Effects of 8-week swimming training on carotid arterial stiffness and hemodynamics in young overweight adults

Abstract

Background
Exercise has been found to either reduce or increase arterial stiffness. Land-based exercise modalities have been documented as effective physical therapies to decrease arterial stiffness. However, these land-based exercise modalities may not be suitable for overweight individuals, in terms of risks of joint injury. The purpose of this study was to determine the effects of 8-week swimming training and 4-week detraining on carotid arterial stiffness and hemodynamics in young overweight adults.

Methods
Twenty young male adults who were overweight were recruited and engaged in 8-week of swimming training and 4-week detraining. Five individuals withdrew due to lack of interest and failure to follow the training protocol. Body Fat Percentage (BFP) and carotid hemodynamic variables were measured on a resting day at the following intervals: baseline, 4 weeks, 8 weeks after swimming training and 4 weeks after detraining. A repeated analysis of variance (ANOVA) was used to assess the differences between baseline and each measurement. When significant differences were detected, Tukey’s test for post hoc comparisons was used.

Results
Eight-week swimming training at moderate intensity decreased BFP, including the trunk and four extremities. Additionally, the BFP of the right and left lower extremities continued to decrease in these overweight adults 4 weeks after ceasing training. Carotid arterial stiffness decreased, while there were no significant changes in arterial diameters. Blood flow velocity, flow rate, maximal and mean wall shear stress increased, while systolic blood pressure and peripheral resistance decreased. No significant differences existed in minimal wall shear stress and oscillatory shear stress.

Conclusions
Eight-week swimming training at moderate intensity exhibited beneficial effects on systolic blood pressure, arterial stiffness and blood supply to the brain in overweight adults. Moreover, maximal and mean wall shear stress increased after training. It is worth noting that these changes in hemodynamics did not last 4 weeks. Therefore, further studies are still warranted to clarify the underlying relationship between improvements in arterial stiffness and alterations in wall shear stress.

