance-trained group was comprised of long distance runners and triathletes who trained for competition more than 5
days/wk and did not engage in resistance training. Resistance-trained
subjects were athletes who played American football. Their training
program consisted mainly of regular heavy resistance training (2–3
days/wk) and anaerobic exercise (5– 6 days/wk). On average, endurance-trained and resistance-trained men had been exercising for 7.1 ⫾
1.8 and 2.6 ⫾ 0.1 yr, respectively. This study was reviewed and
approved by the Institutional Review Board of the National Institute
of Advanced Industrial Science and Technology and was conducted in
Japan. All potential risks and procedures of the study were explained
to the subjects, and they gave their written informed consent to
participate in the study.
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•
Sugawara J et al.
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post hoc test was used to identify significant differences among mean
values. Product-moment correlation analyses were performed to determine relations among physiological characteristics and hemodynamic responses to HUT. Using a forward stepwise multiple regression analysis, we examined which physiological characteristics were
significantly and independently associated with the MAP and SBP
responses to orthostatic stress. Physiological characteristics and
changes in hemodynamic variables (except for blood pressure) were
included in the model if first identified as being significantly associated in product-moment correlation analyses. All data are reported as
means ⫾ SE. Statistical significance was set a priori at P ⬍ 0.05.
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Fig. 1. Responses of blood pressure to the head-up tilt (HUT). Open circles are
sedentary, filled circles are endurance-trained, filled squares are resistancetrained. SBP, systolic blood pressure; DBP, diastolic blood pressure; MAP,
mean arterial pressure; PP, pulse pressure. *P ⬍ 0.05 vs. supine position; ‡P ⬍
0.05 vs. endurance trained.
AVOVA with both between-subject (i.e., sedentary, resistance, endurance) and within-subject factors (i.e., supine vs. tilt) were performed to determine the effects of habitual training on hemodynamic
responses to HUT. In the case of a significant F-value, a Tukey HSD
Fig. 2. Changes in blood pressure from the supine to HUT position. S,
sedentary; E, endurance trained; R, resistance trained.
J Appl Physiol • doi:10.1152/japplphysiol.01460.2011 • www.jappl.org
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Exercise Training, Cardiovascular Adaptation, and Blood Pressure Regulation
RESULTS
Sugawara J et al.
associated with ⌬MAP, explaining ⬃41% of its variability
(R2 ⫽ 0.414, P ⬍ 0.001, Table 4). Changes in SBP (⌬SBP)
during HUT significantly correlated with body mass, BMI,
LVWT, LVM, aortic PWV, and ⌬SV (r ⫽ 0.47– 0.69). Aortic
PWV and ⌬SV were significantly and independently associated with ⌬SBP, explaining ⬃52% of its variability (R2 ⫽
0.519, P ⬍ 0.0001, Table 4). ⌬SV was significantly correlated
with LVWT (r ⫽ 0.39).
DISCUSSION
Our most salient findings are twofold. First, MAP rose with
orthostatic stimulation in resistance-trained men but not in
sedentary and endurance-trained men. LV wall thickening and
aortic stiffening were independently associated with HUTrelated MAP responses. Second, SBP decreased with orthostatic stimulation in endurance-trained men but not in sedentary and resistance-trained men. HUT-related SBP responses
were independently related to aortic PWV and the corresponding change in SV, which itself was associated with LV wall
thickness. Our findings suggest that the BP response to HUT
varies as a function of habitual training modality, and that this
is associated with exercise training-induced morphological
adaptations in LV and large-conduit vessels.
