Key words
aerobic exercise - pulse wave velocity - arterial stiffness - smoking
BP blood pressure
SBP systolic blood pressure
DBP diastolic blood pressure
baPWV brachial – ankle pulse wave velocity
HR heart rate,
MAP mean arterial pressure
CI confidence interval
TG Triglyceride
FBG fasting blood glucose
VO2max maximum oxygen consumption
CV coefficients of variation
Introduction
Arterial stiffness is not only a sign of vascular aging, but is also an independent
risk factor for cardiovascular diseases, renal failure, cognitive dysfunction, and
all-cause mortality [1]
[2]
[3]
[4].
Observational and longitudinal cohort studies have shown that age and blood pressure
(BP) are the main risk factors for arterial stiffness [5]
[6]. However, traditional risk factors,
such as diabetes, smoking, and chronic inflammation, are also risk factors for
arterial stiffness [7]
[8]
[9]. Arterial stiffness is significantly
increased after smoking compared with before smoking in healthy young people [10]. Additionally, Tomiyama et al. (2010) found that
the progression of arterial stiffness was significantly faster in smokers than in
non-smokers of the same age [11].
In 2010, the American Heart Association suggested that an ideal healthy lifestyle,
such as being a non-smoker, moderate exercise, and a healthy diet, can reduce the
risk of cardiovascular disease and all-cause mortality [12]. In particular, long-term regular aerobic exercise is an effective
lifestyle intervention that reduces the damage to blood vessels caused by risk
factors, such as smoking, hypertension, and diabetes [13]
[14]
[15].
However, the results of research on the immediate effect of acute bout of aerobic
exercise on arterial stiffness in individuals with different smoking statuses are
inconsistent [16]
[17].
Doonan et al. (2011) studied 24 smokers and found that arterial stiffness increased
immediately after aerobic exercise [16]. A study of 50
healthy non-smokers showed that arterial stiffness decreased immediately after
aerobic exercise [17]. These studies were small-sample
studies on a Caucasian population.
To the best of our knowledge, few studies have investigated and compared the effect
of acute aerobic exercise-induced changes on arterial stiffness in Asian men with
different smoking statuses. Therefore, we used data from the Kailuan Study to
evaluate short-term changes in arterial stiffness following an acute aerobic
exercise test in men with different smoking statuses.
Materials and Methods
Study design and participants
The data of this study were derived from the subjects in the Kailuan Study
population who were selected to participate in the fifth National Fitness
Monitoring. The Kailuan Study began in 2006 and participants were followed up
every 2 years thereafter in 2008–2009, 2010–2011,
2012–2013, 2014–2015, 2016–2017, and 2018–2019
[18]
[19]. To
systematically assess the nationwide physical fitness of individuals, the State
Sports General Administration initiated the fifth National Physique Monitoring
in 2020. In addition to the general population, special monitoring also had been
carried out on the public security, finance, construction and coal industries of
typical workers [20].
All the participants in this study are workers engaged in the coal industry.
According to the Labor Law, few female employees were underground coal miners or
workers in dangerous occupation [21]. Therefore,
1,200 male coal miners aged 20–49 years were selected by random methods
as subjects of the fifth National Physique Monitoring, using the employee
information database reported and established by the four affiliated companies
of the Kailuan Group. All participants were asked to perform these tests,
including body morphology, physical function, and physical fitness. We also
measured brachial–ankle pulse wave velocity (baPWV) before and
immediately after acute aerobic exercise.
This study was performed in accordance with the Declaration of Helsinki and was
approved by the Ethics Committee of the Kailuan General Hospital. All
participants provided written informed consent.
Inclusion and exclusion criteria
In this study, a total of 1,200 employees of the Kailuan Group participated in
the fifth National Physique Monitoring, of whom 1,138 participated in the
2018–2019 follow-up of the Kailuan Study. Those who did not have baPWV
measured twice before and after exercise (n=185) and those without a
twice-quantitative cycle ergometer exercise (n=13) were excluded.
Finally, 940 individuals were included for analysis ([Fig. 1]).
Fig. 1 Inclusion/exclusion flowchart for study participants.
Caption: The flowchart of 940 participants included in the final
analyses.
