Received: 19 March 2023

| Revised: 10 July 2023

| Accepted: 9 August 2023

DOI: 10.1111/sms.14480

ORIGINAL ARTICLE

Exploring the direct and indirect effects of cardiovascular

disease risk factors on exercise blood pressure

Myles N. Moore1 | Christopher L. Blizzard1 | Terence Dwyer1,2,3,4 |

Costan G. Magnussen1,5,6,7 | James E. Sharman1 | Alison J. Venn1 |
Martin G. Schultz1

1
Menzies Institute for Medical
Research, College of Health and Abstract
Medicine, University of Tasmania, Objective: Exaggerated exercise blood pressure (BP) is independently associated
Hobart, Australia
with cardiovascular disease (CVD) outcomes. However, it is unknown how indi-
2
George Institute for Global
Health, Oxford Martin School and
vidual CVD risk factors may interact with one another to influence exercise BP.
Nuffield Department of Obstetrics The aim of this study was to quantify direct and indirect associations between
& Gynaecology, Oxford University, CVD risk factors and exercise BP, to determine what CVD risk factor/s most-­
Oxford, UK
3
strongly relate to exercise BP.
Murdoch Children's Research
Institute, Melbourne, Australia Methods: In a cross-­sectional design, 660 participants (44 ± 2.6 years, 54% male)
4
Faculty of Medicine, Dentistry from the population-­based Childhood Determinants of Adult Health Study had
and Health Sciences, University of BP measured during low-­intensity fixed-­workload cycling. CVD risk factors were
Melbourne, Melbourne, Australia
5
measured, including body composition, clinic (rest) BP, blood biomarkers, and
Research Centre of Applied and
Preventive Cardiovascular Medicine, cardiorespiratory fitness. Associations between CVD risk factors and exercise BP
University of Turku, Turku, Finland were assessed using linear regression, with direct and indirect pathways of asso-
6
Centre for Population Health ciation assessed via structural equation model.
Research, University of Turku and
Results: Sex, waist-­to-­hip ratio, fitness, and clinic BP were independently associ-
Turku University Hospital, Turku,
Finland ated with exercise systolic BP (SBP), and along with age, had direct associations
7
Baker Heart and Diabetes Institute, with exercise SBP (p < 0.05 all). Most CVD risk factors were indirectly associated
Melbourne, Australia with exercise SBP via a relation with clinic BP (p < 0.05 all). Clinic BP, waist-­to-­
Correspondence hip ratio, and fitness were most-­strongly associated (direct and indirect associa-
Martin G. Schultz, Menzies Institute for tion) with exercise SBP (β[95% CI]: 9.35 [8.04, 10.67], 4.91 [2.56, 7.26], and −2.88
Medical Research, College of Health
[−4.25, −1.51] mm Hg/SD, respectively).
and Medicine, University of Tasmania,
Hobart 7000, Australia. Conclusion: Many CVD risk factors are associated with exercise BP, mostly
Email: martin.schultz@utas.edu.au with indirect effects via clinic BP. Clinic BP, body composition, and fitness were
most-­strongly associated with exercise BP. These results may elucidate how life-
Funding information
National Health and Medical Research style modification could be a primary strategy to decrease exaggerated exercise
Council BP-­related CVD risk.

KEYWORDS
cardiopulmonary, cohort, epidemiology, hemodynamic, hypertension, physiology

© 2023 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.

Scand J Med Sci Sports. 2023;33:2509–2515.  wileyonlinelibrary.com/journal/sms | 2509