Full text

Eects of8‑week swimming training
oncarotid arterial stiness andhemodynamics
inyoung overweight adults
Wen‑Xue Yuan1†, Hai‑Bin Liu1,2†, Feng‑Shan Gao1†, Yan‑Xia Wang3† and Kai‑Rong Qin2*
Background
Arterial stiffness is an independent risk factor of future cardio- and cerebral events
[1]. Common carotid arteries are the main organs that supply blood to the brain. e
changes in structure and function of common carotid arteries are relevant with the
Abstract
Background: Exercise has been found to either reduce or increase arterial stiffness.
Land‑based exercise modalities have been documented as effective physical therapies
to decrease arterial stiffness. However, these land‑based exercise modalities may not be
suitable for overweight individuals, in terms of risks of joint injury. The purpose of this
study was to determine the effects of 8‑week swimming training and 4‑week detrain‑
ing on carotid arterial stiffness and hemodynamics in young overweight adults.
Methods: Twenty young male adults who were overweight were recruited and
engaged in 8‑week of swimming training and 4‑week detraining. Five individuals
withdrew due to lack of interest and failure to follow the training protocol. Body Fat
Percentage (BFP) and carotid hemodynamic variables were measured on a resting
day at the following intervals: baseline, 4 weeks, 8 weeks after swimming training and
4 weeks after detraining. A repeated analysis of variance (ANOVA) was used to assess
the differences between baseline and each measurement. When significant differences
were detected, Tukey’s test for post hoc comparisons was used.
Results: Eight‑week swimming training at moderate intensity decreased BFP, includ‑
ing the trunk and four extremities. Additionally, the BFP of the right and left lower
extremities continued to decrease in these overweight adults 4 weeks after ceasing
training. Carotid arterial stiffness decreased, while there were no significant changes in
arterial diameters. Blood flow velocity, flow rate, maximal and mean wall shear stress
increased, while systolic blood pressure and peripheral resistance decreased. No signifi‑
cant differences existed in minimal wall shear stress and oscillatory shear stress.
Conclusions: Eight‑week swimming training at moderate intensity exhibited benefi‑
cial effects on systolic blood pressure, arterial stiffness and blood supply to the brain in
overweight adults. Moreover, maximal and mean wall shear stress increased after train‑
ing. It is worth noting that these changes in hemodynamics did not last 4 weeks. There‑
fore, further studies are still warranted to clarify the underlying relationship between
improvements in arterial stiffness and alterations in wall shear stress.
Keywords: Swimming training, Overweight adults, Arterial stiffness, Hemodynamics
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RESEARCH
Yuan et al. BioMed Eng OnLine 2016, 15(Suppl 2):151
DOI 10.1186/s12938‑016‑0274‑y
BioMedical Engineering
OnLine
*Correspondence:
krqin@dlut.edu.cn
†Wen‑Xue Yuan, Hai‑Bin Liu,
Feng‑Shan Gao and Yan‑Xia
Wang contributed equally to
this work
2 Department of Biomedical
Engineering, Faculty
of Electronic Information
and Electrical Engineering,
Dalian University
of Technology, Linggong
Road, Dalian, China
Full list of author information
is available at the end of the
article
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occurrence and development of atherosclerosis, coronary ischemia and stroke [2]. Local
hemodynamics plays an important role in mediating arterial stiffness [3]. erefore,
reducing arterial stiffness via hemodynamic modulation is crucial to the prevention and
treatment of cardiovascular disease.
Overweight and obesity are severe public health problems that are common in popula-
tions lacking exercises, combined with a hyper caloric intake. Research conducted post-
mortem on overweight or obesity suggests that overweight adults usually have severe
coronary atherosclerosis, concentric left ventricular hypertrophy, pulmonary embolism,
hypoplastic coronary arteries and dilated cardiomyopathies [4]. e metabolic require-
ments of overweight induce the hemodynamic changes in stroke volume, cardiac output,
systolic and diastolic blood pressure as well as alterations in the hypertrophy of smooth
muscle arterial walls [5]. Consequently, these changes may accelerate the process of arte-
rial stiffening [6].
Exercise, depending on its modality, has been found to either reduce or increase arte-
rial stiffness [7–12]. Land-based exercise modalities [12], such as walking, running and
cycling have been documented as effective physical therapies to decrease arterial stiff-
ness. Unfortunately, these land-based exercise modalities may not be suitable for over-
weight individuals, in terms of risks of joint injury. Swimming, however, with minimum
weight-bearing stress, a humid environment, and a decreased heat load has become an
attractive form of exercise and is always recommended for health promotion, and the
prevention and treatment of risk factors for cardio-vascular disease [13–16]. Nualnim
etal. [16] demonstrated that habitual swimming exercise is an effective endurance exer-
cise for decreasing central arterial stiffness over the age of 50years. In contrast, Walther
etal. [17] suggested that swimmers are more likely to increased arterial stiffness than
cyclists. erefore, additional investigations on the effects of swimming training on arte-
rial stiffness in overweight or obese individuals are needed.
