Journal of Human Hypertension (2015) 29, 351–358

© 2015 Macmillan Publishers Limited All rights reserved 0950-9240/15

www.nature.com/jhh

REVIEW
Exercise blood pressure: clinical relevance
and correct measurement
JE Sharman1 and A LaGerche2

Blood pressure (BP) is a mandatory safety measure during graded intensity clinical exercise stress testing. While it is generally
accepted that exercise hypotension is a poor prognostic sign linked to severe cardiac dysfunction, recent meta-analysis data also
implicate excessive rises in submaximal exercise BP with adverse cardiovascular events and mortality, irrespective of resting BP.
Although more data is needed to derive submaximal normative BP thresholds, the association of a hypertensive response to
exercise with increased cardiovascular risk may be due to underlying hypertension that has gone unnoticed by conventional resting
BP screening methods. Delayed BP decline during recovery is also associated with adverse clinical outcomes. Thus, above and
beyond being used as a routine safety measure during stress testing, exercise (and recovery) BP may be useful for identifying high-
risk individuals and also as an aid to optimise care through appropriate follow-up after exercise stress testing. Accordingly, careful
attention should be paid to correct measurement of exercise stress test BP (before, during and after exercise) using a standardised
approach with trained operators and validated BP monitoring equipment (manual or automated). Recommendations for exercise
BP measurement based on consolidated international guidelines and expert consensus are presented in this review.

Journal of Human Hypertension (2015) 29, 351–358; doi:10.1038/jhh.2014.84; published online 2 October 2014

INTRODUCTION exercise stress testing worldwide each year, the exercise BP

The rationale underpinning exercise stress testing is that
cardiovascular abnormalities not apparent at rest may be revealed
with exercise. Electrocardiographic, hemodynamic (for example,
blood pressure (BP), heart rate) and symptomatic responses to
graded exercise are monitored typically for the purposes of
diagnosing coronary artery disease, or determining severity of
coronary or respiratory disease, but also for gauging exercise
capacity. Compared with cycle ergometry, treadmill testing results
in higher maximal oxygen uptake and has greater sensitivity for
detecting coronary artery disease.1 Accurate BP is expected to be
recorded before, during and after exercise in a standardized
fashion. Pretest BP is used to determine whether exercise testing
should proceed (for example, systolic BP; SBP 4200 mm Hg or
diastolic BP; DBP 4120 mm Hg is a relative contraindication)2 and
also for comparison with exercise BP to ensure appropriate
responses from resting values. BP is recorded during exercise
because excessive or inadequate augmentation of BP may
indicate significant pathology and, if extreme, may be an
indication for terminating testing. Hemodynamic monitoring is
continued into the postexercise period because some abnormal-
ities (including inadequate BP or heart rate reduction) may occur
during this time.
Cycle and treadmill exercise stress test protocols typically start
at very low intensity (and at level gradient for treadmills) and
progressively rise to higher speeds and/or gradients (or resistance
for cycling) each 2–3 min until fatigue or the development of
symptoms or signs of cardiac disease. In recent years data has
emerged suggesting that BP responses to exercise testing could
provide useful clinical information independent from resting BP,
and separate to the acute safety aspect of BP monitoring during
exercise. With many millions of people undergoing clinical
responses could be useful for identifying higher risk individuals
that may otherwise be overlooked using conventional resting BP
screening methods. In this context, the first purpose of this paper
is to review the potential clinical usefulness of exercise BP through
consideration of normal and abnormal exercise BP responses. The
second purpose is to provide recommendations to correctly assess
exercise BP in a standardised fashion according to international
guidelines and accepted protocols. Although there is disparate
information available from independent sources on appropriate
resting and exercise BP measurement, to our knowledge this has
never been presented as a consolidated summary.
WHY DOES BP INCREASE DURING EXERCISE?
During exercise cardiac output (CO) must increase to meet the
greater metabolic requirements of the working muscles. CO
augmentation results from an increase in both heart rate and
stroke volume. According to a simplified Poiseuille's Law, pressure
is proportional to flow and resistance. To extend this further to
incorporate the pulsatile flow in the circulation, it is important
to consider vascular compliance which is inversely proportional to
resistance and can be calculated as the quotient of stroke volume
and arterial pulse pressure. Thus, the ideal circulation is able to
'accommodate' increases in CO by means of (1) active vasodilation
of the arteries of the skeletal muscles and other tissues in which
exercise metabolic requirements are increased and (2) distension
of compliant arteries. However, there is a limit to which the vessels
can dilate and still direct significant CO to the muscles.
Furthermore, increased vascular distension forces the vessels onto
the steeper part of the pressure volume relationship such that the
vessels are stiffer or less compliant. Therefore, in a healthy

1
Menzies Research Institute Tasmania, University of Tasmania, Hobart, Australia and 2Department of Medicine, St Vincent's Hospital, University of Melbourne, Fitzroy, Australia.
Correspondence: Associate Professor JE Sharman, Menzies Research Institute Tasmania, University of Tasmania, Private Bag 23, Hobart 7000, Australia.
E-mail: James.Sharman@menzies.utas.edu.au
Received 19 May 2014; revised 19 August 2014; accepted 22 August 2014; published online 2 October 2014
 Exercise blood pressure: measurement and relevance
JE Sharman and A LaGerche
352
cardiovascular system, CO increases are accompanied by modest
increases in mean BP and pulse pressure. A rapid increase in BP
with only limited increases in CO suggests impaired vasodilation
and vascular compliance. A lack of BP augmentation with exercise
suggests inadequate CO unable to 'fill' the dilated exercise
circulation. Thus, exercise represents an ideal means of testing
both CO and the full range of vascular reserve.
WHAT CONSTITUTES A NORMAL BP CHANGE DURING
EXERCISE?