Exercise protocol
The procedure of performing cycling exercises complies with the Exercise
Standards for Testing and Training released by the American Heart Association
(AHA) and is briefly described below [22]. All
participants and measurements were performed in a quiet, temperature-controlled
room (22°C–25°C). Before cycling exercise, the
participants had avoided alcohol, tobacco, ingest caffeine or perform vigorous
activities within 12 hours. After a preliminary period of
15 minutes of supine rest, pre-exercise measurements of baPWV were made
in the supine position. Cycling exercise was then performed with individually
tailored ramp protocols via upright cycle ergometry (GMCS-GLC3, Beijing, China).
Following a brief warm-up by cycling against unloaded exercise (0 watts) for
30 seconds, according to individual’s fitness conditions,
participants started to cycle at a moderate intensity (50 watts–80
watts) for 3 minutes so that the heart rate reached 60%
~ 80% of their estimated maximum heart (calculated as 220 minus
age in years), and the resistance was increased by 25watts in next
3 minutes. Throughout the exercise, participants were instructed to
maintain a pedaling cadence of 60 revolutions per minute (rpm). The cycling
exercise finished with 30 seconds of unloaded (0 watts). HR was
monitored and recorded continuously. Maximum oxygen consumption (VO2max) was
indirectly estimated based on the cycling exercise and calculated by the
ergometry according to a previously described equation [23].
BaPWV measurement
All participants underwent baPWV measurement after 12 h abstinence from
smoking and fasting. We used the BP-203 RPE III networked arterial stiffness
detection device (Omron Health Medical [China] Co., Ltd.) automation to measure
baPWV. We used the BP-203 RPE III networked arterial stiffness detection device
(Omron Health Medical [China] Co., Ltd.) automation to measure baPWV. BaPWV is
determined by measuring the pulse waves of the brachial artery and ankle, and
dividing the distance between the upper arm and ankle (DAB), which is calculated
using linear regression of body height, by the time difference between the two
pulses (TAB) [24]. Briefly, the calculation
formula is expressed as baPWV=DAB/TAB. BaPWV was recorded before
and immediately (or as soon as possible) after cycling exercise, which
simultaneously records BP, HR following standard operation procedures [25]. For the first measurement, participants in
light clothes had not been smoking and were seated for at least
15 minutes in a room with the temperature controlled between
22°C and 25°C. The participants were asked to lie down on an
examination couch in the supine position and remain quiet during the
measurement. Cuffs were wrapped on both arms and ankles. The lower edges of the
arm cuffs were positioned 2–3 cm above the transverse striation
of the cubital fossa, while the lower edges of the ankle cuffs were positioned
1–2 cm above the superior aspect of the medial malleolus. One
heart sound detector was placed at the left and right edges of the sternum.
Measurements were repeated twice for each subject, and the result of the second
time was used as the final result.
The maximum of the left and right sides of baPWV was used for analysis.
Smoking status
The smoking status of the subjects (i. e., non-smokers, former smokers,
and current smokers) was assessed with a questionnaire. We ensured the accuracy
of smoking information through a telephone follow-up survey. Non-smokers were
defined as having no history of smoking, former smokers [26] as not smoking for at least 6 months, and current smokers [27] as any who had smoked at least one cigarette
per day for 1 year. Additionally, to calculate pack-years in current smokers,
data on the average number of cigarettes smoked per day and the years of
cigarette smoking were collected. Pack-years of smoking were defined as the
average number of packs of cigarettes smoked per day multiplied by the duration
of smoking in years [28]. On the basis of the
number of cigarettes smoked per day, current smokers were classified into the
two following groups: light smokers (1–10 cigarettes/day) and
heavy smokers (>10 cigarettes/day) [29]. To further confirm our findings, we divided the smokers into
light smokers (≤4 pack-years) and heavy smokers (>4 pack-years)
in accordance with the pack-years as described in Celermajer et al.’s
(1993) [30] study as well.
