INTRODUCTION
Clinical exercise testing is performed worldwide for ischemia evaluation and functional assessment, and blood pressure (BP) is routinely recorded both as a safety measure and as a physiological readout [1]. Beyond test safety, the magnitude of the BP rise during exertion carries prognostic information that is not captured by resting BP measurement [2]. An exaggerated rise, termed exaggerated blood pressure response to exercise (EBPR), has been associated with the future development of hypertension and with cardiovascular morbidity and mortality in individuals without overt coronary disease, even after adjustment for office BP and conventional risk factors [2].
EBPR can therefore be conceptualized as an intermediate phenotype linking apparent normotension to established hypertensive disease and its sequelae. It may also unmask elevated out-of-office BP that resting clinic measurement misses. Yet this clinical promise has not translated into guideline recommendations: the 2024 European Society of Cardiology guidelines, for example, address exercise as a therapeutic intervention but do not recognize the exercise BP response as a diagnostic tool, and advise that measurement be preceded by a period without exertion [3].
A principal reason for this disconnect is that the phenomenon lacks a consensus definition and a harmonized measurement standard [4]. More broadly, the incorporation of a novel measure into clinical guidelines requires 3 fundamental elements: standardized measurement, demonstrated incremental value beyond existing diagnostic tools, and clear actionability of an abnormal result. While research on EBPR has made meaningful progress toward standardizing its measurement and definition, considerably greater uncertainty remains regarding its incremental value beyond out-of-office BP monitoring and the clinical actions that should follow an abnormal result.
This review examines the clinical significance of EBPR, identifies the remaining gaps in standardization, incremental value, and actionability that have impeded its broader guideline adoption, and discusses the developments most likely to overcome these barriers.
DEFINITION AND THE PROBLEM OF STANDARDIZATION
The same phenomenon has been described in the literature as an EBPR, a hypertensive response to exercise, exaggerated exercise BP, and exercise hypertension, and these terms are frequently used interchangeably despite resting on different physiological constructs and measurement conventions. As Mariampillai et al. [4] emphasized, there is no consensus definition of an exaggerated rise in systolic blood pressure (SBP) during exercise. This heterogeneity propagates into thresholds, protocols, and measurement timing, and is arguably the proximate reason a phenomenon with decades of supportive data has not been formalized in guidelines.
The most widely cited criterion uses sex-specific peak cut-points: peak SBP ≥ 210 mm Hg in men and ≥ 190 mm Hg in women [256]. American Heart Association exercise standards have additionally incorporated a diastolic component, a diastolic blood pressure (DBP) rise > 10 mm Hg or an absolute value of 90 mm Hg [1]. Moreover, age/sex-specific population-percentile thresholds have been suggested [7].
However, peak BP is strongly confounded by cardiorespiratory fitness: fitter individuals attain higher workloads and therefore higher peak BPs, yet exhibit lower BP relative to metabolic demand. This has motivated indexing peak exercise BP to workload achieved [8910]. Age- and sex-specific reference equations for workload-indexed SBP during cycle ergometry have been derived [11], BP indexed to workload predicts incident hypertension and stroke [12], and the recent EXERcise stress Test collaboratION (EXERTION) study reframed exercise BP as a quantity best interpreted relative to fitness rather than in absolute terms [13].
Despite this promise, the clinical utility of workload-indexed BP remains unproven. The SBP/metabolic equivalent (MET) slope is highly sensitive to how METs are estimated or to the exercise protocol, with limited comparability between treadmill and cycle-ergometer testing. It may also overestimate abnormality in patients with low exercise capacity, in whom small absolute increments in workload translate into disproportionately large changes in the indexed value and externally validated reference ranges and clinically actionable cutoffs are still lacking [8910111213].
Workload-indexed BP should therefore be regarded as a promising but not yet established measure, pending further validation.
