Hypertensive response to exercise: mechanisms and clinical implication.

Jong-Won Ha,Darae Kim

doi:10.1186/s40885-016-0052-y

Jong-Won Ha, Darae Kim

Open Access

https://doi.org/10.1186/s40885-016-0052-y

Copy DOI

Journal: Clinical hypertension	Publication Date: Jul 26, 2016
Citations: 83	License type: cc-by

Affiliation: Yonsei University

Abstract

A hypertensive response to exercise (HRE) is frequently observed in individuals without hypertension or other cardiovascular disease. However, mechanisms and clinical implication of HRE is not fully elucidated. Endothelial dysfunction and increased stiffness of large artery contribute to development of HRE. From neurohormonal aspects, excess stimulation of sympathetic nervous system and augmented rise of angiotensin II seems to be important mechanism in HRE. Increasing evidences indicates that a HRE is associated with functional and structural abnormalities of left ventricle, especially when accompanied by increased central blood pressure. A HRE harbors prognostic significance in future development of hypertension and increased cardiovascular events, particularly if a HRE is documented in moderate intensity of exercise. As supported by previous studies, a HRE is not a benign phenomenon, however, currently, whether to treat a HRE is controversial with uncertain treatment strategy. Considering underlying mechanisms, angiotensin receptor blockers and beta blockers can be suggested in individuals with HRE, however, evidences for efficacy and outcomes of treatment of HRE in individuals without hypertension is scarce and therefore warrants further studies.

Highlights

Systolic blood pressure (BP) normally rises with exercise as cardiac output increases during exercise in responses to the increased demand of oxygen from working muscles via increased sympathetic tone
Some individuals present with abnormally exaggerated rise in systolic BP during exercise
This phenomenon is known as a hypertensive response to exercise (HRE)

Summary

Introduction

Systolic blood pressure (BP) normally rises with exercise as cardiac output increases during exercise in responses to the increased demand of oxygen from working muscles via increased sympathetic tone. Some individuals present with abnormally exaggerated rise in systolic BP during exercise. This phenomenon is known as a hypertensive response to exercise (HRE). A HRE is often observed in individuals without known cardiovascular diseases. It is generally considered as an abnormal response, there are conflicting data regarding its clinical significance. Impaired endothelial function may limit vasodilation in response to increased shear stress from exercise, result in HRE. Consistent with previous studies, Stewart et al [10] demonstrated an independent correlation between flow mediated dilation and exercise BP in normotensive population, suggesting that impaired endothelial vasodilation may contribute to exercise hypertension.

Objectives

Findings

Conclusion