The normal SBP response to each increase in exercise intensity is a
rise that approximates 10 ± 2 mm Hg per metabolic equivalent
(MET) and may plateau at peak exercise.3 DBP generally decreases
but may not change with increasing intensity, thus overall there is
a stepwise increase in pulse pressure from rest to peak exercise.3
There is little clarity in the literature as to what may constitute
normal submaximal or maximal intensity exercise BP, although
maximal responses are commonly cited as being SBP o 210 mm-
Hg (men) and SBP o 190 mm Hg (women) with DBP o 110 mm-
Hg (both sexes) on the basis of these values being below the
upper limits of normal.4 However, older age is associated with
increased maximal exercise BP and these SBP cut points may not
be applicable to people aged 440 years where the BP responses
at below the 90th percentile exceed these values.5 Figure 1
provides an example of maximal exercise BP responses in healthy
men and women.
The Bruce treadmill protocol is widely used, and normal SBP
responses to the first stage (3 min exercise) of the test are
generally about 30 mm Hg above resting values for men and
28 mm Hg for women.6 A small percentage (for example, o 3%) of
apparently healthy people may have a modest decrease in SBP in
the first stage, which could be due to resolution of pretest
sympathetic over activity from the anticipation of exercise.7 The
normal SBP change from rest to peak exercise approximates 50–
60 mm Hg in men and 40–50 mm Hg in women, with a tendency
towards the lower range values in people aged ⩾ 70 years for both
sexes.5 For DBP, the magnitude of decrease is greater in men than
in women, and the size of the decrease becomes smaller with
increasing age (for example, average approximately − 10 mm Hg
at age 20–30 years to approximately 0 mm Hg at age 60–69
years).5 In addition to the influence of age and sex, other factors
positively associated with exercise BP include resting BP, smoking,
Figure 1. Typical values for the mean, 10th and 90th percentile of systolic (SBP) and diastolic (DBP) blood pressure responses to maximal
treadmill exercise (Bruce protocol) in healthy men (n = 7863) and women (n = 2406) from the Cardiovascular Health Clinic database at Mayo
Clinic Rochester. Subjects were not taking cardiovascular medications; had no prior history of hypertension, cardiovascular or pulmonary
disease; with normal resting electrocardiogram findings and no evidence of ischaemia on exercise. Figure produced from data in Daida et al.5
with permission from Elsevier.
Journal of Human Hypertension (2015) 351 – 358
body mass index, dyslipidemia, lower cardiorespiratory fitness and
treadmill time to exhaustion.8–10
HYPOTENSIVE RESPONSE TO EXERCISE: MECHANISMS AND
CLINICAL RELEVANCE
Inappropriately low BP during exercise is an absolute indication to
terminate exercise testing and is defined by the American Heart
Association as a 'drop in SBP 410 mm Hg (persistently below
baseline), despite an increase in workload, when accompanied by
any other evidence of ischaemia.11 Other definition criteria include
an SBP fall 420 mm Hg from the highest value during the test,2 or
failure of SBP to increase with increased workload.3 Reasons for
exercise hypotension relate to major cardiac disease including
severe left ventricular dysfunction, obstruction to aortic outflow or
severe myocardial ischaemia, but can also be precipitated by β-
blocker medications impairing the normal BP (and heart rate) rise
with exercise,11 abnormal sympathetic control, pulmonary vascu-
lar disease or central venous obstruction restricting blood flow.2
Severe coronary artery disease is associated with exercise
hypotension occurring in the early phase of testing (for example,
o5 min), whereas other causes are more likely in patients with
late onset hypotension.12 Incidence of exercise hypotension is
o2% of treadmill exercise-stress tests, with early onset six times
less frequent than late onset.12 Exercise hypotension is assumed
to be a grave prognostic sign due to the relation with severe
disease. Indeed, a recent meta-analysis confirmed the indepen-
dent association of low exercise BP with cardiovascular events and
all-cause mortality in patients undergoing clinically indicated
stress testing.13 Although there was evidence of publication bias
towards positive results, increased risk was evident irrespective of
clinical presentation, exercise mode (treadmill or bike), exercise
intensity or the criteria used to define exercise hypotension.13
HYPERTENSIVE RESPONSE TO EXERCISE: MECHANISMS AND
CLINICAL RELEVANCE
An excessive rise in BP during exercise is a relative indication for
test termination, with SBP 4250 mm Hg and DBP 4115 mm Hg as
the thresholds.11 These cut points are based on expert opinion
that patient safety with respect to myocardial or cerebral vascular
effects may be compromised at high exercise BP levels. While it is
clear that chronic hypertension is a major risk factor for
© 2015 Macmillan Publishers Limited

cardiovascular mortality,14 it is not known if a transient
hypertensive reaction to exercise per se has adverse health effects
during exercise or in the immediate (hours) to mid-term (days,
weeks) period after exercise. In patients with coronary artery
disease, serious adverse events of acute myocardial infarction or
death during exercise stress testing are rare (0.1% incidence)11
and exercise stress testing appears to be safe even in patients with
abdominal aortic aneurysms.15 Large arteries can sustain exceed-
ingly high pressures as there is a 'protective' transfer of load
bearing to stiffened collagen fibres with increasing distending
pressure.16 In the setting of resistance exercise, intra-arterial
brachial BP values have been recorded as high as 480/350 mm Hg
in healthy men,17 although these intravascular pressures probably
overstate the transmural wall stresses in the heart and major
blood vessels because intrathoracic pressures have also been
observed to increase dramatically during power lifting and
valsalva.18 These data tend to reassure that the BP threshold
levels recommended as an indication to stop exercise are
conservative.