 |
2510   
1 | I N T RO DU CT ION
Systolic blood pressure (BP) will normally rise with inten-
sity of dynamic exercise.1 This systolic BP response during
submaximal intensity can, however, be exaggerated,
which pooled data indicate is independently associated
with incident hypertension, cardiovascular morbidity,
and mortality.2,3 An exaggerated BP response during sub-
maximal intensity exercise is also associated with other
hypertension-­related cardiovascular disease (CVD) risk
factors (e.g., raised left ventricular mass and aortic stiff-
ness),4,5 likely because it represents a state of chronic hy-
pertension gone undetected with standard measurement
of BP at rest.6,7 Thus, submaximal exercise BP may be a
useful clinical tool to identify CVD risk.
Several CVD risk factors are known to influence the BP re-
sponse to exercise.8,9 However, CVD risk factors rarely occur
in isolation,10,11 and likely interact with one another via sev-
eral pathways to influence exercise BP. For example, a raised
total and abdominal fat is associated with metabolic-­and
lipid-­related CVD risk factors.12 Metabolic-­and lipid-­related
CVD risk factors may damage the peripheral vasculature
and inhibit vasodilation during exercise,13,14 which when
accompanied with an exercise-­induced elevation in cardiac
output may increase the BP response to exercise.
Pathways of association (i.e., direct and indirect ef-
fects) between exercise BP and different CVD risk factors
have never been explored, and cannot be assessed with
traditional statistical methods (i.e., linear regression). A
structural equation model (SEM) is one method which
can be used to identify, test, and quantify possible path-
ways of association between different CVD risk factors si-
multaneously.15,16 These possible pathways of association
identified from the SEM may help to better understand
the interrelationships between exercise BP and multiple
CVD risk factors, which likely influence one another and
may be missed when traditional linear regression is used
to analyze data.17 The various pathways of association
between exercise BP and CVD risk factors are also im-
portant to understand in order to improve the identifi-
cation and management of CVD risk related to high BP.
Thus, the aim of this study was to quantify the direct and
indirect pathways of association between different CVD
risk factors and exercise BP, while also determining what
CVD risk factor/s most-­strongly relate to exercise BP.
2 | M AT E R IALS AN D M ET H OD S
2.1 | Participants
Participants were initially recruited for the 1985 Austral-
ian Schools Health and Fitness Survey, which involved
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MOORE et al.
collection of lifestyle and physical data on 8498 school
children aged 7–­15 years across Australia.18 Of these par-
ticipants, 1363 attended a follow-­up clinic from 2017 to
2019. Participants were excluded from the current anal-
ysis if: (1) a submaximal exercise (fitness) test was not
completed, and (2) a BP was not measured during the
warm-­up stage of the exercise test at a fixed workload of
75 watts. A total of 660 participants were available for
analysis. Figure S1 illustrates the flow of study partici-
pants. All participants provided informed consent, and
ethics approval was received from the Tasmania Health
and Medical Human Research Ethics Committee.
2.2 | Exercise test
A submaximal exercise test was performed on a cadence-­
independent cycle ergometer (Monark 928G3r; Monark
exercise ab, vansbro, Sweden) to determine physical work
capacity at a heart rate of 170 bpm (PWC170) as an estimate
of cardiorespiratory fitness.19 Specific information on the
protocol of the exercise test (including criteria for the in-
titiation and termination of the test) are described in the
supplementary material (page 3).
2.3 | Exercise BP
A cuff attached to a mercury-­ free manual ausculta-
tory sphygmomanometer (UM-­101, A&D instruments)
was placed onto the left arm of each participant before
the exercise test. A single BP measurement was then
taken during the second minute of the 2-­min warm-­up
stage while participants were cycling at a workload of
75 watts. The technician read the BP values from the
manual sphygmomanometer while listening for the
first and fifth Korotkoff sounds (representing systolic
and diastolic BP, respectively) in accordance with
recommendations.20
2.4 | Cardiorespiratory fitness
Cardiorespiratory fitness was estimated using the heart rate
and workload recorded during the three (or four) incre-
mental exercise test stages. Calculations used to estimate
PWC170 are described in supplementary material (page 3).
2.5 | Clinic (resting) BP and heart rate
At a separate time to the exercise test (but on the same
day), clinic BP and resting heart rate were measured

