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Adi Pranoto, Purwo Sri Rejeki*, Muhammad Miftahussurur, Hayuris Kinandita Setiawan,
Ghana Firsta Yosika, Misbakhul Munir, Siti Maesaroh, Septyaningrum Putri Purwoto, Cakra Waritsu
and Yoshio Yamaoka
Single 30 min treadmill exercise session
suppresses the production of pro-inflammatory
cytokines and oxidative stress in obese female
adolescents
https://doi.org/10.1515/jbcpp-2022-0196
Received September 4, 2022; accepted January 24, 2023;
published online February 20, 2023
Abstract
Objectives: Regular treadmill exercise may result in
changes in pro-inflammatory cytokines and oxidative stress.
However, the way acute treadmill exercise mechanisms
affect the changes in pro-inflammatory cytokines and
oxidative stress in obese has not been comprehensively
exposed. This study aimed to analyze the pro-inflammatory
cytokines and oxidative stress between 30 min before
treadmill exercise and 24 h after treadmill exercise in obese
adolescents.
Methods: A total of 20 obese females aged 19–24 years were
recruited from female students and given one session of
treadmill exercise with an intensity of 60–70% HR
max
. Thi-
obarbituric acid reactive substance (TBARS) was used to
analyze serum levels of MDA, while enzyme-linked immu-
nosorbent assay (ELISA) was used to analyze serum levels of
TNF-αand IL-6. Moreover, the independent samples t-test
with a significance level of 5% was employed to have the
statistical analysis.
Results: The results on 24 h after treadmill exercise and
delta (Δ) between CTRL and TREG showed a significant dif-
ference (p<0.001).
Conclusions: This study found a decrease in pro-
inflammatory cytokines and oxidative stress 24 h after
treadmill exercise in obese adolescents. Therefore, treadmill
exercise can be a promising strategy for preventing adoles-
cents from obesity as well as preventing disease risks asso-
ciated with oxidative stress and chronic inflammation.
Keywords: IL-6; MDA; obesity; TNF-α; treadmill exercise.
Introduction
The increase in the prevalence of obesity has globally
become a major health problem that must be considered [1].
Over the last 30 years, the prevalence of obesity in adults
worldwide has significantly increased [2]. The increase in
the prevalence of obesity directly corresponds to the in-
crease in life expectancy [3]. This happened because the in-
crease in the prevalence of obesity is the main factor that
contributes to the increase in disability and death [4–6].
Obesity in adults in 2016 has currently grown at an alarming
rate because more than 1.9 billion adults aged 18 years and
older were overweight, of these over 650 million adults were
obese [2]. In both developed and developing countries, the
proportion of adults obese has increased from 28.8% in 1980
to 36.9% in 2013 in males and 29.8–38.0% in females [7]. Adult
obesity is affected by the condition of childhood obesity [8]. A
high percentage of children are overweight or obese and
almost half of the parents classified their weight status
*Corresponding author: Purwo Sri Rejeki, Physiology Division,
Department of Medical Physiology and Biochemistry, Faculty of Medicine,
Universitas Airlangga, Surabaya, Indonesia, Phone: +62 8214 1559 388,
E-mail: purwo-s-r@fk.unair.ac.id
Adi Pranoto, Doctoral Program of Medical Science, Faculty of Medicine,
Universitas Airlangga, Surabaya, Indonesia
Muhammad Miftahussurur, Division of Gastroentero-Hepatology,
Department of Internal Medicine, Faculty of Medicine Universitas
Airlangga –Dr. Soetomo Teaching Hospital –Institute of Tropical Disease,
Surabaya, Indonesia
Hayuris Kinandita Setiawan and Misbakhul Munir, Physiology Division,
Department of Medical Physiology and Biochemistry, Faculty of Medicine,
Universitas Airlangga, Surabaya, Indonesia
Ghana Firsta Yosika, Study Program of Sports Coaching Education, Faculty
of Teacher Training and Education, Universitas Tanjungpura, Pontianak,
Indonesia
Siti Maesaroh, Study Program of Sports Coaching Education, Faculty of
Teacher Training and Education, Universitas Riau, Pekanbaru, Indonesia
Septyaningrum Putri Purwoto, Study Program of Physical Education,
STKIP PGRI Bangkalan, Bangkalan, Indonesia
Cakra Waritsu, Study Program of Physiotherapy, Faculty of Health Science,
Universitas Muhammadiyah Surabaya, Surabaya, Indonesia
Yoshio Yamaoka, Department of Environmental and Preventive Medicine,
Faculty of Medicine, Oita University, Yufu, Japan
J Basic Clin Physiol Pharmacol 2023; 34(2): 235–242
incorrectly [9]. However, most childhood has unhealthy
eating habits, low physical fitness, high sedentary behavior,
and poor sleep standards, leading to obesity [10]. Obesity has
been seen as a primary health burden that can impair hu-
man quality of life since it increases the risk of cardiovas-
cular disease, vascular disease, diabetes mellitus type 2,
cancer, osteoarthritis (OA), liver, and kidney dysfunction
[7, 11–15].