As alluded above, data from the general population have
determined that maximal intensity of SBP ⩾ 210 mm Hg (men) and
⩾ 190 mm Hg (women), and DBP ⩾ 110 mm Hg (both sexes)
represent abnormally high exercise BP responses.4 A potential
caveat is that these recommendations are suggested for normal
clinical populations rather than in healthy young subjects and
athletes in which higher BPs have been documented.18–20 There is
some rationale for focusing on BP measurement at standardized
work levels. As an example, a young fit subject may progressively
increase systolic BP well in excess of 200 mm Hg at 20 METS
exercise intensity representing proficient vascular dilation and
compliance which is able to 'absorb' the very large increase in
exercise stroke volumes. This is markedly different to the same BP
being recorded at only six METS. Therefore, as a means of
comparing BP responses at standardized COs, it seems logical to
compare BP at low or moderate exercise intensity. The amplitude
of the SBP rise from resting values, and how this may differ among
patient populations (for example, hypertension ± diabetes or
chronic kidney disease) could also provide meaningful clinical
information, but this is yet to be clarified.
Only desparate information on select populations is available as
to what may constitute a hypertensive response to submaximal
exercise.7,10,21,22 One study indicated that SBP ⩾ 150 mm Hg
experienced at moderate intensity treadmill exercise (five METS/
Bruce protocol stage 2) may denote increased risk related to left
ventricular hypertrophy,23 but more work is needed to clarify
submaximal exercise hypertension thresholds. Moderate, but not
maximal, intensity BP has been shown to independently predict
increased left ventricular mass24 as well as long term (years)
incidence of cardiovascular events and mortality.25 Moreover, only
low intensity exercise is needed to unmask BP irregularities (that
is, masked hypertension) that would otherwise be missed by
resting BP screening methods.26 This may be because resting BP is
subjected to variability from the influence of factors such as noise,
talking or nervousness, whereas exercise BP remains less affected
and thereby able to unveil BP problems.27 Altogether these data
raise the possibility that abnormally high exercise BP at low to
moderate intensity could signal the presence of increased risk
associated with hypertension, and should provide impetus to
consider measuring out-of-clinic BP to confirm true underlying BP
control (that is, according to 24-h ambulatory BP or home BP
monitoring).28,29 This hypothesis is yet to be confirmed with
randomized, controlled data.
People with a hypertensive response to exercise present with
end organ damage similar to that of those with sustained
hypertension (for example, albuminuria,30 left ventricular
hypertrophy31,32 and diastolic dysfunction33). Excessive exercise
BP predicts long term development of sustained hypertension34,35
and is common in patients with higher resting BP (whether
© 2015 Macmillan Publishers Limited
Exercise blood pressure: measurement and relevance
JE Sharman and A LaGerche
353
treated or untreated),9 masked hypertension26,36 and type 2
diabetes mellitus.32 Beyond excessive rises in BP during exercise,
patients with inadequate decline (or paradoxical rise) of SBP in the
postexercise recovery period are at higher risk of new onset
hypertension, coronary artery disease, acute myocardial infarction
and cardiovascular mortality.37–40 Moreover, it seems that co-
occurrence of delayed reductions in both SBP and heart rate
during postexercise recovery interact to provide stronger cardio-
vascular risk prediction than as individual risk components.41
Although there are many definitions of abnormal postexercise
decline in SBP and heart rate, an SBP ratio of ⩾ 0.90 (defined as
third minute recovery SBP to peak exercise SBP ratio) or a heart
rate recovery ⩽ 23 bpm (defined as the difference between peak
exercise heart rate and 1 min of recovery heart rate) have been
shown to have prognostic importance41 and underscore the value
of considering both SBP and heart rate recovery responses when
identifying risk with exercise stress testing.
Mechanistic studies have shown that exaggerated exercise BP
may be mediated by numerous factors including, augmented
reflex pressor responses through enhanced activation of
metaboreceptors,42 increased sympathetic vasoconstriction in
exercising muscles,43 diminished nitric oxide44 and prostaglandin
bioavailability.45 Higher exercise SBP is also associated with
dyslipidaemia, smoking, higher body mass index,8 increased
aortic8,30 and systemic large artery stiffness,46 as well as brachial
endothelial dysfunction8,47 (possibly through an impaired nitric
oxide/cyclic GMP pathway),48 inappropriate aldosterone activity49
and impaired glucose metabolism.50 Reduction in exercise BP is
achievable through antihypertensive medication51 or exercise
training,52,53 even in older men using resistance training.54
Table 1 provides a summary comparison of the definitions, causes
and consequences of exercise hypotension and hypertension.
METHODS TO ASSESS EXERCISE BP
Although automated sphygmomanometry and oscillometric
devices validated to measure BP during exercise are
available,55–57 manual cuff auscultation is the most commonly
employed method because it is easier and does not require
expensive automated equipment.58 Mercury sphygmoman-
ometers have been taken out of use due to toxicity concerns
and have been replaced with aneroid and automated BP
monitors.59 A mercury-free light-emitting diode BP device that
has similar operating features to conventional mercury column
cuff BP also appears to provide a viable alternative.60 Aneroid
devices have intricate mechanical systems that can lose accuracy
over time and have greater variability compared with mercury
sphygmomanometry. Accordingly, they should be regularly
checked for accuracy (6–12 months).61,62 Monitors need to be
tested for validity during exercise according to international
protocol63 because it cannot be assumed that devices that are
accurate at rest will perform satisfactorily during exercise.
Low to moderate intensity exercise BP can be recorded with
greater accuracy than at maximal intensity due to less artefact.64
Noise from subject footfalls, movement or mechanical factors (for
example, treadmill/cycle operation) can mask Korotkoff sounds
and lead to underestimation of SBP (Korotkoff phase I, clear
tapping), as well as difficulty in discerning DBP by separating
Korotkoff phase IV (muffling) from phase V (disappearance of
sound).64 Altogether these problems lead to greater difficulty in
measuring accurate exercise DBP in particular.65 Another method
of measuring exercise BP includes finger photoplethysmography
which enables continuous monitoring and is an advantage for
assessing acute BP changes such as with tilt table testing and in
research at lower exercise intensity,66–68 but is less relevant to
clinical exercise stress testing due to the specialized technique
and greater variability at higher exercise intensities.69,70
Journal of Human Hypertension (2015) 351 – 358
 Exercise blood pressure: measurement and relevance
JE Sharman and A LaGerche
354
Table 1. Summary on the definitions, possible causes and consequences of abnormal exercise blood pressure (BP) responses
Exercise Definitions
response
Hypotension 1. Drop in SBP 410 mm Hg
(persistently below baseline), despite
an increase in workload, when
accompanied by any other evidence
of ischaemia.