SBP measured during submaximal exercise is also an attractive standardization target for standardization. Measurement at a predefined low-to-moderate exercise intensity may offer greater reproducibility and responsiveness to antihypertensive therapy than peak SBP, while an exaggerated response at moderate intensity has been associated with a greater risk of adverse outcomes than a similar response observed at maximal exercise [14]. In the Oslo Ischemia Study, exercise SBP at a fixed 100 Watts workload was linearly related to coronary risk, and resting SBP lost significance once the submaximal value entered the model [15].
Since then, several thresholds based on BP responses at a fixed workload or an exercise intensity have been proposed, including an exercise SBP ≥ 180 mm Hg during moderate dynamic exercise [1617] or SBP ≥ 150 mm Hg at 5 METs [18]. However, the superiority of submaximal over peak BP has not been firmly established, and the proposed thresholds are not interchangeable, as different cutoff values were derived from different populations and exercise protocols [161718]. Furthermore, 2 conceptually distinct approaches should not be conflated: definitions based on a fixed absolute workload (e.g., 100 Watts) and those based on a fixed relative exercise intensity (e.g., 5 METs).
Because a given absolute workload may represent markedly different relative intensities according to age, sex, and cardiorespiratory fitness, thresholds derived using fixed-workload and relative-intensity frameworks are not directly comparable. Accordingly, a threshold established under one framework should not be applied to the other without dedicated validation.
As summarized in Table 1 [125678910111216171819], various definitions of EBPR have been proposed across studies, each with distinct methodological and clinical limitations. One of the main obstacles to defining EBPR is that studies differ in modality (treadmill versus cycle ergometry), in the stage at which BP is recorded, and in measurement timing. Accuracy is itself a concern: auscultatory and automated oscillometric devices are challenged by motion and rapidly changing hemodynamics, and most automated devices are validated under resting conditions per the Association for the Advancement of Medical Instrumentation/European Society of Hypertension/International Organization for Standardization standard rather than during exercise [20].
Measurement technique itself introduces an additional source of variability. Manual auscultatory measurement remains the reference method during exercise but is susceptible to observer variability and the loss of Korotkoff sounds at high cardiac outputs. In contrast, automated oscillometric devices offer greater interobserver reproducibility but may be affected by motion artifacts and rapidly changing hemodynamics [21].
Arm position, including whether the arm is supported or unsupported and whether measurements are obtained on a cycle ergometer or during treadmill exercise, can further influence the recorded BP value. The exercise stage or workload at which cuff inflation is initiated, as well as the interval between cessation of limb movement and cuff inflation, may also affect the recorded value. In the absence of standardized measurement protocols, methodological differences should be carefully considered when interpreting and comparing exercise BP findings across the literature, independently of the definitional heterogeneity described above.
Collectively, this heterogeneity reduces the precision of evidence synthesis, widening confidence intervals and complicating threshold derivation—more plausibly the barrier to guideline recognition than any deficiency in the underlying biology. Recent consensus efforts, notably an Exercise and Sports Science Australia (ESSA) position statement on using exercise BP to identify uncontrolled hypertension, represent a deliberate move toward standardized protocols [22]. Convergence on submaximal or indexed-workload measurement, exercise-validated technology, and harmonized reporting is necessary, but not sufficient, to translate the prognostic signal described below into clinical recommendations.
PATHOPHYSIOLOGY OF EBPR
The normal response to dynamic exercise is a progressive rise in SBP driven by increased cardiac output, with stable or slightly falling DBP as exercising-muscle vasodilation reduces total peripheral resistance. EBPR arises when this compensatory vasodilation is insufficient relative to the rise in cardiac output, producing a disproportionate pressure load [19].
Although the precise pathophysiology underlying EBPR remains incompletely understood, current evidence suggests several plausible mechanisms that may contribute to its development. Endothelial dysfunction and reduced nitric oxide bioavailability impair exercise-induced vasodilation; impaired brachial flow-mediated dilation has been shown to explain variance in maximal exercise SBP and pulse pressure independent of resting BP [23]. Increased large-artery stiffness raises central pressure and pulse pressure during exertion and has been suggested as one of the mechanisms.