MOORE et al.
using an automated BP device (Omron HEM-­ 907,
Omron Healthcare) attached to a cuff on the right arm
of each participant in a seated position after 5 min rest.21
The average of three measurements were used to cal-
culate clinic systolic and diastolic BP and resting heart
rate.
2.6 | Body composition
Supplementary material (page 4) includes details for how
weight, height, waist and hip circumference and triceps,
biceps, subscapular, and suprailiac skinfolds were meas-
ured and calculations used for body mass index, fat and
fat-­free (lean) mass and fat mass percentage.
2.7 | Blood and urine biochemistry
Fasting blood samples were taken from the antecubi-
tal fossa and measured for glucose, insulin, HbA1c, total
cholesterol, high-­and low-­density lipoprotein cholesterol,
triglycerides, high-­sensitivity c-­reactive protein, and creati-
nine. Homeostatic model assessment of insulin resistance
(HOMA-­IR) was also calculated with glucose and insulin,
and these details are described in the supplementary ma-
terial (page 4). Urine samples were collected to calculate
kidney function using the albumin-­to-­creatinine ratio.
2.8 | Muscular strength
Left and right handgrip, shoulder extension and flexion,
and leg extension strength were estimated from maximal
voluntary isometric contractions. Specific information on
the measurement protocols for these strength variables is
outlined in the supplementary methods (page 4).
2.9 | Health history
Participants who attended a follow-­up clinic completed a
lifestyle questionnaire, including questions on previous
diagnosis of hypertension and diabetes mellitus and his-
tory of smoking.
2.10 | Statistical analysis
All statistical analyses were performed using Stata
(Version 16.0, StataCorp). Statistical significance was
defined as a p-­value <0.05. Supplementary material
|
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   2511
(page 5) includes details on the analyses used to assess
the distribution of data and presentation of participant
characteristics.
Exercise systolic and diastolic BP were analyzed as a
continuous variable because of substantial heterogeneity
on thresholds used to define an exaggerated BP response
to exercise.4,5Analyses used to remove skewness in exer-
cise BP and assess linearity and age-­and sex-­interactions
in associations between exercise BP and each study factor
are described in supplementary material (page 5). All as-
sociations were adjusted for age and sex. The estimated
cross-­sectional responses of exercise BP to a one-­ unit
change in each study factor are reported, together with
95% confidence intervals (CI).
Multivariable linear regression analyses were per-
formed to assess the associations between exercise BP and
multiple study factors. Further details on how each study
factor were grouped into broad categories are described
in the supplementary material (page 6). The final multi-
variable linear regression models chosen for each broad
category included only the CVD risk factors that were in-
dependently associated with exercise BP, explaining the
highest variance in the model (i.e., R2). In general, only
one study factor in each category was included in the final
multivariable model.
An SEM was used to assess whether a study factor in-
cluded in the mutually adjusted multivariable linear re-
gression analyses mediated the associations of another
factor on exercise BP. Specific information on specifica-
tion and fit of the SEM are described in supplementary
material (page 6) and illustrated in Figure S2. 17 A direct
effect reported from the SEM was defined as a directional
pathway of association from a study factor to exercise BP.
An indirect effect was defined as a directional pathway of
association from a study factor to exercise BP that was me-
diated through the relationship of another study factor/s.
The joint direct and indirect effects of a study factor on
exercise BP defined the total effect.
3 | RESULTS
Participant characteristics are shown in Table S1.
3.1 | Univariable associations with
exercise BP
The associations between exercise systolic and diastolic
BP and each study factor after adjusting for age and sex
are shown in Table S2 and described on pages 6-­7 of sup-
plementary material.
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2512   
3.2 | Multivariable associations with
exercise BP
Body mass index, waist-­to-­hip ratio (body composition),
HOMA1-­ IR (metabolic), low-­ density lipoprotein cho-
lesterol, triglycerides (lipids), clinic systolic BP, resting
heart rate (hemodynamic), high-­ sensitivity c-­reactive
protein (inflammation), and urine albumin–­ creatine
ratio (kidney function) and PWC170 (fitness) were the
study factors from grouped collections with the strong-
est association with exercise systolic BP (Table S3). Sex
(β, [95% CI]: 3.70 [0.19, 7.20]), waist-­to-­hip ratio (β [95%
CI]: 49.93 [21.96, 77.90]), PWC170 (β [95% CI]: -­0.02