Obesity does not only increase the incidence of meta-
bolic imbalances [15, 16] but also decreases life expectancy
[12] and can affect cellular processes using the same with the
aging process [17]. Besides, the impact of obesity on epige-
netic aging was also reported by Horvath et al. [18] that
obesity can accelerate the epigenetic changes associated
with aging, resulting in an acceleration of 2.7 years older for
every 10 points increase in body mass index (BMI). This
supports the idea that obesity can accelerate aging processes
[19, 20]. The characteristic of aging is the progressive loss of
physiological integrity [21, 22], resulting in increased sus-
ceptibility to disease and death [23–26]. Obesity has also been
associated with an increase in oxidative stress and chronic
inflammation which play a key role in accelerating the aging
processes and is also closely related to the initiation and
progression of various age-related diseases [15, 20, 27, 28].
Exercise has many benefits in alleviating such conditions,
but the effect of exercise on pro-inflammatory parameters
and oxidative stress in obese populations should be further
clarified.
Exercise functions as a stressor during and after exer-
cise and can generate inflammation [29]. However, regular
exercise can be a long-term anti-inflammatory therapy after
the acute inflammatory treatment is resolved [30, 31]. Also,
pro-inflammatory processes that occur after exercise, such
as increased expression of pro-inflammatory cytokines, may
be important for long-term adaptive responses to exercise
[32]. Inflammation is essential to improve processes that
occur, such as those produced during and after exercise [33].
Consequently, the changes in inflammation induced by ex-
ercise can be divided into acute effects (changes during and
immediately after exercise) and long-term effects (changes
in basal level, when the acute effects induced by exercise
have disappeared) [32, 34, 35]. The previous study conducted
by Zheng et al. [20] reported that exercise had a positive
effect on reducing IL-6, and TNF-αlevels in middle-aged and
older adults. However, the study conducted by Andarianto
et al. [36] showed that IL-6 levels increased and TNF-αlevels
decreased immediately after moderate-intensity exercise in
obese female subjects was performed. Several other studies
also reported that obese individuals have greater increases
in oxidative stress and pro-inflammatory parameters after
having acute exercise than those with normal weight [37, 38].
However, other studies showed opposing results [39–41].
Therefore, how pro-inflammatory cytokines and oxidative
stress change after treadmill exercise is still debatable to
date. For this noted background, this study aims to prove the
effects of treadmill exercise on suppressing the production
of pro-inflammatory cytokines and oxidative stress in obese
female adolescents. Understanding these mechanisms can
be an effective strategy for the prevention and physical
therapy for obesity and obesity-related disorders.
Materials and methods
Research subject’s criteria
Twenty subjects aged 19–24 years were rec ruited from female student s
in Malang, East J ava, Indonesia. The inclu sion criteria were individ uals
with a sedentary lifestyle (i.e. individuals who do not exercise >20 min
at least 3x/week based on the subject’s report), BMI of 27.50–33.00 kg/
m2(mean ±SD BMI 30 ±1kg/m
2), blood pressure (BP) (systolic
130 mmHg and diastolic 90 mmHg) (mean ±SD SBP 117 ±8mmHg;DBP
79 ±8 mmHg), resting heart rate (RHR) of 60–80 bpm (mean ±SD RHR
73 ±5 bpm), oxygen saturation (SpO
2
)of97–99% (mean ±SD 98 ±1%).
Subjects enrolled in this study were not actively participating in sports
activities, were not smokers, and were not taking micronutrient sup-
plements. The exclusion criteria were individuals with chronic dis-
eases, such as kidney failure, cancer, liver dysfunction, lung disease,
and diabetes mellitus, individuals currently undergoing a weight loss
program or weight loss surgery, and individuals with a history of
cardiovascular disease as evidenced by the results of medical in-
terviews and physical examinations. All information about the
research has been conveyed to the subject both orally and in writing.
