Physicians' Academy for Cardiovascular Education

BP response to exercise is exaggerated in hypertensives with controlled resting BP

Antihypertensive Treatment Fails to Control Blood Pressure During Exercise

Literature - Chant B, Bakali M, Hinton T, et al. - Hypertension 2018;72:102-109

Introduction and Methods

In individuals with hypertension, the systolic blood pressure (SBP) rises extremely during exercise, which increases their risk of CV morbidity and mortality [1]. Metaboreflex, the group IV afferents in the skeletal muscle, mediates the exaggerated response of sympathetic nerve activity and blood pressure (BP) to exercise, but it is not clear whether antihypertensive medication has an effect on metaboreflex, and on the BP response to exercise [2,3].

In this case-control study, the BP response to incremental exercise testing and metaboreflex activation was evaluated in hypertensive compared with normotensive individuals. For this purpose, 59 participants were recruited, out of which 16 were normotensive, and 43 were hypertensive. Out of participants with hypertension, 16 were treated and controlled, 16 were treated but uncontrolled, and 11 were untreated.

All participants were matched for age, body mass index, and CV fitness. CV fitness was measured by a volume of oxygen inspired (Vo2) peak test, assessed by an incremental exercise test on an upright cycle ergometer. The metaboreflex was assessed using post-exercise ischemia (PEI) 1 minute after isometric handgrip exercise at 30% maximal voluntary contraction.

Main results


BP responses to exercise are similar in patients with treated–controlled hypertension, patients with treated but uncontrolled and untreated hypertension, but higher compared with normotensive individuals, which explains why hypertensive patients on antihypertensive treatment with controlled resting BP are at higher risk of CV events. These data suggest that antihypertensive medications do not favorably influence the BP response to exercise, even though they control resting SBP.

Editorial comment

In his editorial article, Raven [4] acknowledges the work of Chant et al. and discusses the pathophysiology behind the limited control of BP response to exercise by antihypertensive medications. He focuses on the lack of central nitric oxide in hypertensive patients that is necessary to avoid exaggerated BP increase during exercise, and he concludes with a question: ‘Is it possible that investigations into rescuing central NO to buffer the increased central sympathetic nerve activity outflow of the hypersensitive exercise pressor reflex will prove more translational and beneficial for correcting exercise induced hypertension, rather than investigating a multitude of specific mechanisms that are collectively identified as functional sympatholysis?’


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