[-­0.04. -­0.002]), and clinic systolic BP (β [95% CI]: 0.63
[0.53, 0.73]) were independently associated with exer-
cise systolic BP after mutual adjustment of all the CVD
risk factors found from grouped collections (p < 0.05 all;
Table S4).
The direct and indirect pathways of association of each
study factor with exercise systolic BP in the SEM are il-
lustrated in Figure S3 and described on supplementary
material (page 7; Table S5). Age, body mass index, waist-­
to-­hip ratio, HOMA1-­IR, high-­sensitivity c-­reactive pro-
tein, low-­ density lipoprotein cholesterol, triglycerides,
clinic systolic BP, and resting heart rate had a positive total
effect (association) on exercise systolic BP, while female
sex and PWC170 had a negative total effect (association)
on exercise systolic BP (Table S4). Based on comparisons
of the estimated response of exercise systolic BP to a one
standard deviation change in each study factor, the study
factor that had largest effect on exercise systolic BP was
clinic systolic BP (β [95% CI]: 9.35 [8.04, 10.67] mmHg/SD,
p < 0.05), followed by waist-­to-­hip ratio (β [95% CI]: 4.91
[2.56, 7.26] mmHg/SD, p < 0.05) and then PWC170 (β [95%
CI]: -­2.88 [-­4.25, -­1.51] mmHg/SD, p < 0.05; Table S4). Sup-
plementary material (page 7) describes the details for why
albumin-­creatine ratio was excluded from the multivari-
able linear regression and SEM.
Details and results on the multivariable associations
and direct, indirect and total effects between exercise dia-
stolic BP and each study factor are reported in supplemen-
tary material (page 7; Figure S4; Tables S7 and S8).
4 | DI S C USSION
This study aimed to quantify the direct and indirect
pathways of association between different CVD risk fac-
tors and exercise BP to determine the CVD risk factor/s
most-­strongly related to exercise BP. The novel findings
of this study are that many CVD risk factors have a path-
way of association with exercise systolic BP, mostly with
indirect relationship via clinic BP. The study factors that
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MOORE et al.
were most-­strongly associated with exercise systolic BP
were clinic BP, waist-­to-­hip ratio, and PWC170 (as a de-
terminant of cardiorespiratory fitness). This highlights
that lifestyle modification of these CVD risk factors is
likely a primary strategy to decrease BP-­related CVD
risk.
The statistical methods used in this study are dis-
tinctly different to those in previous studies that have
investigated the relationship between exercise BP and
various CVD risk factors via traditional linear models
(i.e., Pearson's correlation or regression).4,8,9 A limitation
of previous findings and traditional statistical methods
is that the association between exercise BP and a indi-
vidual CVD risk factor may be indirect via a relationship
with another factor. The novelty of this study is the SEM
utilized enabled simultaneously tested multiple path-
ways of association between exercise BP and different
CVD risk factors. For example, the SEM showed that
while waist-­to-­hip ratio had a direct pathway of associ-
ation with exercise BP, an indirect pathway of associa-
tion was also simultaneously present via relationships
with HOMA1-­IR, low-­density lipoprotein cholesterol,
triglycerides, high-­sensitivity c-­reactive protein, resting
heart rate, and clinic systolic BP. Thus, the results from
the SEM in the present study have enabled the interre-
lationships between different CVD risk factors and exer-
cise BP to be better understood.
The measurement of BP is a mandatory requirement
of clinical exercise testing and is regularly performed in
cardiology and exercise physiology clinics. Although an
exaggerated exercise BP response is likely a signal of high
BP-­ CVD risk missed from resting clinic measures,5-­7
those with this exercise BP response often present with
slightly raised clinic BP (i.e., pre-­hypertension).9,22 This
may provide an explanation for why clinic BP was most-­
strongly associated with exercise BP in this study, and
why this relationship was also mediated via other CVD
risk factors that typically appear in concert with high
BP.10,11 However, an exaggerated exercise BP response
can still occur even when clinic BP is normal.6,7 The re-
sults of this study also support this idea because exercise
BP was associated with age, sex, waist-­to-­hip ratio, and
PWC170 independently of clinic BP. Thus, these results
highlight that the measurement of exercise BP could
offer an opportunity to identify individuals at high BP-­
related CVD risk that may have been otherwise missed
from clinic BP taken under resting conditions,5-­7 and
prompt further testing with ambulatory or home BP
monitoring for a definitive diagnosis.
There is a complex interplay between body compo-
sition and cardiorespiratory fitness in relation to CVD
risk. While raised body fatness is associated with in-
creased risk of CVD, this relationship can be reduced