Informed consent was obtained before the students were enrolled as
subjects. All protocols applied in this study have been designed ac-
cording to the 1975 Declaration of Helsinki on the ethics of research
using human subjects.
Anthropometric and body composition measurements
Anthropometric measurements such as height, weight, and BMI using
TANITA (TANITA WB 380 H, TANITA Corporation, Tokyo, JAPAN). Body
composition measurements which include FAT, FM, FFM, and MM used
the TANITA Body Composition Analyzer DC-360 (TANITA Corporation,
Inc., IL 60005, USA).
Physiological parameters measurements
Physiological parameters measurements including BP and RHR were
employed using OMRON Digital Tensimeter (OMRON Model HBP-9030,
JAPAN) on the non-dominant arm three times with a rest interval
between measurements of 1 min. SpO
2
was measured using a Pulse
Oximeter (Beurer PO30 Pulse Oximeter, USA). Meanwhile, body tem-
perature (BT) was evaluated using Omron Digital Thermometer (Omron
Model MC-343F, Osaka, Japan) which was administered orally.
236 Pranoto et al.: Acute exercise decreases oxidative stress and pro-inflammatory markers
Mechanism of treadmill exercise and blood sampling
The treadmill exercise protocol was implemented and supervised by a
personal trainer from Atlas Sports Club Malang, East Java 65,146,
Indonesia. Subjects were grouped into two parts, namely CTRL (n=10;
control group), and TREG (n=10; treadmill exercise group). The treadmill
exercise was performed using an intensity of 60–70% HRmax (calcu-
lated as 220-age) for 30 min. Warming up and cooling down are carried
out for 5 min [42–46]. Treadmill exercise was performed between 8.00–
9.00 a.m [39]. using a treadmill (Richter Treadmill (4.0HP DC), Taipei,
Taiwan, R.O.C) with a slope of 0% [47]. Heart rate monitoring during the
intervention was evaluated using Polar (Polar H10 Sensor, Inc., USA).
The exercise room has a temperature of 26 ±1°C with a humidity level of
50–70% [42, 48–49]. Blood samples were taken 30 min before treadmill
exercise and 24 h after treadmill exercise on the cubital vein each as
much as 4 mL. The before and after treadmill exercise blood samples
were taken after the subject had fasted overnight for 12 h. Blood samples
were centrifuged for 15 min at 3,000 rpm, then the separated serum was
immediately processed for analysis of the levels of MDA, TNF-α, and IL-6.
Oxidative stress and pro-inflammatory parameters
measurements
The oxidative stress parameters were evaluated by examining serum
MDA levels using the TBARs [50, 51]. Pro-inflammatory parameters were
evaluated by examining serum IL-6 levels using commercial ELISA Kits
(Cat.No.:E-EL-H6156; Elabscience Biotechnology Inc., Houston, TX 77079,
USA), while serum TNF-αlevels were evaluated using commercial ELISA
Kits (Cat.No.:E-EL-H0109; Elabscience Biotechnology Inc., Houston, TX
77079, USA). The ELISA Kits accuracy used to evaluate IL-6 and TNF-α
serum levels had been validated by several studies [36, 52].
Statistical analysis
The data in Tables 1, 2 are presented with Mean ±SD. Paired samples
t-test was used to compare the mean of the dependent variable (MDA,
TNF-α, IL-6) between 30 min before treadmill exercise and 24 h after
treadmill exercise. Independent Samples t-Test was used to assess
changes in MDA, TNF-α, and IL-6 levels between TREG and CTRL.
Pearson’s correlation coefficient test was performed to evaluate the
correlation between variables. The p<value of 0.05 was statistically
significant. Analyzed all data using SPSS for Windows version 21 (IBM®
SPSS®Statistics Inc., Chicago, IL, USA).
Results
The basic characteristics such as demographics, anthro-
pometry, and physiology of the population are presented in
Table 1. The participants were randomly divided into two
groups, namely the control group (CTRL) and treadmill ex-
ercise group (TREG).