Resistance training seems to be associated with superior
orthostatic tolerance (8, 17). For example, Lightfoot et al. (8)
indicated that men who were chronically resistance trained
exhibited an elevation in MAP with maximal lower-body
negative pressure administered until the onset of presyncopal
signs. However, the exact mechanisms underlying the observations are unclear. Levine et al. (6) suggested that in endurance-trained athletes greater LV chamber compliance (i.e., a
steeper Frank-Staring cardiac function curve) could lead to a
substantial fall of SV during orthostatic stress, and hence
orthostatic hypotension. Therefore, we reasoned that an increase in LV wall thickness in resistance-trained individuals
would result in a reduction in LV chamber compliance, and
thus may improve orthostatic tolerance. As expected, endurance-trained and resistance-trained individuals exhibited distinct BP responses to the orthostatic stimulation. During shortterm orthostatic stimulation (e.g., 5 min HUT) resistancetrained men exhibited a significant increase in MAP and an
unchanged SBP, whereas endurance-trained men showed an
unchanged MAP and a significant reduction in SBP. Further-
Table 2. Hemodynamic responses to the orthostatic stimulation
Variables
HR, beats/min
SV, ml
SV index, ml/m2
Q, l/min
Cardiac index, l 䡠 min⫺1 䡠 m⫺2
TPR, unit
TPR index, unit
Posture
Sedentary
Endurance Trained
Resistance Trained
Supine
HUT
Supine
HUT
Supine
HUT
Supine
HUT
Supine
HUT
Supine
HUT
Supine
HUT
55 ⫾ 2
77 ⫾ 3*
104 ⫾ 4
75 ⫾ 5*
58 ⫾ 3
42 ⫾ 3*
5.7 ⫾ 0.3
5.7 ⫾ 0.3
3.2 ⫾ 0.1
3.2 ⫾ 0.2
15.5 ⫾ 0.8
16.3 ⫾ 1.1
8.7 ⫾ 0.5
9.1 ⫾ 0.7
50 ⫾ 3
66 ⫾ 5*
112 ⫾ 7
84 ⫾ 8*
64 ⫾ 4
48 ⫾ 4*
5.6 ⫾ 0.4
5.4 ⫾ 0.5
3.2 ⫾ 0.2
3.1 ⫾ 0.3
15.4 ⫾ 1.4
16.2 ⫾ 1.8
8.8 ⫾ 0.8
9.3 ⫾ 1.1
53 ⫾ 2
70 ⫾ 3*
113 ⫾ 4
93 ⫾ 3*
57 ⫾ 2
47 ⫾ 1*
6 ⫾ 0.3
6.4 ⫾ 0.3
3 ⫾ 0.1
3.2 ⫾ 0.4
15.9 ⫾ 0.4
15.7 ⫾ 0.4
8.1 ⫾ 0.3
8 ⫾ 0.3
Data are means ⫾ SE. HUT, head-up tilt; HR, heart rate; SV, stroke volume; Q, cardiac output; TPR, total peripheral resistance. *P ⬍ 0.05 vs. supine position.
J Appl Physiol • doi:10.1152/japplphysiol.01460.2011 • www.jappl.org
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Selected physiological characteristics are summarized in
Table 1. Resistance-trained men had a significantly greater
body mass, body mass index, thigh circumference, and leg
volume compared with the sedentary and endurance-trained
group. LVEDV and body surface area-normalized LVEDV
(i.e., LVEDV index) were significantly larger in the endurancetrained group than in the other groups. Significantly greater
LVWT was seen in the resistance-trained group compared with
the other groups. There was no significant difference in FS
among the three groups. Aortic PWV was significantly higher
in the resistance-trained group than in the endurance-trained
group.
Figure 1 depicts the BP responses to the HUT. There were
no significant differences in baseline BP between groups. With
HUT, SBP significantly decreased by 8 ⫾ 2 mmHg in the
endurance-trained group but remained unchanged in the resistance-trained and sedentary groups. DBP rose significantly
with HUT in the resistance-trained and sedentary groups, but
not in the endurance-trained group. MAP increased with HUT
in the resistance-trained group but not in the sedentary and
endurance-trained groups. PP was reduced with HUT in the
endurance-trained and sedentary groups, but not in the resistance-trained group. Consequently, HUT-mediated BP responses of the endurance- and resistance-trained groups were
divergent, as seen in Fig. 2.