In community-based data, both arterial stiffness and impaired endothelial function correlated with the BP response to low-intensity exercise [2425]. Neurohormonal activation including sympathetic nervous system overactivity, heightened vascular responsiveness to adrenergic stimulation, and an augmented rise in angiotensin II further limits vasodilatory reserve [2225]. Additional contributors include microvascular and structural vascular changes, baroreflex dysfunction, and metabolic abnormalities such as hyperglycemia, dyslipidemia, and adiposity that cluster with EBPR and may act through vascular inflammation [25].
These mechanisms are not mutually exclusive. Rather, EBPR likely reflects an early, integrated vascular–autonomic phenotype. Importantly, the same abnormalities, such as endothelial dysfunction, arterial stiffening, and elevated central pressure, plausibly mediate the link between EBPR and downstream left ventricular (LV) remodeling, providing a mechanistic bridge from the hemodynamic phenotype to structural cardiac disease [22].
CLINICAL IMPLICATIONS
Prediction of incident hypertension
In normotensive individuals, EBPR is among the more robust predictors of future hypertension. Systematic review of normotensive cohorts has consistently linked an exaggerated exercise BP to new-onset hypertension [26], and contemporary data show that the exercise SBP response during cycle ergometry predicts incident hypertension in normotensive adults [12]. The association persists after adjustment for resting BP and conventional risk factors [1226], consistent with EBPR marking a pre-hypertensive trajectory rather than merely reflecting current BP.
Cardiovascular events and mortality
The landmark synthesis is the meta-analysis by Schultz et al. [2], which pooled 12 longitudinal studies comprising 46,314 individuals without significant coronary disease followed for a mean of 15.2 ± 4.0 years. After adjustment for age, office BP, and cardiovascular risk factors, an exaggerated response at moderate exercise intensity was associated with a 36% higher rate of cardiovascular events and mortality than in those without an exaggerated response (95% confidential interval, 1.02–1.83) [2]. Individual cohorts link exercise BP to stroke [27] and to combined cardiovascular events and new-onset hypertension during treadmill testing [28].
However, some reports have suggested a paradoxical association between EBPR and lower cardiovascular risk [2930], highlighting the heterogeneity and complexity of its prognostic implications. This apparent paradox likely reflects, at least in part, the fact that a low peak exercise SBP may itself be a marker of adverse prognosis. Chronotropic or inotropic incompetence, deconditioning, and premature test termination due to symptoms or comorbidities can all result in a low peak SBP in individuals who are nevertheless at elevated cardiovascular risk.
Accordingly, the association between peak exercise SBP and clinical outcomes may be U-shaped rather than monotonic, with both an exaggerated response and a blunted response, particularly when exercise is terminated prematurely, identifying individuals at increased risk through distinct mechanisms. Reverse causation also warrants consideration, as subclinical cardiac or vascular disease may simultaneously limit the peak SBP response and independently worsen prognosis, thereby generating an inverse association that could be mistaken for a protective effect of lower peak SBP. These interpretive challenges further underscore the limitations of peak SBP as a standalone metric and reinforce the rationale for indexing the BP response to workload or cardiorespiratory fitness.
To address this limitation, it has recently been suggested that the interpretation of peak SBP should take fitness level into account [1031]. The recent EXERTION study advanced this field by demonstrating that the prognostic interpretation of exercise BP is refined when considered relative to fitness, addressing a long-standing confounder and pointing toward more clinically actionable risk stratification [13].
Masked hypertension (MH)
EBPR is closely linked to MH, which is a phenomenon of normal clinic BP with elevated out-of-office BP. A meta-analysis by Cuspidi et al. [32] found the likelihood of EBPR markedly higher in individuals with MH than in sustained normotensives, with higher peak exercise BP in the MH group. Low-intensity exercise BP can thus unmask elevated out-of-office BP otherwise missed by resting measurement [33], supporting a role for exercise BP in detecting individuals at high risk owing to undiagnosed hypertension.