Based on Table 1, all data on basic characteristics such as
demographics, anthropometry, and physiology are normal
in both groups. The results of the independent samples t-test
on the basic characteristics did not show any significant
difference between the two groups (p>0.05). The results of
the analysis of oxidative stress and pro-inflammatory pa-
rameters are presented in Figure 1.
Based on Figure 1, the results of the statistical analysis
of paired samples t-test blood circulation levels of oxida-
tive stress parameters (MDA) between 30 min before
treadmill exercise and 24 h after treadmill exercise on
the CTRL and the TREG show 879.00 ±148.38 vs.
933.00 ±204.57 ng/mL (p>0.05) and 867.00 ±131.57 vs.
Table :Basic characteristics of the population.
Parameters n CTRL TREG p-Value
Age, years . ±. . ±. N.S.
BW, kg . ±. . ±. N.S.
BH, m . ±. . ±. N.S.
BMI, kg/m . ±. . ±. N.S.
FAT, % . ±. . ±. N.S.
FM, kg . ±. . ±. N.S.
FFM, kg . ±. . ±. N.S.
MM, kg . ±. . ±. N.S.
SBP, mmHg . ±. . ±. N.S.
DBP, mmHg . ±. . ±. N.S.
RHR, bpm . ±. . ±. N.S.
SpO
,% . ±. . ±. N.S.
BT, °C . ±. . ±. N.S.
BH, body height; BMI, body mass index; BT, body temperature; BW, body
weight; DBP, diastolic blood pressure; FM, fat mass; FFM, free fat mass; MM,
muscle mass; RHR, resting heart rate; SBP, systolic blood pressure; SpO
,
oxygen saturation. The data are stated as mean ±SD. The p-value was
determined using the Independent Samples t-Test. N.S., not significant.
Table :Analysis of circulating blood levels of oxidative stress and pro-
inflammatory markers based on the observation points of min before
treadmill exercise, h after treadmill exercise, and delta (Δ) in both
groups.
Parameters Unit n CTRL TREG p-Value
Pre-MDA ng/mL . ±. . ±. N.S
Post-MDA ng/mL . ±. . ±.a<.
ΔMDA ng/mL . ±. −. ±.a<.
Pre-IL-pg/mL . ±. . ±. N.S
Post-IL-pg/mL . ±. . ±.a<.
ΔIL-pg/mL . ±. −. ±.a<.
Pre-TNF-αpg/mL . ±. . ±. N.S
Post-TNF-αpg/mL . ±. . ±.a<.
ΔTNF-αpg/mL . ±. −. ±.a<.
The analysis was determined based on the observation points of min
before treadmill exercise, h after treadmill exercise, and delta (Δ) in both
groups using the independent samples t-test. The data were stated as
mean ±SD. (a) Shows the statistical difference between CTRL and TREG
(p<.). N.S., not significant.
Pranoto et al.: Acute exercise decreases oxidative stress and pro-inflammatory markers 237
597.00 ±56.37 ng/mL (p<0.001), respectively. Paired sam-
ples t-test analysis of pro-inflammatory parameters (IL-6)
between 30 min before treadmill exercise and 24 h after
treadmill exercise on the CTRL and the TREG show
97.10 ±12.26 vs. 98.77 ±29.43 pg/mL (p>0.05) and
104.82 ±18.17 vs. 41.92 ±10.38 pg/mL (p<0.001), respectively.
Paired Samples t-Test analysis of pro-inflammatory pa-
rameters (TNF-α) between 30 min before treadmill exer-
cise and 24 h after treadmill exercise on the CTRL and the
TREG show 184.18 ±12.74 vs. 186.05 ±17.14 pg/mL (p>0.05)
and 185.42 ±13.62 vs. 154.31 ±10.01 pg/mL (p<0.001),
respectively.
Based on Table 2, there are no significant differences in
pro-inflammatory (TNF-α, IL-6) and oxidative stress (MDA)
parameters based on the observation point of 30 min before
treadmill exercise between CTRL and TREG (p>0.05), while
pro-inflammatory parameters (TNF-α, IL-6) and oxidative
stress (MDA) based on 24 h after treadmill exercise obser-
vation points and delta (Δ) between CTRL and TREG show a
significant difference (p<0.001).
The results of Pearson’s product-moment correlation
coefficient analysis presented in Table 3 indicate a strong
positive correlation between pro-inflammatory parameters
(TNF-α, IL-6) and oxidative stress (MDA).