Data collection
Information on demographic data and lifestyle factors (e. g., age, sex,
alcohol consumption) and medical history (e. g., diabetes, hypertension)
were collected using a self-reported questionnaire. Anthropometric indicators,
including height, weight were derived from the fifth National Physique
Monitoring data. BMI was calculated as weight (kg) divided by height squared
(m2). The physical exercise was defined as taking
exercise≥3 times/week with at least 30 mins each time
[31]. All participants underwent blood tests
after 12 h fasting at each physical examination. The blood samples were
analyzed using an auto-analyzer (Hitachi 747, Hitachi, Tokyo, Japan) on the day
of the blood draw. The biochemical indicators tested included fasting blood
glucose (FBG), triglycerides (TG) levels. Hypertension was defined as (i)
systolic blood pressure (SBP)≥140 mmHg or diastolic blood
pressure (DBP)≥90 mmHg, or (ii) formerly diagnosed hypertension
or using antihypertensive drugs [32]. Diabetes was
defined as either a fasting blood glucose (FBG)
level≥7.0 mmol/L, self-reporting of a
physician’s diagnosis, or self-reported use of antidiabetic medication
[33].
Statistical analysis
Continuous variables that conformed to a normal distribution are presented as the
mean±standard deviation (x̅
±s). Data with a
non-normal distribution are expressed as the median (interquartile range).
Categorical variables are expressed as the number of samples (percentage).
Demographic factors and hemodynamic parameters were compared between the groups
using the one-way analysis of variance or the Wilcoxon rank sum test, as
appropriate. Categorical variables were assessed using the χ2
test for independence. The paired-sample t test was used to compare baPWV, HR,
and BP values in each group post-exercise and pre-exercise.
Linear regression models were established to evaluate group changes in baPWV, HR
and BP post-exercise and pre-exercise. In the linear regression models, we
adjusted for age (continuous variable), the pre-exercise value of BMI
(continuous variable), and TG level (continuous variable), education level
(categorical variable), alcohol consumption (categorical variable), physical
activity (categorical variable) and the timing of post-exercise measurements
(continuous variable).
Generalized linear models were used to analyze differences in the change in baPWV
between the groups. In generalized linear models, we adjusted for age and the
pre-exercise values of baPWV in model 1. In model 2, we further adjusted for the
pre-exercise values of BMI, HR, MAP, and TG level, the timing of post-exercise
measurements, education level, alcohol consumption, physical activity. In model
3, we further adjusted for the change in MAP and HR. Between-group differences
are described by β-value and 95% confidence interval (CI).
Stratified analyses were performed based on the different physical activity
levels among participants. To test the robustness of our findings, the following
sensitivity analyses were performed: 1) We repeated the above-mentioned
generalized linear model for sensitivity analysis of smokers classified by
pack-years. 2) We excluded participants with diabetes mellitus, which is
associated with a high baPWV and is a potential risk factor for arterial
stiffness. 3) We also excluded participants with hypertension, which is
associated with a high baPWV and is a potential risk factor for arterial
stiffness. 4) To reduce the effect of the timing of post-exercise measurements,
we also conducted another sensitivity analysis by excluding participants with
the timing of post-exercise measurements exceeding 95%
percent (26.7 minutes).
A P value<0.05 was considered statistically significant with a
two-sided test. SAS 9.4 (Version 9.4; SAS Institute, Cary, NC) was used for data
analysis.
Results
Baseline characteristics of the study population
The study population had a mean age of 36.82±7.76 years ([Table 1]). On the basis of smoking status, the
study population was divided into non-smokers (n=231), former smokers
(n=165), light smokers (n=254), and heavy smokers
(n=290). Participants with heavy smoke had higher pre-exercise SBP,
pre-exercise DBP, pre-exercise MAP, pre-exercise baPWV, TG level, and rate of
alcohol consumption, lower education level than those in the other three groups
(all P<0.05). The heavy smoker group had higher rate of taking
exercise than those in the other three groups, but there were no statistical
difference among groups (P=0.64). After the cycling exercise,
baPWV of all participants significantly decreased
(1375.08±209.09 cm/s vs.
1341.53±208.04 cm/s, P<0.05), and their
HR increased (80.24±12.54 bpm vs. 85.73±13.56 bpm,
P<0.05). There were no significant changes in SBP, DBP, or
MAP before and after exercise ([Table 1]).