A number of investigations [18, 19] have shown that hemodynamic variables includ-
ing blood pressure, blood-flow-induced wall shear stress (WSS), and oscillatory shear
index (OSI) play vital roles in modulating arterial stiffness. Exercise can directly alter
systemic and local hemodynamic variables [7]. Vascular endothelial and smooth muscle
cells in the blood vessels may sense these hemodynamic responses, resulting in cellu-
lar responses, such as changes in cell morphology, cell function, and gene expression,
which are more relevant with changes in arterial stiffness [20]. To date, most studies
[9, 21] have focused on the effects of acute exercise on arterial stiffness and hemody-
namics, without full consideration of the alteration in hemodynamic responses to long
term exercise. Lawrence [4] manifested hemodynamic changes (heart rate, systolic and
diastolic blood pressure) in overweight and obese individuals, following 8 weeks of
home-based calisthenics training. Recently, Shaw [22] reported the effects of 8weeks
concurrent resistance and aerobic training on hemodynamics (resting heart rate, sys-
tolic, diastolic and mean blood pressure) in overweight and obese populations. Despite
substantial progress, relatively little information is available concerning the effects of
swimming training on arterial stiffness and hemodynamics (blood pressure, peripheral
resistance, wall shear stress, and oscillatory shear index) in overweight individuals.
e purpose of this study was to explore the effects of swimming training on carotid
arterial stiffness and hemodynamics in overweight adults. e study used 8 weeks of
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supervised swimming training and a further 4weeks of ceased training to assess the out-
comes of training and detraining.
Methods
Subjects
Twenty male volunteers, aged from 19 to 21, were recruited from the surrounding dis-
tricts of the university in this study. e subjects had no history of cardiovascular disease
or any other medical disorder were overweight (body mass index (BMI), 30±3kgm−2)
and were not involved in any regular, planned exercise program [23] during the past
3months. Subjects were required to have swimming skills including crawl, breaststroke
or both. None of the subjects had taken cardiovascular or blood pressure medicines.
During the swimming intervention, three individuals withdrew, due to lack of interest
in the study. A further two individuals withdrew from the detraining, due to not ceas-
ing swimming activity. e present study was approved by the Ethics Committee, Dalian
University of Technology, China. All subjects provided written informed consent before
inclusion.
Experimental design
Subjects visited the lab four times during the supervised swimming training (Fig.1), and
each subject’s visit was performed at the same time. At the intervals of baseline, 4 and
8weeks after swimming training and 4weeks of detraining, body fat percentage and
hemodynamics were measured on a resting day.
Swimming training protocol
Swimming training was organized at an indoor swimming pool with mean water tem-
perature of 25.5°C. Subjects completed supervised training three times per week for
8weeks. Each training session consisted of 5min stretching on land, a 5min kicking
exercise in the water, 30min swimming, a 10 min cool down, and 5 min stretching.
Swimming, including front crawl and breaststroke, was performed as interval training
with rest times declining, as fitness improved. In the first 2weeks, subjects swimming,
exercised at 50% maximal heart rate (HRmax), and exercised at 65–80% HRmax intensity
from 3weeks to 8weeks. HR was accessed by heart rate monitor (Geonaute 8360801,
France).
Fig. 1 Protocol of swimming training and study methodology
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Body fat percentage andhemodynamics measurement
Body fat percentage (BFP) measurement
Body fat percentage was measured by bioelectrical impedance (model TBF-418B, Tanita
Corp, Japan). Subjects wore light clothing and no shoes. During the measurements, the
subjects stood erect with feet shoulder-width apart.
Hemodynamics measurement
e inner arterial diameters and blood flow velocity waveforms measurements were
examined using a high-resolution Doppler ultrasound (ProSound Alpha 7, Aloka). e
heart rate, brachial systolic pressure (ps_mea), and diastolic pressure (pd_mea) were simul-
taneously assessed on the left upper arm with a cuff-type manometer (Patient Monitor
PM8000, Mindray) and repeated in triplicate, and the average of the three values was
calculated.
Calculation ofhemodynamic variables
Blood pressure (BP)
In this study, the mean value of the carotid arterial pressure pm and diastolic pressure pd
were assumed to be equal to the mean value of the brachial pressure pm_mea and diastolic
pressure pd_mea, as performed in a previous investigation [10]. e mean arterial pres-
sure (pm) was calculated using the following equation:
erefore, the carotid artery blood pressure waveform was calibrated using the brachial
mean arterial pm_mea and diastolic pressure pd_mea. e maximal value of the carotid arte-
rial pressure waveform was then calculated and assumed to be the systolic pressure ps.
Flow rate (FR)
e FR was computed as
where R0 is the time-averaged value of the carotid artery radius in one cardiac cycle,
y=r/R0 in which r is the radial coordinate, and u(y) satisfies [24]
where n is the harmonic number, J0 is the 0th-order Bessel function of the first kind,
and
j=√−1
,
α
n
=
R0