Other hemodynamic responses to orthostatic stimulation are
summarized in Table 2. There were no significant intergroup
differences in these variables. HR significantly increased during HUT in all groups presumably due to a significant reduction in SV (⌬SV correlated significantly with ⌬HR, r ⫽ ⫺0.49,
P ⬍ 0.01). SV index significantly decreased with HUT in all
groups (P ⬍ 0.05 for all). Main effects for group and treatment
(i.e., HUT) were not significant in Q, cardiac index, TPR, and
TPR index. The group-treatment interactions were also nonsignificant
Table 3 summarizes the results of product-moment correlation analyses among baseline physiological characteristics and
hemodynamic responses to HUT. Changes in MAP (⌬MAP)
during HUT were significantly correlated with LVWT, LVM,
and corresponding changes in SV (⌬SV) (r ⫽ 0.38 – 0.52). A
forward stepwise multiple regression analysis revealed that
LVWT and aortic PWV were significantly and independently
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Table 3. Result of product-moment correlation analyses of physiological characteristics and hemodynamic responses to HUT
BMI LVEDV LVEDV Index LVWT LVWT Index LVM LVM Index Aortic PWV
Body mass
0.93
BMI
LVEDV
LVEDV index
LVWT
LVWT index
LVM
LVM index
Aortic PWV
DHR
⌬SV
⌬Q
⌬TPR
⌬MAP
⌬SBP
⌬DBP
0.07
0.01
⫺0.31
⫺0.32
0.92
0.53
0.58
⫺0.20
⫺0.39
0.41
0.48
⫺0.60
⫺0.71
0.90
0.55
0.56
0.36
0.14
0.84
0.51
0.27
0.31
0.40
0.29
0.76
0.44
0.95
0.38
0.39
0.01
⫺0.13
0.30
0.25
0.30
0.20
⌬HR
⌬SV
⌬Q
⌬TPR
⌬MAP ⌬SBP ⌬DBP
⌬PP
⫺0.15
0.34 0.27 ⫺0.22
0.27 0.47 0.10 0.61
⫺0.22
0.43 0.28 ⫺0.21
0.34 0.52 0.17 0.62
⫺0.02 ⫺0.05 0.21 ⫺0.21 ⫺0.23 ⫺0.03 ⫺0.26 0.14
0.00 ⫺0.15 0.09 ⫺0.09 ⫺0.29 ⫺0.18 ⫺0.26 ⫺0.07
⫺0.12
0.39 0.34 ⫺0.22
0.52 0.49 0.42 0.41
⫺0.08
0.33 0.20 ⫺0.10
0.52 0.40 0.45 0.26
⫺0.12
0.35 0.42 ⫺0.31
0.38 0.47 0.27 0.49
⫺0.10
0.29 0.40 ⫺0.29
0.33 0.36 0.25 0.34
⫺0.09
0.32 0.21
0.05
0.51 0.64 0.47 0.59
⫺0.49 0.30 ⫺0.26 ⫺0.20 ⫺0.34 ⫺0.04 ⫺0.46
0.48 ⫺0.36
0.44 0.52 0.19 0.62
⫺0.86
0.16 0.11 0.08 0.11
0.22 0.25 0.34 0.12
0.88 0.95 0.60
0.77 0.90
0.41
Bold numbers mean significant correlation (r ⬎ 0.35, P ⬍ 0.05; r ⬎ 0.45, P ⬍ 0.01). Delta (⌬) means HUT-mediated change. MAP, mean arterial pressure;
SBP, systolic blood pressure; DBP, diastolic blood pressure; PP, pulse pressure.
orthostatic stress remains unclear, our findings might imply
that age-related and resistance training-induced alterations of
central arterial stiffness are functionally different.
Overall, the results of the present study suggest that the
morphological adaptations in the LV and large-conduit arteries
resulting from chronic exercise training are accompanied by
alterations in BP regulation during orthostatic stimulation. Our
findings support and extend the notion advanced by Levine et
al. (6) that LV morphological adaptations are associated with
orthostatic intolerance in endurance-trained individuals. However, in the present study training-related cardiovascular morphological adaptation explained only ⬃41–52% of the variance
in the MAP and SBP responses to HUT. The physiological
mechanism(s) that account for the remaining variance are
unclear but may involve exercise training-related changes in
baroreflex control (12, 15), peripheral arterial structure and
function (5), blood volume and/or hydration status (4). Further
studies are required to explore these possibilities.
There are several limitations to the present study. First,
because we used a cross-sectional study design, potential
genetic influences cannot be completely ruled out. Additionally, correlational and regression analyses could not provide
causation. Second, we did not measure either aerobic capacity
(i.e., maximal oxygen uptake) or maximal muscle strength of
subjects. The average length of exercise training was also
Table 4. Result of forward stepwise multiregression analysis
␤
P Value
R2 Change
Dependent Variable: Changes in MAP with HUT
Independent variables
LVWT, mm
Aortic PWV, cm/s
Independent variables
Aortic PWV, cm/s
⌬SV, ml
0.406
⬍0.05
0.274
0.392
⬍0.05
0.140
(R2 ⫽ 0.414, P ⬍ 0.01. Excluded were LVWT index, LVM,
and ⌬SV)
Dependent Variable: Changes in SBP with HUT
0.523
⬍0.0001
0.405
0.356
⬍0.05
0.114
(R2 ⫽ 0.519, P ⬍ 0.01. Excluded were body mass, BMI, LVWT,
LVWT index, and LVM)
␤ ⫽ standard regression coefficient.