Table 1 Baseline participant
characteristics.
|
All n=940
|
Never n=231
|
Former n=165
|
Light Smoker n=254
|
Heavy Smoker n=290
|
P
|
|
Demographic factors
|
|
Age (year)
|
36.82±7.76
|
37.18±8.11
|
39.20±6.97
|
34.36±7.70
|
37.50±7.64
|
<0.01
|
|
BMI (kg/m2)
|
26.25±3.89
|
26.45±3.61
|
26.28±3.50
|
25.82±4.15
|
26.45±4.05
|
0.14
|
|
Laboratory parameters
|
|
TG (mmol/L)
|
1.20(0.83,1.91)
|
1.15(0.77,1.88)
|
1.19(0.79,1.78)
|
1.09(0.84,1.72)
|
1.35(0.90,2.12)
|
<0.01
|
|
FBG (mmol/L)
|
5.51±0.94
|
5.54±0.76
|
5.52±0.81
|
5.47±0.79
|
5.51±1.22
|
0.89
|
|
Current drinker, n (%)
|
523(55.64)
|
108(46.75)
|
83(50.30)
|
144(56.69)
|
188(64.83)
|
<0.01
|
|
Physical activity, n (%)
|
352(37.45)
|
79(34.20)
|
63(38.18)
|
96(37.80)
|
114(39.31)
|
0.64
|
|
Senior college or above, n (%)
|
184(19.57)
|
62(26.84)
|
36(21.82)
|
51(20.08)
|
35(12.07)
|
<0.01
|
|
Diabetes mellitus, n (%)
|
66(7.02)
|
20(8.66)
|
14(8.48)
|
15(5.91)
|
17(5.86)
|
0.46
|
|
Hypertension, n (%)
|
319(33.94)
|
80(34.63)
|
50(30.30)
|
86(33.86)
|
103(35.52)
|
0.22
|
|
Arterial stiffness and hemodynamics (measured
supine)
|
|
Pre-exercise SBP (mmHg)
|
131.84±15.97
|
132.38±17.61
|
130.16±15.46
|
129.99±14.81
|
133.99±15.66
|
0.01
|
|
Post-exercise SBP (mmHg)
|
132.34±14.83
|
133.09±14.45
|
131.20±15.18
|
130.88±14.57
|
133.67±15.05
|
0.10
|
|
Pre-exercise DBP (mmHg)
|
78.99±11.27
|
78.65±12.04
|
78.87±11.13
|
77.27±11.51
|
80.84±10.26
|
<0.01
|
|
Post-exercise DBP (mmHg)
|
79.35±10.92
|
79.79±10.75*
|
79.34±11.12
|
77.51±11.43
|
80.63±10.30
|
<0.01
|
|
Pre-exercise MAP (mmHg)
|
99.09±12.91
|
98.35±13.88
|
98.28±12.84
|
97.54±12.32
|
101.50±12.38
|
<0.01
|
|
Post-exercise MAP (mmHg)
|
99.42±11.95
|
99.74±11.76*
|
99.24±12.45
|
97.71±11.67
|
100.77±11.94
|
0.03
|
|
Pre-exercise HR (bpm)
|
80.24±12.54
|
79.04±13.97
|
77.85±12.54
|
81.82±12.51
|
81.18±11.03
|
<0.01
|
|
Post-exercise HR (bpm)
|
85.73±13.56*
|
84.13±14.46*
|
82.67±13.59*
|
87.23±13.71*
|
86.64±12.40*
|
<0.01
|
|
Pre-exercise baPWV (cm/s)
|
1375.08±209.09
|
1384.32+220.35
|
1368.85±218.41
|
1345.80±194.43
|
1396.92±204.75
|
0.03
|
|
Post-exercise baPWV (cm/s)
|
1341.53±208.04*
|
1361.32±216.35*
|
1341.83±221.97*
|
1305.55±195.90*
|
1357.10±200.32*
|
<0.01
|
|
VO2max (ml/kg/min)
|
3.19±0.58
|
3.27±0.68
|
3.18±0.54
|
3.16±0.52
|
3.17±0.57
|
0.58
|
|
Peak heat rate (bpm)
|
139.39±14.47
|
138.42±13.90
|
137.33±13.95
|
142.19±14.60
|
138.88±14.80
|
<0.01
|
|
Time interval (min)
|
7.13(4.93,11.16)
|
6.98(5.13,10.43)
|
7.57(4.95,12.60)
|
6.89(5.00,11.05)
|
7.02(4.73,11.15)
|
0.42
|
|
CVbaPWV
|
4.00(1.57,5.53)
|
3.95(1.58,5.55)
|
3.81(1.24,5.23)
|
3.77(1.30,5.27)
|
4.35(2.00,5.80)
|
0.04
|
|
CVSBP
|
3.90(1.40,5.43)
|
4.13(1.55,4.98)
|
3.74(1.55,5.46)
|
3.92(1.29,5.66)
|
3.80(1.26,5.42)
|
0.94
|
|
CVDBP
|
4.40(1.49,5.85)
|
4.61(1.45,6.01)
|
4.39(1.31,5.64)
|
4.44(1.44,5.64)
|
4.22(1.63,5.91)
|
0.93
|
|
CVMAP
|
4.24(1.45,6.07)
|
4.89(1.70,6.39)
|
4.02(1.42,5.22)
|
4.08(1.49,6.03)
|
3.99(1.19,6.20)
|
0.50
|
|
CVHR
|
6.57(2.49,9.10)
|
6.98(2.74,9.64)
|
6.49(1.96,9.98)
|
7.04(2.64,9.82)
|
5.87(2.45,8.22)
|
0.13
|
Note: BMI, body mass index; TG, triglyceride; FBG, fasting blood glucose;
SBP, systolic blood pressure; DBP, diastolic blood pressure; MAP, mean
arterial pressure; HR, heart rate; baPWV, brachial-ankle pulse wave
velocity; VO2max: maximum oxygen consumption; Time interval: the timing
of post-exercise measurements; CV: coefficients of variation;
*P<0.05 against pre-exercise value.