2. SBP fall 420 mm Hg from the
highest value during the test.
3. Failure of SBP to increase with
increased workload.
Hypertension 1. Maximal exercise SBP ⩾ 210 mm Hg
(men) or ⩾ 190 mm Hg (women).
Maximal exercise DBP ⩾ 110 mm Hg
(men and women).
2. Limited data with respect to
submaximal exercise BP, but SBP
⩾ 150 mm Hg at moderate intensity
(five METS) may be a discriminatory
threshold.
Abbreviations: DBP, diastolic BP; METS, metabolic equivalents; SBP, systolic BP.
Table 2. Summary of methods to measure exercise blood pressure (BP)
Method Technique
Manual Auscultation using aneroid or
brachial cuff mercury-free light-emitting diode
devices
Automated Automated auscultation or
brachial cuff oscillometry
Finger cuff Digit photo/plethysmography
Indwelling Direct pressure waveform analysis
catheter
Abbreviation: SBP, systolic BP.
A summary of the methods that may be used to measure exercise
BP are provided in Table 2.
RECOMMENDED METHOD FOR MEASUREMENT OF
EXERCISE BP
The guide to measuring BP (before, during and after exercise)
described below, and summarised in Table 3, is a compilation of
recommendations from peak professional bodies3,11,58,71,72 and
basic BP measurement principles.61,70 The BP operator should
Journal of Human Hypertension (2015) 351 – 358
Possible causes Possible consequences
Cardiac Increased risk for cardiovascular
Severe left ventricular dysfunction, events and all-cause mortality.
obstruction to aortic outflow or severe
myocardial ischaemia.
Other
Abnormal sympathetic control, pulmonary
vascular disease, central venous obstruction
restricting blood flow, β-blocker medications.
Correlates Increased risk for cardiovascular
Pre-existing hypertension, masked events and cardiovascular mortality.
hypertension, impaired glucose metabolism Higher prevalence of end organ
(type 2 diabetes mellitus), dyslipidaemia, damage related to hypertension
smoking, higher body mass index, aortic (albuminuria, left ventricular
and large artery stiffness, impaired brachial hypertrophy/diastolic dysfunction).
endothelial function.
Mechanisms
Augmented reflex pressor responses through
enhanced activation of metaboreceptors,
increased sympathetic vasoconstriction in
exercising muscles, decreased nitric oxide
and prostaglandin bioavailability,
Advantages Disadvantages
Similar mode of operation to conventional Aneroid—intricate mechanical parts,
mercury sphygmomanometry prone to inaccuracy over time—need
Inexpensive regular checking
Relatively easy to use Operator skill required
Movement and noise artefact disrupt
accuracy
Operator free Expensive specialized equipment not
widely available
Occasional erratic readings due to
artefact
Continuous monitoring of acute BP Amplification of SBP from upper arm
responses (for example, tilt table, drugs) to finger overestimates brachial SBP
Other haemodynamic variables able to be Synthesised brachial BP from finger
estimated from pulse contour algorithms waveform algorithm
(for example, cardiac output, pulse rate Finger must be at heart level
variability) Wide variability at higher exercise
intensities
High level accuracy Invasive; specialized, expensive
Continuous monitoring of acute BP equipment—not available for
responses widespread use
Not without risk to patients
have adequate hearing and sight, be appropriately trained,
measure BP to the nearest 2 mm Hg and immediately record
after each measurement.63,73 For manual BP, the monitor should
be within 1 m of the observer and viewed straight on to the centre
of the face of the gauge.61 A correct sized cuff should be used
because an undersized cuff will overestimate BP, whereas an
oversized cuff will underestimate BP. The location of cuff
placement should be free of clothing and the cuff placed with
the lower edge about 2–3 cm above the point of brachial artery
auscultation.61 Place the bell (better sound production) or
© 2015 Macmillan Publishers Limited

Table 3. Summary of recommendations for exercise blood pressure
(BP) monitoring
Pre-exercise
Measure supine BP
Measure BP in the posture of exercise (e.g., standing for treadmill,
seated for cycling)
SBP or DBP 4200/110 mm Hg is a relative contraindication to
exercise testing
During exercise
Measure BP each 2–3 min (last 45 s of each stage/interval) or more
frequently in high-risk subjects
For manual measurement inflate to ~ 30 mm Hg above SBP and
deflate at 2–3 mm Hg s − 1
Due to wide pulse pressure during exercise, once SBP is
determined manually, rapid cuff deflation to ~ 10 mm Hg above
previously measured DBP can be used before returning to deflate
at 2–3 mm Hg s − 1 to measure DBP
For manual measurement use Korotokoff phase I and V for SBP
and DBP, respectively, but take phase IV as DBP where sounds can
be heard to very low DBP
Report BP within 2 mm Hg where possible
Confirm abnormal hypotensive or hypertensive responses using
automatic devices with manual cuff auscultation and respond
with test termination as appropriate
Technical difficulties with inability to measure SBP is an absolute
indication for test termination
After exercise
Measure BP immediately postexercise and every 2 min for 6–8 min
or longer if BP has not returned to near baseline levels
Organise follow-up testing for subjects with abnormal exercise BP
responses
Clean BP cuffs and tubing by wiping with a cleaning solution after
each use
Inspect equipment for leakage/damage
Abbreviations: DBP, diastolic BP; SBP, systolic BP. Adapted from3,52,64–66.
diaphragm (better surface coverage) end of the stethoscope
gently over the brachial artery, avoiding clothing and tubing.
