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.
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 >200 mm Hg or diastolic BP; DBP >120 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 abnormalities (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 exercise stress testing worldwide each year, the exercise BP 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 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 <210 mm Hg (men) and SBP <190 mm Hg (women) with DBP <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 >40 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, <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, body mass index, dyslipidemia, lower cardiorespiratory fitness and treadmill time to exhaustion.8, 9, 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 >10 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 >20 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 vascular 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, <5 min), whereas other causes are more likely in patients with late onset hypotension.12 Incidence of exercise hypotension is <2% 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 independent 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 >250 mm Hg and DBP >115 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 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 exceedingly 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, 19, 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 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, 38, 39, 40 Moreover, it seems that co-occurrence of delayed reductions in both SBP and heart rate during postexercise recovery interact to provide stronger cardiovascular 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, 56, 57 manual cuff auscultation is the most commonly employed method because it is easier and does not require expensive automated equipment.58 Mercury sphygmomanometers 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, 67, 68 but is less relevant to clinical exercise stress testing due to the specialized technique and greater variability at higher exercise intensities.69,70 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 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 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 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 internationally each year, accurate exercise BP measures offer additional clinical information as well as opportunity to improve patient care above and beyond other conventional exercise-stress test parameters.
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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.
The authors declare no conflict of interest.
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Sharman, J., LaGerche, A. Exercise blood pressure: clinical relevance and correct measurement. J Hum Hypertens 29, 351–358 (2015). https://doi.org/10.1038/jhh.2014.84
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