Comparison of changes in BP, HR, and baPWV between the groups
In adjusted analyses, the changes in baPWV of all participants post-exercise were
−33.55 cm/s (95% CI, −39.69 to
−27.42), and the change in the heavy smoking group was more
significantly than other three groups. The changes in HR of all participants
were 5.59 bpm (95% CI, 4.94 to 6.24). The changes in MAP of all
participants post-exercise were 0.33 mmHg (95% CI, −0.19
to 0.85) ([Table 2]).
Table 2 Adjusted values of changes in arterial stiffness
and hemodynamics.
|
All n=940
|
Never n=231
|
Former n=165
|
Light Smoker n=254
|
Heavy Smoker n=290
|
|
△MAP (mmHg)
|
0.33 (−0.19 to 0.85)
|
1.15 (0.28 to 2.01)
|
0.50 (−0.54 to 1.53)
|
0.20 (−0.64 to 1.04)
|
−0.20 (−0.98 to 0.57)
|
|
△HR (bpm)
|
5.59 (4.94 to 6.24)
|
5.10 (4.96 to 5.24)
|
4.79 (4.52 to 5.06)
|
5.36 (5.11 to 5.61)
|
5.50 (5.38 to 5.62)
|
|
△ baPWV (cm/s)
|
−33.55 (−39.69 to −27.42)
|
−23.53 (−35.89 to −11.16)
|
−29.46 (−44.20 to −14.71)
|
−37.21 (−49.18 to −25.24)
|
−40.67 (−51.72 to −29.63)
|
Note: Adjusted means (95% CI) are presented; Adjusted for Age,
the pre-exercise value BMI, and TG level; VO2mx; Education level;
Alcohol consumption; Physical activity; and Time interval; Abbreviation:
MAP, mean arterial pressure; HR, heart rate; baPWV, brachial-ankle pulse
wave velocity; VO2max: Maximum oxygen consumption; Time interval: the
timing of post-exercise measurements;
△MAP/△HR/△baPWV, post-exercise
value minus pre-exercise value.
Generalized linear model estimation of between-group differences in the
change in baPWV
We used the generalized linear model to compare between-group differences in the
change in baPWV. In Model 3, with the non-smokers as the control, the
β-values and 95% CI of former smokers, light smoking smokers,
and heavy smoking smokers were −12.17 cm/s (95%
CI, −30.08 to 5.75), −18.43 cm/s (95%
CI, −34.69 to −2.16), and −22.46 cm/s
(95% CI, −38.39 to −6.54), respectively ([Table 3]). For every increase in one standard
deviation (6.26 cigarettes/day) in the number of cigarettes smoked, the
β-value and 95% CI were −18.11 cm/s
(95% CI, −114.16 to 77.95) ([Table
3]).