Excessive pressure of the stethoscope should be prevented as this
can produce sounds below DBP due to distortion of the artery.61
There is scarce data on the reproducibility of manual BP
measurement during exercise. There is a potential for 'regression
to the mean' by which the challenges of exercise BP measurement
results in estimation toward normative values.
Measure pretest resting BP in the supine position, as well as the
posture of exercise. Minimise error by avoiding talking with the
subject during the pre-exercise BP measures and ensure the arm is
supported with the cuff at heart level for all measures.70 For
standing and exercise BP, this can be achieved by having the
subject place their hand or forearm on the shoulder of the
operator (padded/protected with a folded towel) standing at
lower level to the subject on the treadmill or bicycle. The subject
should be advised to relax all tension in the arm and shoulder
when measuring BP, because isometric muscle contraction may
increase recorded BP values.70 Inflate the cuff rapidly to ~ 30
mm Hg above SBP and deflate at 2–3 mm Hg s − 1. Once SBP is
determined, rapid cuff deflation to ~ 10 mm Hg above previously
measured DBP can be used to traverse the wide pulse pressure
before resuming deflation at 2–3 mm Hg s − 1. In some subjects,
Korotkoff phase IV can continue to very low DBP including all the
way to 0 mm Hg. In such cases the onset of phase IV should be
taken as DBP.9,61
During exercise, BP should be recorded every 2–3 min, which is
usually in the last 45 s of each exercise stage or interval. However,
more frequent measurement may be needed with higher risk
© 2015 Macmillan Publishers Limited
Exercise blood pressure: measurement and relevance
JE Sharman and A LaGerche
355
Table 4. General operator information on exercise blood pressure (BP)
measurement
Use manual cuff auscultation or validated automatic BP device
with correct sized cuff
Ensure that a variety of cuff sizes are available (small, normal and
large)
Position the BP monitor within 1 m of the operator and view the
gauge straight on
Avoid excess stethoscope pressure as this can distort artery and
produce sounds below diastolic BP
Measure BP each time with the cuff supported at heart level,
shoulder/arm relaxed and no talking during pre-exercise measures
(subject can place hand on the shoulder of the operator—covered
with folded towel)
Subjects to avoid gripping tightly to the treadmill rails
Use a rating of perceived exertion scale in the last 5 s of each
minute as a guide to when the last BP measure may be acquired
relative to stopping
If using an automatic BP device, test reliability by comparison with
manual cuff auscultation before routine use
Follow calibration and maintenance procedures for the BP device
according to manufacturer's directions
Compare readings of automated devices with manual cuff
auscultation on a monthly basis
subjects.71 Due to time constraints of graded exercise protocols,
singular BP measures are usually acquired at each interval,
although duplicates can be recorded in the event of uncertainty
as to correct measurement or to confirm abnormal (hypotensive
or hypertensive) responses measured by automated device. The
BP operator should keep good verbal contact with the exercising
subject to gauge an estimation of time to stopping exercise due to
fatigue, and take measures of BP accordingly. Objective measures
of effort such as the Borg scale administered in the final seconds
of each exercise level is useful to guide the amount of time left
within a stage to measure BP. Subjects can steady themselves by
lightly holding the front or side rails of the treadmill, but should
not grip tightly as this can reduce workload by supporting body
weight.11 Follow up tests to confirm BP control (for example,
home BP or 24-h ambulatory BP) is advised in subjects with
exercise hypertension.29 A hypotensive response to exercise
should be considered a serious sign given its association with
serious cardiac disease and adverse outcomes. Patients should be
investigated further with tests of greater specificity pertinent to
the suspected pathology—for example, coronary angiography for
ischaemic heart disease, echocardiography and/or catheterization
for heart failure, pulmonary hypertension or valvular heart disease.
General BP operator principles are summarised in Table 4 and
Figure 2.
SUMMARY AND CONCLUSIONS
Aerobic exercise is an excellent modality for exposing BP
abnormalities and serious underlying disease that may not be
evident under resting conditions. Thus, an important component
of clinical exercise stress testing is vigilant care to correctly
measure BP using a standardized protocol with appropriately
validated equipment. Abnormal exercise BP responses can then
be acted on with confidence. Although a significant body of
evidence indicates that exercise hypotension is a serious sign of
disease, there are several evidence gaps with respect to exercise
hypertension. In particular, the establishment of normative and
reference values for excessive submaximal exercise BP responses,
and suitable clinical pathway/s for 'hypertensive responders' are
needed. With millions of exercise stress tests performed inter-
nationally each year, accurate exercise BP measures offer
Journal of Human Hypertension (2015) 351 – 358
 Exercise blood pressure: measurement and relevance
JE Sharman and A LaGerche
356
Figure 2. Example set up for appropriate blood pressure (BP) measurement by manual auscultation during exercise stress testing.
additional clinical information as well as opportunity to improve
patient care above and beyond other conventional exercise-stress
test parameters.
CONFLICT OF INTEREST
The authors declare no conflict of interest.
ACKNOWLEDGEMENTS
JES was supported by a National Health and Medical Research Council of Australia
Career Development Award (reference 1045373). AL was supported by a National
Health and Medical Research Council of Australia post-doctoral scholarship.
REFERENCES
1 Hambrecht RP, Schuler GC, Muth T, Grunze MF, Marburger CT, Niebauer J et al.
Greater diagnostic sensitivity of treadmill versus cycle exercise testing of
asymptomatic men with coronary artery disease. Am J Cardiol 1992; 70: 141–146.
2 American Thoracic Society American College of Chest Physicians. ATS/ACCP
Statement on cardiopulmonary exercise testing. Am J Respir Crit Care Med 2003;
167: 211–277.
3 Linda SP (eds). American College of Sports Medicine. ACSM's Guidelines for Exercise
Testing and Prescription. 9th edn Wolters Kluwer: Philadelphia, PA, USA, 2014.