CTRL
0
500
1000
1500 30-min before exercise
24-hr after exercise
MDA (ng/mL)
TREG
0
500
1000
1500 30-min before exercise
24-hr after exercise
*
MDA (ng/mL)
CTRL
0
50
100
150 30-min before exercise
24-hr after exercise
IL-6(pg/mL)
TREG
0
50
100
150 30-min before exercise
24-hr after exercise
*
IL-6 (pg/mL)
CTRL
0
50
100
150
200
250 30-min before exercise
24-hr after exercise
TNF- (pg/mL)
TREG
0
50
100
150
200
250 30-min before exercise
24-hr after exercise
TNF- (pg/mL)
Figure 1: Thirty min before treadmill exercise and 24 h after treadmill exercise circulating blood levels of oxidative stress and pro-inflammatory markers
in the two groups. The statistical analysis was determined 30 min before and 24 h after a single 30 min treadmill-exercise session with an intensity of 60–
70% HR
max
. The data were stated as mean ±SD. (*) shows the statistical difference between 30 min before treadmill exercise and 24 h after treadmill
exercise (p≤0.001).
238 Pranoto et al.: Acute exercise decreases oxidative stress and pro-inflammatory markers
Discussion
This study investigated the effects of treadmill exercise on
suppressing the production of pro-inflammatory cytokines
and oxidative stress in obese female adolescents. Exercise
has been considered a promising approach to minimizing
the negative impact of obesity [53–55]. Recent studies show
that exercise can decrease oxidative stress parameters and
increase antioxidant defense systems in obese individuals
[39, 56, 57], exercise can also reduce levels of inflammation in
obese individuals [36]. This is in line with the main finding of
this study which reported that exercise has a significant ef-
fect on the changes in oxidative stress and pro-inflammatory
parameters. The results of the statistical analysis confirmed
that moderate-intensity exercise significantly reduced
oxidative stress (MDA) and pro-inflammatory parameters
(reduced IL-6, TNF-α) in sedentary obese female adolescents
(Figure 1). Also, the results of the study by Abd El-Kader & Al-
Shreef [58] reported that moderate-intensity aerobic exer-
cise significantly reduced inflammatory parameters, such as
IL-6 and TNF-α. Likewise, the study by Santos et al. [59] re-
ported that moderate-intensity aerobic exercise can modu-
late cytokine profiles (reduce IL-6, TNF-α, and increase
IL-10), and reduce oxidative stress [39]. Sellami et al. [60]
added that moderate-intensity exercise is an appropriate
method for lowering systemic inflammation parameters and
promoting anti-inflammatory processes.
Obesity is often associated with low-grade inflamma-
tion, which may have a role in the development of many
degenerative diseases [61]. Low-grade inflammation may
lead to the release of pro-inflammatory cytokines, which
results in the activation of pathways involved in the increase
in the production of reactive oxygen species (ROS), thereby
increasing oxidative stress conditions [56, 61]. The increase
in chronic inflammation and oxidative stress in obesity have
a central role in accelerating aging processes [62]. Therefore,
it is essential to reduce obesity, one of which is exercise [63].
Exercise can reduce obesity by lowering body fat mass [64,
65]. On the other hand, exercise is also a potential strategy
for reducing oxidative stress and chronic inflammation
[57, 66]. It can be proven in our study that showed a decrease
in oxidative stress and inflammatory parameters 24 h after
treadmill exercise (Table 1). The decrease is caused by the
exercise that can induce metabolic changes in the organism,
which then leads to the activation of adaptive mechanisms to
form a new dynamic balance [67]. One of the most significant
changes in this regard is an increase in antioxidant activity
in skeletal muscle, heart, and liver, and thus, it can inhibit
the production of free radicals and oxidative damage [68].
Besides, exercise can also decrease the production of in-
flammatory parameters in skeletal muscle under the control
of endogenous and exogenous modulators [50].
Exercise is beneficial for the prevention, treatment, and
rehabilitation of several diseases, such as metabolic syn-
drome, cancer, lung and cardiovascular disease [69]. The
increase in the metabolic capacity of muscle tissue also in-
duces an increase in insulin sensitivity, thus explaining the
significant decrease in blood glucose detected in this group
of patients [70]. Sustained hyperglycemia is bad for the body
because it can increase the production of free radicals and
cause low-level inflammation [71]. Reducing blood glucose
levels is very important, especially for health and mental
health [11]. This proves that exercise is beneficial for
improving health-related quality of life [72].