ρωn
η
is the Womersley number. ρ is the density of blood, η
is blood viscosity. η and ρ, in the present study, were taken as the same values for all
subjects, i.e., η=0.004Pa·s and ρ=1050kg/m3, respectively. ωn=2nπf is the angu-
lar frequency, and f is the base frequency. u(0, ωn) is the n harmonic component of the
measured center-line velocities. e maximal harmonic number n was computed as 20
and satisfies
(1)
pm
=
pm_mea
=
pd_mea
+1
3
ps_mea
−
pd_mea

(2)
Q=
2πR2
0
1
0
y
·
u(y)
·
dy
,
(3)
u
(y,t)=
+∞

n=−∞
J0(αnj
3
2)−J0(αnj
3
2y)
J0
(α
nj
3
2)
−1
u(0, ωn)ejωnt
,
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Vmax, Vmin, and Vmean are the maximal, minimal, and mean center-line velocities, after
one cardiac cycle. Qmax, Qmin, and Qmean are the maximal, minimal, and mean blood flow
FR, after one cardiac cycle.
β‑stiness index (β)
β was calculated as a means of adjusting arterial compliance for changes in distending
pressure as follows [8]:
Peripheral resistance (RP)
Wall shear stress (WSS)
e blood flowing along the vascular vessel creates a tangential friction force, known as
wall shear stress (τw), and was computed as [24]:
where J1 is the first-order Bessel function of the first kind. τw_max, τw_min, and τw_mean refer
to the maximal, minimal, and mean shear stress waveforms, after a cardiac cycle.
Oscillatory shear index (OSI)
e OSI is an index that describes the shear stress acting in directions other than the
direction of the temporal mean shear stress vector and was defined by Ku etal. [25] as
where, T is the period of one cardiac cycle.
Statistical analysis
For data management and analysis, SPSS 20.0 software (SPSS Inc., Chicago, IL, USA)
was used. All values were presented as the mean±SD. e repeated ANOVA was used
to assess differences between baseline and each measurement. When significant differ-
ences were detected, Tukey’s test was used for post hoc comparisons. e significance
level was set at P=0.05.
(4)
u
(0, t)=
+∞