4 Lauer MS, Levy D, Anderson KM, Plehn JF. Is there a relationship between exercise
systolic blood pressure response and left ventricular mass? The Framingham
Heart Study. Ann Intern Med 1992; 116: 203–210.
5 Daida H, Allison TG, Squires RW, Miller TD, Gau GT. Peak exercise blood pressure
stratified by age and gender in apparently healthy subjects. Mayo Clin Proc 1996;
71: 445–452.
6 Criqui MH, Haskell WL, Heiss G, Tyroler HA, Green P, Rubenstein CJ. Predictors of
systolic blood pressure response to treadmill exercise: the Lipid Research Clinics
Program Prevalence Study. Circulation 1983; 68: 225–233.
7 Menghini F, Dally L, Fazzini PF, Menotti A, Prati PL, Rovelli F et al. Normal beha-
viour of circulatory parameters during exercise. Reference values for heart rate
and systemic blood pressure. The ECCIS Project data. Epidemiologia e Clinica della
Cardiopatia Ischemica Silente. G Ital Cardiol 1995; 25: 967–975.
Journal of Human Hypertension (2015) 351 – 358
8 Thanassoulis G, Lyass A, Benjamin EJ, Larson MG, Vita JA, Levy D et al. Relations of
exercise blood pressure response to cardiovascular risk factors and vascular
function in the framingham heart study. Circulation 2012; 125: 2836–2843.
9 Irving JB, Bruce RA, DeRouen TA. Variations in and significance of systolic pressure
during maximal exercise (treadmill) testing. Am J Cardiol 1977; 39: 841–848.
10 Kokkinos PF, Andreas PE, Coutoulakis E, Colleran JA, Narayan P, Dotson CO et al.
Determinants of exercise blood pressure response in normotensive and hyper-
tensive women: role of cardiorespiratory fitness. J Cardiopulm Rehabil 2002; 22:
178–183.
11 Fletcher GF, Balady GJ, Amsterdam EA, Chaitman B, Eckel R, Fleg J et al. Exercise
standards for testing and training: a statement for healthcare professionals from
the American Heart Association. Circulation 2001; 104: 1694–1740.
12 Watson G, Mechling E, Ewy GA. Clinical significance of early vs late hypotensive
blood pressure response to treadmill exercise. Arch Intern Med 1992; 152:
1005–1008.
13 Barlow PA, Otahal P, Schultz MG, Shing CM, Sharman JE. Low exercise blood
pressure and risk of cardiovascular events and all-cause mortality: systematic
review and meta-analysis. Atherosclerosis 2014; 237: 13–22.
14 Lewington S, Clarke R, Qizilbash N, Peto R, Collins R. Age-specific relevance of
usual blood pressure to vascular mortality: a meta-analysis of individual data for
one million adults in 61 prospective studies. Lancet 2002; 360: 1903–1913.
15 Best PJ, Tajik AJ, Gibbons RJ, Pellikka PA. The safety of treadmill exercise stress
testing in patients with abdominal aortic aneurysms. Ann Intern Med 1998; 129:
628–631.
16 Armentano RL, Levenson J, Barra JG, Fischer EI, Breitbart GJ, Pichel RH et al.
Assessment of elastin and collagen contribution to aortic elasticity in
conscious dogs. Am J Physiol 1991; 260: H1870–H1877.
17 MacDougall JD, Tuxen D, Sale DG, Moroz JR, Sutton JR. Arterial blood pressure
response to heavy resistance exercise. J Appl Physiol 1985; 58: 785–790.
18 Haykowsky M, Taylor D, Teo K, Quinney A, Humen D. Left ventricular wall stress
during leg-press exercise performed with a brief Valsalva maneuver. Chest 2001;
119: 150–154.
19 La Gerche A, MacIsaac AI, Burns AT, Mooney DJ, Inder WJ, Voigt JU et al. Pul-
monary transit of agitated contrast is associated with enhanced pulmonary vas-
cular reserve and right ventricular function during exercise. J Appl Physiol 2010;
109: 1307–1317.
20 Palatini P, Mos L, Mormino P, Munari L, Del Torre M, Valle F et al. Intra-arterial
blood pressure monitoring in the evaluation of the hypertensive athlete. Eur Heart
J 1990; 11: 348–354.
© 2015 Macmillan Publishers Limited

21 Itoh H, Ajisaka R, Koike A, Makita S, Omiya K, Kato Y et al. Heart rate and
blood pressure response to ramp exercise and exercise capacity in relation
to age, gender, and mode of exercise in a healthy population. J Cardiol 2013; 61:
71–78.
22 Wolthuis R, Froelicher V Jr, Fischer J, Triebwasser J. The response of healthy men
to treadmill exercise. Circulation 1977; 55: 153–157.
23 Kokkinos P, Pittaras A, Narayan P, Faselis C, Singh S, Manolis A. Exercise capacity
and blood pressure associations with left ventricular mass in prehypertensive
individuals. Hypertension 2007; 49: 55–61.
24 Lim PO, Donnan PT, MacDonald TM. Blood pressure determinants of left ven-
tricular wall thickness and mass index in hypertension: comparing office, ambu-
latory and exercise blood pressures. J Hum Hypertens 2001; 15: 627–633.
25 Schultz MG, Otahal P, Cleland VJ, Blizzard L, Marwick TH, Sharman JE. Exercise-
induced hypertension, cardiovascular events, and mortality in patients under-
going exercise stress testing: a systematic review and meta-analysis. Am J
Hypertens 2013; 26: 357–366.
26 Schultz MG, Hare JL, Marwick TH, Stowasser M, Sharman JE. Masked hypertension
is ‘unmasked’ by low-intensity exercise blood pressure. Blood Press 2011; 20:
284–289.
27 Sharman JE. New insights into cardiovascular risk from the exercise central
waveform. Artery Research 2009; 2: 132–137.