Table 3 Generalized linear model analysis results of the
between-group difference of △baPWV with different smoking
statuses.
|
Smoking status
|
N
|
β
|
95% CI
|
|
Model 1
|
Never
|
231
|
Ref
|
|
|
Former
|
165
|
−11.32
|
−29.72 to 7.08
|
|
Light smoker,≤10 cigarettes/day
|
254
|
−15.80
|
−32.27 to −0.68
|
|
Heavy smoker,>10 cigarettes/day
|
290
|
−15.77
|
−31.61 to −0.07
|
|
P for trend
|
–
|
0.05
|
|
|
Daily cigarette consumption, per SD (6.26)
|
–
|
6.99
|
−118.27 to 75.59
|
|
Model 2
|
Never
|
231
|
Ref
|
|
|
Former
|
165
|
−13.67
|
−30.73 to 4.40
|
|
Light smoker,≤10 cigarettes/day
|
254
|
−20.76
|
−37.17 to −4.36
|
|
Heavy smoker,>10 cigarettes/day
|
290
|
−24.80
|
−40.86 to −8.73
|
|
P for trend
|
–
|
<0.01
|
|
|
Daily cigarette consumption, per SD (6.26)
|
–
|
−21.34
|
−118.27 to 75.59
|
|
Model 3
|
Never
|
231
|
Ref
|
|
|
Former
|
165
|
−12.17
|
−30.08 to 5.75
|
|
Light Smoker,≤10 cigarettes/day
|
254
|
−18.43
|
−34.69 to −2.16
|
|
Heavy Smoker,>10 cigarettes/day
|
290
|
−22.46
|
−38.39 to −6.54
|
|
P for trend
|
–
|
<0.01
|
|
|
Daily Cigarette Consumption, per SD (6.26)
|
–
|
−18.11
|
−114.16 to 77.95
|
Model 1: included Age, the pre-exercise values of baPWV; Model 2:
included Model 1 covariates plus BMI, the pre-exercise values of HR,
MAP, and TG level; VO2max, Time interval; Alcohol consumption; Education
level; Model 3: included Model 2 covariates plus △HR;
△MAP; Abbreviation: MAP, mean arterial pressure; HR, heart rate;
baPWV, brachial-ankle pulse wave velocity, BMI, body mass index; TG,
triglyceride; VO2max: maximum oxygen consumption; Time interval: the
timing of post-exercise measurements; △HR/△MAP,
post-exercise value minus pre-exercise value.
Stratified analysis
In the stratified analysis, after adjustment for covariates, the result was
consistent with the main analysis among participants without regular exercise
habit. But for those with regular exercise habit, there were no significant
difference in the change of baPWV in former smoker, light smoker, and heavy
smoker, compared with non-smokers (Table S1).
Sensitivity analysis
The results of the sensitivity analysis were consistent with those of the main
analysis, which indicated that the main results were robust (Table
S2).
Discussion
Using a functional community population, this study showed that aerobic exercise
immediately improved arterial stiffness in individuals with different smoking
statuses. Remarkably, the beneficial effects of exercise on arterial stiffness
appeared to be more evident in light and heavy smoker than in non-smoker.
Following a 7-minute bout of exercise, we observed a significant reduction in baPWV
of 33.55 cm/s from resting values in young and middle-aged
(36.82±7.76 years) subjects. This finding is similar to that by Yamato et
al. (2016) [34]. They found that baPWV in non-smoking
healthy men (n=26, age: 21.0±1.0 years) was decreased by
33.5 cm/s after 15 minutes of aerobic exercise for
40 minutes. However, Doonan et al.’s (2011) [16] study of 24 healthy young smoking men and 53 non-smokers showed that
carotid-femoral pulse wave velocity in smokers and non-smokers increased by
80 cm/s and 60 cm/s, respectively, after
5 minutes of exhausting exercise. There are several possible reasons for
this discrepancy between our study and Doonan et al.’s (2011) study. The
sample size of Doonan et al.’s study was small, the population was
relatively young (26.06±6.70 years), and the exercise style was more intense
compared with our study. Additionally, the difference in the type of pulse wave
velocity could be the reason for the inconsistent conclusion between the studies.
A
meta-analysis suggested that aerobic exercise had different effects on arterial
stiffness of different segments. In this meta-analysis, after aerobic exercise,
arterial stiffness in the peripheral segments was significantly improved, but it did
not significantly improve arterial stiffness in the central segment [35].