Exercise can increase the activation of anti-inflammatory
responses, which is influenced by an increase in interleukin-
10 (IL-10), interleukin-1 receptor antagonist (IL-1RA), and sol-
uble tumor necrosis factor- receptors (sTNFr) level, thereby
causing a decrease in pro-inflammatory cytokines, such as
IL-6 and TNF-α[73–76]. During such conditions, the inflam-
matory IL-6 will limit the expression of genes encoding pro-
inflammatory cytokines (e.g., TNF-α,IL1β, NOS2) and the
activation of c-Jun N-Terminal Kinase (JNK) to increase
macrophage responsiveness to interleukin-4 (IL-4), thus it will
reduce the level of inflammation [77]. Also, exercise can
decrease the activity of pro-inflammatory macrophage sub-
type 1 (M1) and increase the activity of anti-inflammatory
macrophage subtype 2 (M2) [78]. Therefore, treadmill exercise
can be a non-pharmacological treatment modality to prevent
premature aging in obese individuals through oxidative stress
and inflammation mechanism.
After having provided the above description, this study
shows a special significance that the research was conducted
at the same place and time, with the same subject conditions,
and all blood samples were processed immediately after the
Table :The relationship between oxidative stress and pro-inflammatory
markers.
Parameters Oxidative stress
h after exer-
cise MDA,
ng/mL
ΔMDA, ng/mL
rp-Value rp-Value
Pro-inflammatory markers
h after exercise IL-, pg/mL .a<. ––
h after exercise TNF-α, pg/mL .b<. ––
ΔIL-, pg/mL ––.b<.
ΔTNF-α, pg/mL ––.b<.
aSignificant with p<. by Pearson’s product-moment correlation
coefficient test. bSignificant with p<. by Pearson’s product-moment
correlation coefficient test.
Pranoto et al.: Acute exercise decreases oxidative stress and pro-inflammatory markers 239
blood sampling to obtain optimal analysis results. However,
this study also has limitations, such as the small number of
subjects since the authors found some difficulties in getting
the subjects who are willing to voluntarily give their blood
twice in a row as the samples in a short time. Therefore, the
data interpretation to compare both groups should carefully
be completed. In addition, this study was only conducted on
sedentary obese female adolescents who were, thereby it
needs careful treatment to generalize the conclusion. Future
studies are recommended to compare these results in the
two sexes and different age groups.
Conclusions
By having a thorough analysis, this study established that
a single 30 min treadmill exercise session with an intensity
of 60–70% HRmax suppresses the production of pro-
inflammatory cytokines and oxidative stress in obese fe-
male adolescents. This also shows a strong positive corre-
lation between variables. The findings of this study can be
the basis for further research by providing chronic exer-
cise interventions and adding the identification of new bio
parameters. Therefore, they can be used as an effective
strategy and new therapies in preventing adolescents from
obesity as well as the negative effects of obesity, especially
on chronic inflammation and oxidative stress.
Acknowledgments: We would like to express our gratitude to
the Management of Atlas Sports Club Malang for providing
good facilities for making the process of screening prospective
subjects and conducting research a success. We also thank
Mrs. Eli Ning Khabidah, Amd. Kep, a medical analyst from the
Patimura Clinical Laboratory Malang, for her kind help in the
process of taking blood samples and blood centrifuge as well
as Mrs. Umi Salamah, Amd as stafffrom the Laboratory of
Physiology, Faculty of Medicine, Universitas Brawijaya who
has helped us complete the process of analyzing the MDA,
IL-6, TNF-αserum the levels. Last but not least is all subjects
who have participated in this study.
Research funding: This study is supported by the
Directorate of Research and Community Services, Deputy
for Strengthening Research and Development of the
Ministry of Research and Technology/National Research
and Innovation Agency, Indonesia, under Grand Number:
4/E1/KP.PTNBH/2021 and 292/UN3.15/PT/2021.
Author contributions: All authors have accepted
responsibility for the entire content of this manuscript and
approved its submission.
Competing interests: Authors state no conflict of interest.
Informed consent: Written informed consent was obtained
before the students were enrolled as the subjects.
Ethical approval: This study has been approved by the Health
Research Ethics Committee of the Faculty of Medicine,
Universitas Airlangga, Surabaya, under registered number
192/KEPK/FKUA/2021.
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