28 Cuspidi C. Is exaggerated exercise blood pressure increase related to masked
hypertension. Am J Hypertens 2011; 24: 861.
29 Mancia G, Fagard R, Narkiewicz K, Redón J, Zanchetti A, Böhm M et al. 2013 ESH/
ESC Guidelines for the management of arterial hypertension: the Task Force for
the management of arterial hypertension of the European Society of Hyperten-
sion (ESH) and of the European Society of Cardiology (ESC). J Hypertens 2013; 31:
1281–1357.
30 Tsioufis C, Dimitriadis K, Thomopoulos C, Tsiachris D, Selima M, Stefanadi E et al.
Exercise blood pressure response, albuminuria, and arterial stiffness in hyper-
tension. Am J Med 2008; 121: 894–902.
31 Sharman JE, Hare JL, Thomas S, Davies JE, Leano R, Jenkins C et al. Association of
masked hypertension and left ventricular remodeling with the hypertensive
response to exercise. Am J Hypertens 2011; 24: 898–903.
32 Scott JA, Coombes JS, Prins JB, Leano RL, Marwick TH, Sharman JE. Patients with
type 2 diabetes have exaggerated brachial and central exercise blood pressure:
Relation to left ventricular relative wall thickness. Am J Hypertens 2008; 21:
715–721.
33 Tsioufis C, Chatzis D, Tsiachris D, Katsi V, Toutouzas K, Tousoulis D et al. Exag-
gerated exercise blood pressure response is related to tissue Doppler imaging
estimated diastolic dysfunction in the early stages of hypertension. J Am Soc
Hypertens 2008; 2: 158–164.
34 Holmqvist L, Mortensen L, Kanckos C, Ljungman C, Mehlig K, Manhem K. Exercise
blood pressure and the risk of future hypertension. J Hum Hypertens 2012; 26:
691–695.
35 Laukkanen JA, Kurl S. Blood pressure responses during exercise testing-is up best
for prognosis?. Ann Med 2012; 44: 218–224.
36 Kayrak M, Bacaksiz A, Vatankulu MA, Ayhan SS, Kaya Z, Ari H et al. Exaggerated
Blood Pressure Response to Exercise—A New Portent of Masked Hypertension.
Clin Exp Hypertens 2010; 32: 560–568.
37 Singh JP, Larson MG, Manolio TA, O'Donnell CJ, Lauer M, Evans JC et al. Blood
pressure response during treadmill testing as a risk factor for new-onset hyper-
tension: the Framingham Heart Study. Circulation 1999; 99: 1831–1836.
38 McHam SA, Marwick TH, Pashkow FJ, Lauer MS. Delayed systolic blood pressure
recovery after graded exercise: an independent correlate of angiographic cor-
onary disease. J Am Coll Cardiol 1999; 34: 754–759.
39 Laukkanen JA, Kurl S, Salonen R, Lakka TA, Rauramaa R, Salonen JT. Systolic blood
pressure during recovery from exercise and the risk of acute myocardial infarction
in middle-aged men. Hypertension 2004; 44: 820–825.
40 Huang C-L, Su T-C, Chen W-J, Lin L-Y, Wang W-L, Feng M-H et al. Usefulness of
paradoxical systolic blood pressure increase after exercise as a predictor of car-
diovascular mortality. Am J Cardiol 2008; 102: 518–523.
41 Michaelides AP, Liakos CI, Vyssoulis GP, Chatzistamatiou EI, Markou MI, Tzamou V
et al. The interplay of exercise heart rate and blood pressure as a predictor of
coronary artery disease and arterial hypertension. J Clin Hypertens 2013; 15:
162–170.
42 Choi HM, Stebbins CL, Lee OT, Nho H, Lee JH, Chun JM et al. Augmentation of the
exercise pressor reflex in prehypertension: roles of the muscle metaboreflex and
mechanoreflex. Appl Physiol Nutr Metab 2013; 38: 209–215.
43 Vongpatanasin W, Wang Z, Arbique D, Arbique G, Adams-Huet B, Mitchell JH et al.
Functional sympatholysis is impaired in hypertensive humans. J Physiol 2011; 589:
1209–1220.
44 Campbell R, Fisher JP, Sharman JE, McDonnell BJ, Frenneaux MP. Contribution of
nitric oxide to the blood pressure and arterial responses to exercise in humans.
J Hum Hypertens 2011; 25: 262–270.
© 2015 Macmillan Publishers Limited
Exercise blood pressure: measurement and relevance
JE Sharman and A LaGerche
357
45 Cowley AJ, Stainer K, Rowley JM, Wilcox RG. Effect of aspirin and indomethacin on
exercise-induced changes in blood pressure and limb blood flow in normal
volunteers. Cardiovasc Res 1985; 19: 177–180.
46 Sung J, Choi SH, Choi YH, Kim DK, Park WH. The relationship between arterial
stiffness and increase in blood pressure during exercise in normotensive persons.
J Hypertens 2012; 30: 587–591.
47 Stewart KJ, Sung J, Silber HA, Fleg JL, Kelemen MD, Turner KL et al. Exaggerated
exercise blood pressure is related to impaired endothelial vasodilator function.
Am J Hypertens 2004; 17: 314–320.
48 Chang HJ, Chung JH, Choi BJ, Choi TY, Choi SY, Yoon MH et al. Endothelial
dysfunction and alteration of nitric oxide/cyclic GMP pathway in patients with
exercise-induced hypertension. Yonsei Med J 2003; 44: 1014–1020.
49 Lim PO, Donnan PT, MacDonald TM. Aldosterone to renin ratio as a determinant
of exercise blood pressure response in hypertensive patients. J Hum Hypertens
2001; 15: 119–123.
50 Papavasileiou MV, Thomopoulos C, Antoniou I, Papadimitriou G, Seferou M,
Makris TK. Impaired glucose metabolism and the exaggerated blood pressure
response to exercise treadmill testing in normotensive patients. J Clin Hypertens
2009; 11: 627–635.