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more, forward stepwise multiple regression analyses in pooled
subjects indicated that the MAP response to HUT was independently associated with LV wall thickness, whereas the SBP
response to HUT was independently associated with the corresponding change in SV, which itself was modestly associated
with LV wall thickness. LV wall thickening may be accompanied with lower LV chamber compliance and limit a drop of
SV with HUT. Taken together, these results suggest that the
divergent BP responses to HUT are associated with exercise
training-specific morphological adaptations of the heart.
Regular endurance training reduces central arterial stiffness,
whereas regular vigorous resistance exercise training elicits a
stiffening of the central arteries (10, 13). In line with these
previous findings, we observed that resistance-trained individuals have significantly higher aortic PWV compared with
endurance-trained individuals. It should be emphasized that a
forward stepwise multiple regression analysis showed that
aortic PWV was positively associated with both MAP and SBP
responses to HUT, such that greater conduit artery stiffness
was related to a greater BP increase to HUT. These results are
inconsistent with a previous observation made in an elderly
cohort, in which an increase in central arterial stiffness was
suggested to precipitate falls in BP during orthostatic stress.
Although the precise contribution of exercise training-related
adaptations of the central arteries on BP regulation during
1896
Exercise Training, Cardiovascular Adaptation, and Blood Pressure Regulation
GRANTS
This study was supported by the Uehara Memorial Foundation (J. Sugawara) and Mizuno Sports Promotion Foundation (J. Sugawara).
DISCLOSURES
No conflicts of interest, financial or otherwise, are declared by the author(s).
AUTHOR CONTRIBUTIONS
Author contributions: J.S., H.K., and S.O. conception and design of research; J.S., H.K., T.M., T.I., and S.O. performed experiments; J.S., H.K.,
T.M., and T.I. analyzed data; J.S., H.K., T.M., T.I., J.P.F., and S.O. interpreted
results of experiments; J.S. prepared figures; J.S. drafted manuscript; J.S.,
J.P.F., and S.O. edited and revised manuscript; J.S., H.K., T.M., T.I., J.P.F.,
and S.O. approved final version of manuscript.
REFERENCES
1. Cheitlin MD, Armstrong WF, Aurigemma GP, Beller GA, Bierman
FZ, Davis JL, Douglas PS, Faxon DP, Gillam LD, Kimball TR,
Kussmaul WG, Pearlman AS, Philbrick JT, Rakowski H, Thys DM,
Antman EM, Smith SC Jr, Alpert JS, Gregoratos G, Anderson JL,
Hiratzka LF, Hunt SA, Fuster V, Jacobs AK, Gibbons RJ, Russell
RO. ACC/AHA/ASE 2003 guideline update for the clinical application of
echocardiography. Summary article: a report of the American College of
Cardiology/American Heart Association Task Force on Practice Guidelines (ACC/AHA/ASE Committee to Update the 1997 Guidelines for the
Clinical Application of Echocardiography). Circulation 108: 1146 –1162,
2003.
2. Convertino VA. Endurance exercise training: conditions of enhanced
hemodynamic responses and tolerance to LBNP. Med Sci Sports Exerc 25:
705–712, 1993.
3. Devereux RB, Reichek N. Echocardiographic determination of left ventricular mass in man. Anatomic validation of the method. Circulation 55:
613–618, 1977.
Sugawara J et al.
4. Frey MA, Lathers C, Davis J, Fortney S, Charles JB. Cardiovascular
responses to standing: effect of hydration. J Clin Pharmacol 34: 387–393,
1994.
5. Levine BD, Buckey JC, Fritsch JM, Yancy CW Jr, Watenpaugh DE,
Snell PG, Lane LD, Eckberg DL, Blomqvist CG. Physical fitness and
cardiovascular regulation: mechanisms of orthostatic intolerance. J Appl
Physiol 70: 112–122, 1991.
6. Levine BD, Lane LD, Buckey JC, Friedman DB, Blomqvist CG. Left
ventricular pressure-volume and Frank-Starling relations in endurance
athletes. Implications for orthostatic tolerance and exercise performance.
Circulation 84: 1016 –1023, 1991.
7. Lewis JF, Kuo LC, Nelson JG, Limacher MC, Quinones MA. Pulsed
Doppler echocardiographic determination of stroke volume and cardiac
output: clinical validation of two new methods using the apical window.
Circulation 70: 425–431, 1984.
8. Lightfoot JT, Torok DJ, Journell TW, Turner MJ, Claytor RP.
Resistance training increases lower body negative pressure tolerance. Med
Sci Sports Exerc 26: 1003–1011, 1994.