Subclinical target-organ damage and LV remodeling
Among markers of subclinical target-organ damage, LV remodeling has been consistently associated with EBPR and has been proposed as a potential structural mediator through which repeated exercise-related pressure loading may contribute to excess cardiovascular risk, although this mediating role has not been directly demonstrated. The most comprehensive synthesis, by Moore et al. [34], pooled 49 cross-sectional studies and found exercise SBP consistently associated with greater LV mass, LV mass index and relative wall thickness. Individuals with EBPR carried a 2.6-fold higher risk of LV hypertrophy and, on average, 47 g greater LV mass and 7 g/m2 greater LV mass index than those without [34].
However, because this synthesis was based exclusively on cross-sectional studies, it establishes association rather than a temporal or causal relationship, and longitudinal data directly linking exercise BP trajectories to incident LV remodeling remain lacking. A parallel meta-analysis links exercise BP to cardiovascular disease risk across cross-sectional studies [35]. These associations were broadly consistent across populations with and without resting hypertension, suggesting the structural signal is not merely a consequence of established office hypertension.
A graded relationship is also evident: in prehypertensive individuals, a submaximal exercise SBP of 150 mm Hg at 5 METs marked a threshold above which LV hypertrophy risk rose steeply, with an approximately 4-fold increase per 10 mm Hg increment beyond it [18]. Structural change is frequently accompanied by subclinical functional impairment, that is, impaired systolic function even without overt hypertrophy [36], and impaired diastolic function [37], suggesting EBPR may identify an early phase of hypertensive heart disease. Exercise BP predicts LV mass independently of office and ambulatory pressures [38], supporting an incremental, possibly mechanistic contribution, although the predominantly cross-sectional evidence base limits causal inference.
Supporting the incremental value of workload-indexed measures, one study combining the SBP/MET slope with conventional EBPR criteria found that adding the slope to EBPR significantly improved prediction of reduced diastolic relaxation, particularly among individuals without overt EBPR [10].
SPECIAL POPULATIONS
High cardiac output during intense exercise produces high absolute peak pressures in endurance athletes, so conventional thresholds may misclassify physiological adaptation as pathology. Existing criteria cannot be directly transposed to highly trained individuals, and elevated exercise SBP may reflect training adaptation rather than disease [39]. This reinforces the case for fitness- or workload-indexed interpretation [31].
It has been shown that even when absolute exercise BP was not high, patients with a higher SBP/MET slope exhibited worse indices of diastolic function [10], suggesting that fitness-adjusted SBP may be a better indicator for assessing EBPR than absolute exercise BP alone. Notably, it was suggested that individuals without EBPR are not a homogeneous low-risk group. Some exhibit a small, stiff “sedentary” left ventricle with premature exercise termination and a deceptively low peak SBP despite an elevated SBP/MET slope, whereas others show a genuinely normal BP response, suggesting distinguishing between these phenotypes may refine risk stratification [10].
This population dependence also extends to patients with established coronary artery disease or other cardiovascular disease, in whom the prognostic significance of exercise SBP may differ substantially from that observed in generally healthy individuals. In these patients, a higher exercise SBP may reflect preserved cardiac output, LV function, and exercise capacity, whereas a blunted SBP response may indicate more advanced cardiac disease, chronotropic or inotropic incompetence, or premature exercise termination [2930]. Accordingly, the prognostic significance of exercise SBP should be interpreted within the clinical context and should not be extrapolated uncritically from generally healthy cohorts to patients with established cardiovascular disease.
There are sex differences in the exercise BP rise. The traditional lower threshold for women compared to men reflects sex differences in the exercise BP response, and recent normative data characterize these differences across the age and fitness spectrum [40]. Elevated exercise BP in women has been associated with distinct LV and vascular stiffening [41], warranting sex-specific reference values.
Type 2 diabetes and metabolic syndrome are associated with a high prevalence of MH and EBPR, with elevated exercise SBP independent of other risk factors, suggesting residual, undetected BP-related risk that exercise BP may reveal [42]. Chronic kidney disease patients exhibit exaggerated exercise pressor responses associated with sympathetic overactivity, endothelial dysfunction, and reduced nitric oxide bioavailability, illustrating the mechanistic pathways in a high-risk group [43].
