Impact of Exercise Training on Blood Pressure and Endothelial Function in Individuals with Systemic Hypertension

Mini Review

Austin Sports Med. 2016; 1(2): 1006.

Impact of Exercise Training on Blood Pressure and Endothelial Function in Individuals with Systemic Hypertension

Pedralli ML1,2, Waclawovsky G1 and Lehnen AM1,3*

1Laboratório de Investigaço Clínica, Instituto de Cardiologia / Fundaço Universitária de Cardiologia, Brazil

2Universidade Luterana do Brasil, Brazil

3Faculdade Sogipa de Educaço Fisica, Brazil

*Corresponding author: Alexandre Machado Lehnen, Instituto de Cardiologia / Fundaço Universitaria de Cardiologia, Porto Alegre, Brazil

Received: February 11, 2016; Accepted: April 20, 2016; Published: April 22, 2016


Ischemic heart diseases are largely determined by multifactorial risk factors that are associated with systemic arterial hypertension. Furthermore, high levels of total cholesterol, high body mass index, and high fasting glucose are also major risk factors that can lead to atherosclerosis. Endothelial dysfunction is a characteristic feature of systemic arterial hypertension and an early marker of atherosclerosis. Evidence shows that high blood pressure can result in vascular remodeling and damage to vascular endothelial cells and may partly explain endothelial dysfunction found in hypertensive individuals. There is a consensus that regular exercise can help control blood pressure levels in hypertensive individuals and all leading health organizations consider it the first-line nonpharmacological strategy for blood pressure control. Moreover, regular exercise has shown to improve endothelial function in different populations. However, different modalities of exercises, i.e. aerobic, resistance or combined (aerobic + resistance), could have different effects on blood pressure and endothelial response and they need to be further investigated. Thus, this review aims to better understand the behavior of blood pressure and endothelium-dependent vasodilator capacity in hypertensive individuals engaging in different forms of exercise training.

Keywords: Exercise; Endothelium; Hypertension


SAH: Systemic Arterial Hypertension; CVD: Cardiovascular Disease; NOS: Nitric Oxide Synthase; NO: Nitric Oxide; eNOS: endothelial Nitric Oxide Synthase; LDL-C: Low-Density Lipoprotein Cholesterol; EPCs: Endothelial Progenitor Cells; BP: Blood Pressure; SBP: Systolic Blood Pressure; DBP: Diastolic Blood Pressure; NOx: Nitrate/Nitrite; 1 RM: One Repetition Maximum


Systemic Arterial Hypertension (SAH) is characterized by high Blood Pressure (BP) resulting in a failure of vascular regulation due to malfunction in pressure control mechanisms [1,2]. It is likely that a large number of interrelated factors contribute to increased blood pressure in hypertensive subject, and their relative roles may differ between individuals. Factors associated with SAH are excess sodium intake [3], elevated levels of circulating angiotensin-converting enzyme [4], increased sympathetic nervous system activation [5], genetic factors [6], and endothelial dysfunction [7,8]. It is estimated that, by 2025, approximately 29% of the world population will have hypertension, accounting for about 1.56 billion individuals affected, mostly in developing countries [9]. These data are concerning given the high incidence of coronary artery disease, peripheral artery disease, stroke, and heart failure in this population [10,11]. Of all risk factors for developing coronary artery disease, hypertension is described as the most important, followed by high levels of total cholesterol, high body mass index, and high fasting glucose [12].

Obesity [13,14], physical inactivity [15], and insulin resistance [16] are all risk factors closely associated with SAH. These risk factors may individually contribute to the development of atherosclerosis and consequent mortality from ischemic Cardiovascular Disease (CVD) [17].

The vascular endothelium has an important function in modulating angiogenesis, inflammatory responses, homeostasis as well as and vascular tone and permeability [18]. This important vascular protection function results from a balance of factors released by vascular endothelium that determine vasodilation or vasoconstriction [19]. Vasodilation is primarily mediated by factors such as prostacyclin, Endothelium-Derived Hyperpolarizing Factor (EDHF), and Nitric Oxide (NO), whereas a vasoconstrictor state is mediated by factors such as angiotensin II, Endothelin-1 (ET-1), thromboxane A2, and prostaglandin H2 [20,21]. Among these factors, NO is considered to be the most potent endogenous vasodilator [22,23]. NO is produced from L-arginine and released by the activity of endothelial NO Synthase (eNOS) through the action of chemical agonists that act on specific endothelial chemoreceptors or respond to mechanical forces on mechanoreceptors such as shear stress [24]. A decrease in NO production, low local bioavailability, and inadequate vasomotor response characterize endothelial dysfunction, [19] a hallmark of diabetes mellitus type 2 [25], SAH [26] and dyslipidemia [27] and an early marker of atherosclerosis [28].

Evidence exists that clearly shows that physical exercise can improve the endothelium-dependent vasodilatory capacity in different populations [29]. Increasing physical activity levels and/ or physical exercise is a recommended treatment for SAH in major guidelines [30]. Accumulated evidence supports exercise as a nonpharmacological strategy for the prevention of CVD including ischemic heart disease as endothelial dysfunction precedes the development of these conditions and has a major role in the pathogenesis of atherosclerosis [28].

Regular exercise is a non-pharmacological intervention recommended by all leading health organizations because it provides the most comprehensive benefits among modifiable risk factors [31]. Thus, considering that regular exercise is part of antihypertensive therapy and has shown to improve endothelial function in different populations, this review seeks to provide an overview of the effects of different types of physical exercise on BP levels and endothelial function in hypertensive patients.


The endothelium is a single layer of cells lining the tunica intima of blood vessels and it plays a major role in the modulation of vascular angiogenesis, inflammatory responses, and vascular tone and permeability [18,32]. Endothelial protection particularly involves the activity of eNOS, an enzyme involved in the production of NO.

Endothelium-dependent NO release can be stimulated by different physiological factors including physical stress (shear stress), circulating hormones (catecholamines, vasopressin, and aldosterone), platelet agonists (serotonin and adenosine diphosphate), autacoids (histamine and bradykinin), and prostaglandins [33]. The NO dilates all types of blood vessels by stimulating soluble guanylyl cyclase and increasing cyclic GMP in smooth muscle cells [34]. A decreased production of NO, low local bioavailability, and/or insufficient vasomotor response characterize endothelial dysfunction evidenced in patients with SAH, [19] which has an important role in the pathogenesis of atherosclerosis (Figure 1) [28,35].

Citation:Pedralli ML, Waclawovsky G and Lehnen AM. Impact of Exercise Training on Blood Pressure and Endothelial Function in Individuals with Systemic Hypertension. Austin Sports Med. 2016; 1(2): 1006.