n=−∞
u(0, ωn)ejωnt
.
(5)
β=
ln

ps

pd

Rs−Rd
·
Rd
.
(6)
R
p
=
pmean
Qmean
(7)
τ
w=η
R0
+∞

n=−∞
αnj
3
2J1(αnj
3
2)
J0(αnj
3
2
)−1
u(0, ωn)ejωnt
,
(8)
OSI =
1
2


1−


T
0τwdt




T
0
|
τw
|
dt


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Results
Eects onbody fat percentage
e changes in body fat percentage of subjects during 8-week training and 4-week
detraining are presented in Table1. ere were significant differences between baseline
and after 8-week training in the fat percentages of the whole body, trunk, left UE, left
LE, right UE, and right LE. Compared with baseline, after 4weeks detraining, there were
significant differences in the fat percentages of the left LE, and right LE.
Eects onarterial stiness anddiameters
Figure2 shows the changes in arterial stiffness and diameters before and after swim-
ming training. Compared to baseline, carotid arterial stiffness was significantly lower at
8weeks after training. ere were no significant differences in mean arterial diameters
between baseline, post training and detraining.
Eects onblood ow velocity andblood ow rate tobrain
Figure3a, b and c illustrate that maximal, mean center line velocities were significantly
increased after 8-week swimming training. Figure3d, e and f display, compared with
baseline, the maximal, mean and minimal flow rates, which were significantly increased
after 8-week swimming training.
Table 1 Eects ofswimming training onthe body fat percentage
UE upper extremity, LE lower extremity, Unit: %
*Signicant dierence from baseline: P<0.05
Fat percentage Pretraining Swimming training Detraining
Baseline 4weeks 8weeks 12weeks
Whole body 28.6 ± 5.7 27.3 ± 6.1 25.4 ± 5.6* 25.8 ± 6.1
Trunk 29.8 ± 5.8 28.8 ± 5.6 26.1 ± 6.0* 27.1 ± 5.2
Left UE 25.9 ± 6.4 24.6 ± 6.2 23.9 ± 5.1* 24.6 ± 6.3
Left LE 27.8 ± 6.1 27.2 ± 5.9 25.2 ± 6.1* 25.5 ± 5.8*
Right UE 25.3 ± 6.2 24.8 ± 5.6 23.2 ± 5.0* 23.9 ± 6.0
Right LE 27.9 ± 6.2 27.3 ± 5.7 25.1 ± 6.2* 26.1 ± 5.8*
Fig. 2 Effects on arterial stiffness and mean arterial diameters. a Arterial stifness (β). b Mean arterial diam‑
eters (Dmean)
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Eects onblood pressure, peripheral resistance, wall shear stress andOSI
Figure4 shows that compared with baseline, both systolic blood pressure and peripheral
resistance decreased after 8-week swimming training. Figure5 illustrates that maximal
and mean wall shear stress increased after 8-week training, while no significant differ-
ence existed in oscillatory shear stress.
Discussion
Swimming is always recommended for overweight individuals to improve cardiovascu-
lar function [13–16]. However, research on the effects of swimming exercise on arterial
stiffness are extremely limited and controversial [16, 17]. Additionally, the hemody-
namic variables, induced by exercise, play vital roles in modulating arterial stiffness
Fig. 3 Effects on blood flow to brain. a Maximal center‑line velocity (vmax). b Mean center‑line velocity (vmean).
c Minimal center‑line velocity (vmin). d Maximal flow rate ( Qmax). e Mean flow rate ( Qmean). f Minimal flow
rate (Qmin)
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Fig. 4 Effects on blood pressure and peripheral resistance. a Systolic blood pressure (Ps). b Mean blood pres‑
sure (Pm). c Diastolic blood pressure (Pd). d Peripheral resistance (Rp)
Fig. 5 Effects on wall shear stress (WSS) and OSI. a Maximal wall shear stress (τw−max). b Mean wall shear
stress (τw−mean). c Minimal wall shear stress (τw−min). d Oscillatory shear index (OSI)
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[3, 18, 19]. Some studies have reported the effects of home-based training on hemody-
namic changes in overweight individuals [4, 22]. To date, little information is available
concerning the effects of swimming training on arterial stiffness and hemodynamics
in overweight individuals. e purpose of this study was to detect the effects of swim-
ming training on carotid arterial stiffness and hemodynamics in overweight adults. e
main results of 8weeks of moderate intensity swimming training can be summarized
as follows: (1) Carotid arterial stiffness was decreased while arterial diameters were not
changed. (2) Blood supply to the brain via carotid arteries was improved. (3) All hemo-
dynamic variables, including blood pressure, peripheral resistance, wall shear stress and
OSI in this study were significantly changed but returned to baseline levels by 4weeks
after detraining.
e decreases in body fat percentage with swimming have important implications for
overweight individuals in this study. Previous studies [26] have suggested that water-
based exercise may be less effective than land-based modalities, such as walking or run-
ning, because of different effects on energy balance and weight loss mechanisms. e
findings in this paper indicate that 8weeks of swimming training, at moderate intensity,
reduced whole body fat percentage and had a continuous effect on the lower extremities.
Swimming training is perceived as an excellent form of exercise, especially for the
overweight who suffers from increased risk of cardiovascular disease, because swimming
involves minimum weight-bearing stress [13]. However, research on the effects of swim-
ming exercise, on cardiovascular health profile is extremely limited. e results in this
paper demonstrated that 8weeks of swimming training at moderate intensity can sig-
nificantly increase blood velocity and flow rate, and decrease systolic BP and peripheral
resistance. Tanaka etal. [27] presented the results of 10weeks of a swimming program,
demonstrating a decrease in systolic and diastolic blood pressure. Recently, Alkatan’s
group [13] reported that systolic BP was reduced after both 12weeks of swimming and
cycling training. e results in this study confirm, and extend the above findings by
demonstrating that 8weeks of swimming training at moderate intensity decreased sys-
tolic BP, instead of mean and diastolic BP.
Several cross-sectional and longitudinal studies have indicated that exercise train-