Our study showed that there was a difference in the decrease in baPWV after aerobic
exercise in individuals with different smoking statuses. After adjusting for related
confounding factors, baPWV was more significantly immediately decreased in
low-intensity and high-intensity smokers than in never smokers (by 18.43 and
22.46 cm/s, respectively). A more likely explanation is that
short-term aerobic exercise may have ameliorated the adverse effects of oxidative
chemicals contained in cigarette smoke on vascular endothelial function and
sympathetic nervous system activity [36]. Oxidative
chemicals in cigarette smoke can affect vascular endothelial function through
inflammatory response [37] and oxidative stress [38], which reduce the activity of endothelial nitric
oxide synthase and the production of nitric oxide [39]. Because aerobic exercise can stimulate the expression of antioxidant
enzymes [40] and vasodilatory substances [41]. We speculate that the augmented antioxidant
defense mechanism in current smokers is the reason why baPWV improvement is more
significant than that in non-smokers after exercise.
Although we found that there was a difference in the decrease in baPWV after aerobic
exercise in individuals with different smoking statuses, and this decrease in heavy
smokers was more obvious, we did not examine the specific mechanism(s). Previous
studies have shown that arterial stiffness is mainly determined by two factors. One
factor is that the structure of arteries affects arterial stiffness. A decrease in
elastin in the middle layer of the arterial wall and an increase in fibrin cause
changes in vascular structure, which increases arterial stiffness [42]
[43]
[44]
[45]. The other factor
is that the functional status of arteries also affects arterial stiffness. Vascular
endothelial dysfunction and nervous system activity disorders can affect vascular
function, resulting in increased arterial stiffness [46]
[47]. Short-term aerobic exercise
increases blood flow by stimulating the production of endothelial nitric oxide,
prostaglandin, and other vasodilator factors, and decreases vasoconstrictors
(e. g., endothelin) [41]
[48]
[49]
[50], or vascular modifications [51]. These processes can improve vascular endothelial function and
arterial stiffness. In addition, an improvement in arterial stiffness after aerobic
exercise may also be related to changes in the levels of circulatory metabolites.
The Framingham study showed a significant reduction in circulating blood metabolites
after aerobic exercise, which resulted in insulin resistance, body inflammation, and
oxidative stress. Metabolites related to cardio-cerebral vascular protection were
significantly increased [52].
Improving lifestyles and preventing and controlling multiple risk factors are still
primary prevention measures for cardiovascular disease, which can effectively reduce
the probability of adverse cardiovascular events [53].
Hamdy et al. (2005) found that long-term regular aerobic exercise delayed and
reversed the process of vascular aging [54]. Our study
showed that arterial stiffness in individuals with different smoking statuses were
significantly immediately decreased after exercise compared with before exercise.
However, this might not be a continuous change. If the exercise time is prolonged
and the exercise frequency is increased, arterial stiffness may be maintained.
Therefore, smokers can adopt a healthy lifestyle such as aerobic exercise to improve
arterial stiffness, delay vascular aging, and reduce the damage to blood vessels
caused by smoking.
This study has some limitations: (1) This was a cross-sectional study that was
performed to examine the causal relationships between various factors and the
difference in baPWV before and after exercise. (2) We did not find a
dose–response relationship of the change in baPWV after aerobic exercise,
possibly because we had difficulty in determining the specific number of cigarettes
smoked per day. The number of cigarettes smoked was treated as a classification
variable (1–10, 11–20, 21–30, 31–40, and>40
cigarettes/day). Therefore, it is difficult to observe a
dose–response relationship. (3) We used baPWV as a measurement of arterial
stiffness instead of carotid–femoral pulse wave velocity, which is the gold
standard. The validity and accuracy of baPWV against carotid–femoral pulse
wave velocity have been demonstrated in previous studies [55], and the American Heart Association has also recommended baPWV as a
common indicator for arterial stiffness [56]. (4) The
study was conducted only in men, and findings could not be readily generalizable to
female working populations or to workers in other settings or other countries. (5)
Because of space and personnel constraints, the timing of baPWV measurement after
aerobic exercise could not be unified. But baPWV was measured immediately (or as
soon as possible) after aerobic exercise. In addition, when evaluating the
short-term effect of acute aerobic exercise on arterial stiffness, we adjusted for
the timing of baPWV measurement.
In summary, this study shows that a single aerobic exercise can immediately decrease
baPWV in individuals with different smoking statuses. Additionally, compared with
non-smokers, baPWV decreased more significantly in light and heavy smokers.