CLINICAL APPROACH AND MANAGEMENT
At present, no guideline endorses routine screening for EBPR, and assessment is opportunistic, typically arising when BP is recorded during exercise testing performed for other indications. Where an exaggerated response is observed, a pragmatic approach is to pursue out-of-office BP assessment to detect MH or masked uncontrolled hypertension [3233], and to intensify surveillance of conventional risk factors and target-organ damage. The ESSA consensus statement frames exercise BP specifically as a tool to identify uncontrolled hypertension, offering practical recommendations toward this end [22].
EBPR is substantially more common among individuals with MH than among sustained normotensives, and low-intensity exercise BP has been shown to unmask elevated out-of-office BP that resting measurement misses [3233]. However, the incremental value of exercise BP lies less in replacing out-of-office BP such as ambulatory or home BP monitoring, than in identifying individuals who may benefit from such testing. This triage function can be achieved opportunistically, without substantial additional cost, when BP is already measured during routine exercise testing.
Formal head-to-head comparisons of the diagnostic performance of exercise BP versus out-of-office BP monitoring for detecting MH, as well as cost-effectiveness analyses of exercise BP-triggered ambulatory monitoring, are still needed to establish the clinical utility of this approach. Thus, exercise BP should not be viewed as a substitute for established out-of-office BP measurements, but rather as an opportunistic trigger for identifying individuals who might otherwise not undergo out-of-office monitoring. Because clinic BP is normal by definition in MH, there is often no immediate clinical indication to obtain ambulatory or home BP monitoring unless another finding raises suspicion.
An exaggerated exercise BP response detected incidentally during testing performed for another indication may provide such a trigger.
The clinical action prompted by an exaggerated exercise BP response should then be tailored to the patient's clinical context. In patients receiving antihypertensive therapy, EBPR should raise suspicion of masked uncontrolled hypertension and prompt out-of-office BP assessment to confirm BP control, together with reassessment of treatment adherence and regimen intensity. In untreated individuals with otherwise normal resting BP, the primary role of EBPR is risk stratification rather than diagnosis of established hypertension.
In this setting, EBPR may signal an adverse BP trajectory and an increased likelihood of subclinical LV remodeling, supporting closer surveillance of BP and cardiovascular risk factors rather than immediate pharmacological intervention. If out-of-office BP confirms BP above goal, treatment should be initiated or intensified according to the patient's overall cardiovascular risk and treatment status. If out-of-office BP remains normal, echocardiographic assessment for subclinical LV remodeling may be considered, particularly in individuals with a marked EBPR or concomitant abnormalities in workload-indexed BP measures.
Periodic reassessment of BP and cardiovascular risk factors is also reasonable given the adverse BP trajectory associated with EBPR. A practical approach to the clinical management of EBPR is presented in Fig. 1.
Management is otherwise guideline-directed for any hypertension or risk that is unmasked. Regular aerobic exercise lowers resting and ambulatory BP and is recommended by guidelines as first-line lifestyle therapy [3]; notably, aerobic training also tends to lower submaximal exercise BP, whereas its effect on maximal exercise BP is inconsistent [14]. Antihypertensive therapy can reduce exercise BP and an effect most clearly appreciated at a fixed submaximal workload, where improvements in fitness do not obscure the pharmacological response [44].
However, no trial has yet tested whether treating EBPR in the absence of established hypertension improves outcomes, so pharmacotherapy directed at EBPR alone remains unsupported by evidence and is not currently recommended.
UNSOLVED PROBLEMS AND FUTURE PERSPECTIVES
The foremost unmet need is consensus on definition and protocol: a harmonized, preferably submaximal and fitness- or workload-indexed measurement, with agreed thresholds and reporting standards [132231]. Equally important, but less well established, is the evidence for incremental diagnostic value beyond out-of-office BP and for clinical actionability. Comparative studies assessing the diagnostic performance of exercise BP against ambulatory or home BP monitoring, as well as outcome studies determining whether exercise BP-triggered evaluation or intervention changes clinical management or improves prognosis, remain limited.