9. Mattace-Raso FU, van der Cammen TJ, Knetsch AM, van den
Meiracker AH, Schalekamp MA, Hofman A, Witteman JC. Arterial
stiffness as the candidate underlying mechanism for postural blood pressure changes and orthostatic hypotension in older adults: the Rotterdam
Study. J Hypertens 24: 339 –344, 2006.
10. Miyachi M, Donato AJ, Yamamoto K, Takahashi K, Gates PE,
Moreau KL, Tanaka H. Greater age-related reductions in central arterial
compliance in resistance-trained men. Hypertension 41: 130 –135, 2003.
11. Nardo CJ, Chambless LE, Light KC, Rosamond WD, Sharrett AR,
Tell GS, Heiss G. Descriptive epidemiology of blood pressure response to
change in body position. The ARIC study. Hypertension 33: 1123–1129,
1999.
12. Ogoh S, Volianitis S, Nissen P, Wray DW, Secher NH, Raven PB.
Carotid baroreflex responsiveness to head-up tilt-induced central hypovolaemia: effect of aerobic fitness. J Physiol 551: 601–608, 2003.
13. Otsuki T, Maeda S, Iernitsu M, Saito Y, Tanimura Y, Ajisaka R,
Miyauchi T. Relationship between arterial stiffness and athletic training
programs in young adult men. Am J Hypertens 20: 967–973, 2007.
14. Pluim BM, Zwinderman AH, van der Laarse A, van der Wall EE. The
athlete’s heart. A meta-analysis of cardiac structure and function. Circulation 101: 336 –344, 2000.
15. Raven PB, Pawelczyk JA. Chronic endurance exercise training: a condition of inadequate blood pressure regulation and reduced tolerance to
LBNP. Med Sci Sports Exerc 25: 713–721, 1993.
16. Rose KM, Holme I, Light KC, Sharrett AR, Tyroler HA, Heiss G.
Association between the blood pressure response to a change in posture
and the 6-year incidence of hypertension: prospective findings from the
ARIC study. J Hum Hypertens 16: 771–777, 2002.
17. Smith ML, Raven PB. Cardiovascular responses to lower body negative
pressure in endurance and static exercise-trained men. Med Sci Sports
Exerc 18: 545–550, 1986.
18. Sugawara J, Hayashi K, Yokoi T, Cortez-Cooper MY, DeVan AE,
Anton MA, Tanaka H. Brachial-ankle pulse wave velocity: an index of
central arterial stiffness? J Hum Hypertens 19: 401–406, 2005.
19. Sugawara J, Tanabe T, Miyachi M, Yamamoto K, Takahashi K,
Iemitsu M, Otsuki T, Homma S, Maeda S, Ajisaka R, Matsuda M.
Noninvasive assessment of cardiac output during exercise in healthy
young humans: comparison between Modelflow method and Doppler
echocardiography method. Acta Physiol Scand 179: 361–366, 2003.
20. Victor RG, Leimbach WN Jr. Effects of lower body negative pressure on
sympathetic discharge to leg muscles in humans. J Appl Physiol 63:
2558 –2562, 1987.
21. Wesseling KH, Jansen JR, Settels JJ, Schreuder JJ. Computation of
aortic flow from pressure in humans using a nonlinear, three-element
model. J Appl Physiol 74: 2566 –2573, 1993.
J Appl Physiol • doi:10.1152/japplphysiol.01460.2011 • www.jappl.org
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different between endurance- and resistance-trained groups.
However, as expected endurance-trained and resistance-trained
groups exhibited distinct cardiovascular morphological adaptations (i.e., increased LV chamber vs. increased LV wall
thickness, lower vs. higher large-conduit arterial PWV) as
previously reported (13, 14), suggesting that the habitual exercise training regimes of our trained individuals were sufficient to test our hypothesis. Third, we measured steady-state
BP responses to the short-term orthostatic stimulation because
such measures could provide useful clinical and pathophysiological information (11, 16). However, it remains unclear if an
individual’s BP response to 5 min HUT is indicative of their
tolerance to prolonged orthostatic stress.
In summary, we investigated the influence of chronic exercise training (e.g., endurance exercise training vs. resistance
exercise training) on the BP responses to the orthostatic stimulation. Our findings suggest that the BP response to HUT
varies as a function of habitual training modality, and that this
is related to exercise training-induced morphological adaptations of the LV and large-conduit arteries.
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