MOORE et al.
with higher cardiorespiratory fitness levels.23 Moreover,
the poor CVD risk profile related to elevated body fat-
ness can be improved, but not fully eliminated, with an
increase in cardiorespiratory fitness.24 In this study, ex-
ercise BP also had a stronger positive association with
elevated body fatness compared to the independent neg-
ative relationship with PWC170. These findings are con-
sistent with other cross-­sectional studies where exercise
systolic BP was higher among individuals with elevated
body fatness irrespective of cardiorespiratory fitness.25,26
A decrease in exercise BP has also been found to be inde-
pendently associated with a reduction in waist circum-
ference and improvement in cardiorespiratory fitness
following an exercise intervention.27 The current study
also expands on this understanding between exercise BP,
body fatness, and PWC170 and shows these relationships
were partly mediated via relations with general CVD risk
factors, suggesting other contributory factors may also
influence the BP response. Indeed, another potential
contributory factor associated with exercise BP is raised
arterial stiffness,4 which also shares a relationship with
elevated body fatness parameters, low cardiorespiratory
fitness, and a poorer metabolic-­and lipid-­related CVD
risk profile.28,29 Overall, the results in this study may
suggest that lifestyle modification of body fatness and
fitness could be a primary strategy to decrease exercise
BP-­related CVD risk that is independent and additive of
clinic BP and other general CVD risk factors.
4.1 | Strengths and limitations
This study includes a large nationally representative sam-
ple of middle-­aged and healthy Australians. However,
the cohort has a relatively narrow age band, and results
may not be generalizable to other population groups. Re-
sults are also only specific to exercise BP measured dur-
ing submaximal (rather than peak) intensities. However,
a strength of this study was that exercise BP can be in-
terpreted free from the influence of cardiorespiratory fit-
ness and less influenced by movement and noise artifact
because it was measured during a standardized fixed and
submaximal workload rather than at a specific intensity.30
The manual measurement of BP is also feasible (and is
the recommended method outlined within exercise test-
ing guidelines) in clinical practice.31 In the absence of the
gold-­standard measurements, cardiorespiratory fitness
and body fatness were estimated in this study. However,
PWC170 and the measurement of skin folds have shown to
be suitable methods to estimate cardiorespiratory fitness
and body fatness within large scale field-­based studies.32,33
Behavioral variables such as physical activity, diet, and al-
cohol consumption might also influence the BP response
|
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   2513
to exercise, as well as one or more CVD risk factors that
were not included in the current study. Self-­reported be-
havioral factors can also be unreliable and inaccurately
estimate objective measures,34,35 which is why these fac-
tors were excluded from the current analyses. An analysis
with longitudinal data would improve understanding of
the different casual relationships between exercise BP and
different CVD risk factors compared to this cross-­sectional
study. Nevertheless, the direction of each relationship
and total effect (i.e., the combined direct and indirect as-
sociations) between exercise BP and individual CVD risk
factors in the SEM were as hypothesized in the original
model specification, and thus, likely represent biologically
plausible pathways to be tested in future studies. More-
over, the SEM in this study was sufficiently powered to
evaluate the multiple pathways of association between ex-
ercise BP and different CVD risk factors simultaneously,
which cannot be undertaken with a multivariable linear
regression model. Future studies should aim to replicate
the SEM approach included in this study.
5 | PERSPECTIVES
There are many pathways of association between exercise
BP and different CVD risk factors, mostly that occur via an
indirect relationship with clinic BP. These interrelation-
ships between exercise BP and different CVD risk factors
are important to understand in order to improve the iden-
tification and management of high BP-­related CVD risk
been otherwise missed by clinic BP taken under resting
conditions. While longitudinal analyses are needed to bet-
ter understand the casual relationships between exercise
BP and different CVD risk factors, interventions that tar-
get modification of both body composition and cardiores-
piratory fitness could be a primary strategy to decrease
exercise BP-­related CVD risk that is independent and ad-
ditive of clinic BP and other general CVD risk factors.
AUTHOR CONTRIBUTIONS
MNM contributed to the study conception, statistical
analysis, and drafting manuscript. MNM, CLB, and MGS
contributed to the study design and interpretated findings.
MNM and CGM contributed to the data collection. TD
and AJV contributed to the data custodian. CLB contrib-
uted to the statistical support. CLB, TD, CGM, AJV, JES,
and MGS critically revised manuscript. All authors gave
final approval and agreed to be accountable for all aspects
of work ensuring integrity and accuracy.
ACKNO​WLE​DGE​MENTS
We acknowledge the contribution of the project man-
agers (Marita Dalton, Karen Patterson and Jasmine
 |
2514   
Pritchard), staff and volunteers who assisted with this
study, and ongoing commitment of participants to the
study.
FUNDING INFORMATION
Data used for this study were able to be collected because
of a project grant from the National Health and Medical
Research Council (reference: 1128373). MGS is supported
by a National Heart Foundation of Australia Future
Leader Fellowship (reference: 102553).
CONFLICT OF INTEREST STATEMENT
Nothing to declare.
DATA AVAILABILITY STATEMENT
The data that support the findings of this study are avail-
able from the corresponding author upon reasonable
request.
ORCID
Terence Dwyer https://orcid.org/0000-0002-2091-7663
Martin G. Schultz https://orcid.
org/0000-0003-3458-1811
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SUPPORTING INFORMATION
Additional supporting information can be found online
in the Supporting Information section at the end of this
article.
How to cite this article: Moore MN, Blizzard CL,
Dwyer T, et al. Exploring the direct and indirect
effects of cardiovascular disease risk factors on
exercise blood pressure. Scand J Med Sci Sports.
2023;33:2509-2515. doi:10.1111/sms.14480