ing is correlated with enlargement of the large arteries (aorta, carotid and femoral
artery) in humans. Endurance-trained athletes were reported to possess larger arteries
than control individuals [10, 28, 29]. Additionally, the resting femoral artery diameter
was enhanced after walking training in sedentary men [30]. No significant increase in
carotid arterial diameter was detected in this study. Conversely, it is well-documented
that regular land-based exercise training, such as running and cycling, can reduce arte-
rial stiffness [12], even if the changes in arterial stiffness are obtained after 1week of
aerobic running exercise [31]. e arterial stiffness in this study decreased significantly
after 8weeks of swimming training. is finding is consistent with the notion [15] that
regular swimming exercise plays an important role in preventing arterial stiffening. e
above-mentioned contrary conclusions [15–17] may be drawn from different subjects,
exercise intensity, or different intervention protocols.
One potential explanation for the vascular adaptations to exercise training relates to
shear stress [32]. Endothelial cells (ECs) along blood vessels can sense variations of WSS
and contribute to the endothelial production of vasoactive mediators, such as nitric
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oxide, which can cause changes in arterial function and structure [20]. It is well estab-
lished that low wall shear stress (WSS) may be involved in the early stages of the athero-
sclerotic process [33, 34]. Gnasso etal. [35] proposed that WSS in the common carotid
artery is inversely associated with intima-media thickness, age, systolic BP and BMI in
healthy male subjects. More recent investigations [36, 37] suggested that the mean WSS
significantly decreases in both sexes with age, while peak WSS decreases significantly
only in men. Despite the fact that hemodynamic shear stress is a major determinant of
vessel diameter and vascular remodeling [18, 19], little information is available regarding
the influence of regular swimming on WSS. e results in this study suggest that maxi-
mal and mean WSS significantly increased after 8weeks of swimming training. Accord-
ing to the formula [24], WSS is determined by flow velocity and whole blood viscosity and
is inversely related to vessel diameter [33]. e data in this study are limited by the fact
that blood viscosity was at the same value for all subjects. e changes in arterial struc-
ture and function may relate to the impact of swimming training on blood flow and shear
stress patterns. erefore, the impact of increases in maximal and mean WSS at carotid
artery, in relation to the changes in structure and function, remain to be established.
e investigations of home-based training on the hemodynamic variables in over-
weight and obese populations are limited only to heart rate, and systolic and diastolic
blood pressure [4, 22]. In this study, hemodynamics, including blood pressure, periph-
eral resistance, wall shear stress, and oscillatory shear index were measured and com-
puted to examine the effects of swimming training on carotid arterial stiffness and
hemodynamics. is study not only presents hemodynamic information for identifying
an effective form of exercise for improving arterial stiffness but also serves as a basis for
a further understanding of the hemodynamic mechanisms underlying the modulation of
arterial stiffness via exercise training.
Conclusions
In this study, 8-week swimming training at moderate intensity exhibited beneficial
effects on systolic blood pressure, arterial stiffness and blood supply to the brain in
overweight adults. Additionally, maximal and mean WSS were increased after 8weeks
training. It is worth noting that these changes in hemodynamics did not last 4weeks.
erefore, further studies are still needed to clarify the underlying relationship between
improvements in arterial stiffness and alterations in WSS.
Declarations
Authors’ contributions
Yuan and Qin designed the study. Liu and Gao conducted the supervised swimming training. Wang collected the
experimental data. Liu and Qin wrote the manuscript. All authors read and approved the final manuscript.
Authors’ information
Qin’s group has been researching the regulation of arterial function via exercise intervention and associated hemody‑
namic mechanisms see website:
Homepage:http://gs1.dlut.edu.cn/Supervisor/qinkr.page
Author details
1 Department of Physical Education, Dalian University of Technology, Linggong Road, Dalian, China. 2 Department
of Biomedical Engineering, Faculty of Electronic Information and Electrical Engineering, Dalian University of Technology,
Linggong Road, Dalian, China. 3 Department of Engineering Mechanics, Dalian University of Technology, Linggong Road,
Dalian, China.
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Acknowledgements
The research described in this report was supported in part by the National Natural Science Foundation of China (Grant
No. 31370948), the Fundamental Research Funds for the Central Universities in China (Grant No. DUT15QY12).
Competing interests
The authors declare that they have no competing interests.
About this supplement
This article has been published as part of BioMedical Engineering OnLine Volume 15 Supplement 2, 2016. Compu‑
tational and experimental methods for biological research: cardiovascular diseases and beyond. The full contents of
the supplement are available online http://biomedical‑engineering‑online.biomedcentral.com/articles/supplements/
volume‑15‑supplement‑2.
Ethics approval and consent to participate
The present study was approved by the Ethics Committee, Dalian University of Technology, China. The subject provided
written informed consent before measurement.
Funding
Publication of this article was paid for with funding from the Fundamental Research Funds for the Central Universities in
China, Grant No. DUT15QY12.
Published: 28 December 2016
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