51 Omvik P, Lund-Johansen P. Long-term hemodynamic effects at rest and during
exercise of newer antihypertensive agents and salt restriction in essential
hypertension: review of epanolol, doxazosin, amlodipine, felodipine, diltiazem,
lisinopril, dilevalol, carvedilol, and ketanserin. Cardiovasc Drugs Ther 1993; 7:
193–206.
52 Swift DL, Earnest CP, Katzmarzyk PT, Rankinen T, Blair SN, Church TS. The
effect of different doses of aerobic exercise training on exercise blood pressure
in overweight and obese postmenopausal women. Menopause 2012; 19:
503–509.
53 Cornelissen VA, Verheyden B, Aubert AE, Fagard RH. Effects of aerobic training
intensity on resting, exercise and post-exercise blood pressure, heart rate and
heart-rate variability. J Hum Hypertens 2010; 24: 175–182.
54 Lovell DI, Cuneo R, Gass GC. Resistance training reduces the blood pressure
response of older men during submaximum aerobic exercise. Blood Press Monit
2009; 14: 137–144.
55 Griffin SE, Robergs RA, Heyward VH. Blood pressure measurement during exercise:
a review. Med Sci Sports Exerc 1997; 29: 149–159.
56 Cameron JD, Stevenson I, Reed E, McGrath BP, Dart AM, Kingwell BA. Accuracy of
automated auscultatory blood pressure measurement during supine exercise
and treadmill stress electrocardiogram-testing. Blood Press Monit 2004; 9:
269–275.
57 MacRae HS, Allen PJ. Automated blood pressure measurement at rest and during
exercise: evaluation of the motion tolerant CardioDyne NBP 2000. Med Sci Sports
Exerc 1998; 30: 328–331.
58 Myers J, Arena R, Franklin B, Pina I, Kraus WE, McInnis K et al. Recommendations
for clinical exercise laboratories: a scientific statement from the american heart
association. Circulation 2009; 119: 3144–3161.
59 O'Brien E. Replacing the mercury sphygmomanometer. Br Med J 2000; 320(7238):
815–816.
60 Stergiou GS, Giovas PP, Gkinos CP, Tzamouranis DG. Validation of the A&D
UM-101 professional hybrid device for office blood pressure measurement
according to the International Protocol. Blood Press Monit 2008; 13: 37–42.
61 Beevers G, Lip GY, O'Brien E. ABC of hypertension: blood pressure measurement.
Part II-conventional sphygmomanometry: technique of auscultatory blood pres-
sure measurement. Br Med J 2001; 322: 1043–1047.
62 Burke MJ, Towers HM, O'Malley K, Fitzgerald DJ, O'Brien ET. Sphygmomanometers
in hospital and family practice: problems and recommendations. Br Med J 1982;
285: 469–471.
63 O'Brien E, Atkins N, Stergiou G, Karpettas N, Parati G, Asmar R et al.
European Society of Hypertension International Protocol revision 2010 for the
validation of blood pressure measuring devices in adults. Blood Press Monit 2010;
15: 23–38.
64 Lightfoot JT, Tuller B, Williams DF. Ambient noise interferes with auscultatory
blood pressure measurement during exercise. Med Sci Sports Exerc 1996; 28:
502–508.
65 Sagiv M, Ben-Sira D, Goldhammer E. Direct vs indirect blood pressure measure-
ment at peak anaerobic exercise. Int J Sports Med 1999; 20: 275–278.
66 Jellema WT, Imholz BP, van Goudoever J, Wesseling KH, van Lieshout JJ. Finger
arterial versus intrabrachial pressure and continuous cardiac output during head-
up tilt testing in healthy subjects. Clin Sci 1996; 91: 193–200.
67 Eckert S, Horstkotte D. Comparison of Portapres non-invasive blood pressure
measurement in the finger with intra-aortic pressure measurement during
incremental bicycle exercise. Blood Press Monit 2002; 7: 179–183.
68 Eeftinck Schattenkerk DW, van Lieshout JJ, van den Meiracker AH, Wesseling KR,
Blanc S, Wieling W et al. Nexfin noninvasive continuous blood pressure validated
against Riva-Rocci/Korotkoff. Am J Hypertens 2009; 22: 378–383.
Journal of Human Hypertension (2015) 351 – 358
 Exercise blood pressure: measurement and relevance
JE Sharman and A LaGerche
358
69 Buclin T, Buchwalder-Csajka C, Brunner HR, Biollaz J. Evaluation of noninvasive
blood pressure recording by photoplethysmography in clinical studies using
angiotensin challenges. Br J Clin Pharmacol 1999; 48: 586–593.
70 Pickering TG, Hall JE, Appel LJ, Falkner BE, Graves J, Hill MN et al. Recommen-
dations for blood pressure measurement in humans and experimental animals:
Part 1: blood pressure measurement in humans: a statement for professionals
from the Subcommittee of Professional and Public Education of the American
Heart Association Council on High Blood Pressure Research. Hypertension 2005;
45: 142–161.
Journal of Human Hypertension (2015) 351 – 358
71 Balady GJ, Arena R, Sietsema K, Myers J, Coke L, Fletcher GF et al. Clinician’s guide
to cardiopulmonary exercise testing in adults: a scientific statement from the
American Heart Association. Circulation 2010; 122: 191–225.
72 Fletcher GF, Ades PA, Kligfield P, Arena R, Balady GJ, Bittner VA et al. Exercise
standards for testing and training: a scientific statement from the American Heart
Association. Circulation 2013; 128: 873–934.
73 O'Brien E, Mee F, Tan KS, Atkins N, O'Malley K. Training and assessment of
observers for blood pressure measurement in hypertension research. J Hum
Hypertens 1991; 5: 7–10.
© 2015 Macmillan Publishers Limited