Without progress across all 3 domains—standardization, incremental value, and actionability—evidence synthesis and translation into clinical guidelines will remain constrained.
The promise of workload- or fitness-indexed measurement is itself limited by how fitness is estimated. Much of the available evidence, including the EXERTION study, derives the SBP/MET slope from estimated rather than directly measured peak METs, and estimated METs are influenced by exercise protocol, biomechanics, body composition, and musculoskeletal limitations [13]. Direct validation studies comparing SBP/MET slopes based on estimated METs with those derived from directly measured oxygen uptake are needed to establish the optimal approach for fitness-adjusted exercise BP assessment [4546].
Continuous, cuffless technologies such as smartwatches, rings, patches, and optical sensors offer the theoretical ability to capture the dynamic BP trajectory across exercise and recovery, which intermittent cuff measurement cannot. This is particularly relevant to EBPR, where the shape and submaximal portion of the response carry prognostic value. However, accuracy during motion and rapid hemodynamic change remains unproven.
Current devices are largely validated under static conditions; validation protocols suited to exercise are still maturing; and major statements, including from the American Heart Association and European Society of Cardiology caution that cuffless devices are not yet recommended for clinical use, especially during activity [347]. Although the recently published 2026 Korean Society of Hypertension guidelines for the management of hypertension are the first to provide a class IIb recommendation for the use of validated cuffless BP devices for out-of-office BP assessment [48], this recommendation is limited to measurements obtained under static conditions, and evidence supporting their use for BP assessment during exercise remains lacking. Bridging this gap through exercise-specific validation, dynamic calibration, and machine-learning approaches to motion-robust estimation represents a longer-term technological opportunity for capturing the full BP trajectory rather than an immediate research or clinical priority [49].
Given that these fundamental gaps remain unresolved even for conventional exercise BP, research efforts should first prioritize standardized definitions and measurement protocols, validated thresholds, reproducibility, identification of the optimal exercise BP metric, demonstration of incremental prognostic value, and evidence that exercise BP–guided assessment or intervention improves clinical outcomes.
The evidence linking EBPR to outcomes is observational. Randomized controlled trials are needed to determine whether identifying and treating EBPR through lifestyle or pharmacological interventions modifies cardiovascular risk, and to establish whether EBPR-guided management adds value beyond standard risk stratification. Longitudinal designs pairing standardized exercise testing with contemporaneous cardiac imaging can clarify whether EBPR-associated LV remodeling is a modifiable target or a risk marker, by characterizing the hemodynamic phenotype and its structural correlate under matched conditions.
Overall, the current evidence for EBPR is closer to meeting the standardization requirements for guideline adoption than the requirements for incremental value and actionability. Although approaches based on submaximal and fitness-indexed exercise BP are increasingly converging, comparative diagnostic-performance data against out-of-office BP monitoring and outcome studies evaluating exercise BP-guided management are still needed before EBPR can reasonably be considered for formal guideline incorporation.
CONCLUSION
EBPR is a biologically coherent phenotype that predicts incident hypertension, unmasks elevated out-of-office BP, associates with adverse LV remodeling, and forecasts cardiovascular events and mortality largely independent of resting BP. The persistent gap between this evidence and formal guideline recognition reflects not only the absence of a standardized definition and measurement approach, but also unresolved questions regarding the incremental value of EBPR beyond ambulatory and home BP monitoring and the specific clinical actions that an abnormal response should trigger. Progress will likely depend on convergence toward standardized submaximal and fitness-indexed measurement, comparative and outcome studies establishing the incremental diagnostic value and clinical actionability of an exercise BP–triggered evaluation pathway, and advances in exercise-validated cuffless technologies capable of capturing the full BP trajectory.
Ultimately, outcome studies are needed to determine whether acting on EBPR improves clinical outcomes and thereby justifies its incorporation into clinical guidelines (Fig. 2). Until then, an exaggerated exercise BP is best regarded as a clinically meaningful signal that should prompt out-of-office BP assessment and closer cardiovascular risk surveillance.