Abstract-The effects of exercise training on baroreflex control of sympathetic nerve activity in human hypertension are unknown. We hypothesized that exercise training would improve baroreflex control of muscle sympathetic nerve activity (MSNA) and heart rate (HR) in patients with hypertension and that exercise training would reduce MSNA and blood pressure (BP) in hypertensive patients. Twenty never-treated hypertensive patients were randomly divided into 2 groups: exercise-trained (nϭ11; age: 46Ϯ2 years) and untrained (nϭ9; age: 42Ϯ2 years) patients. An age-matched normotensive exercise-trained group (nϭ12; age: 42Ϯ2 years) was also studied. Key Words: hypertension Ⅲ baroreflex sensitivity Ⅲ sympathetic nerve activity Ⅲ exercise Ⅲ blood pressure T here is accumulated evidence that arterial baroreflex plays an important role in the regulation of the cardiovascular system. During spontaneous variation of blood pressure (BP), stimulation or deactivation of the arterial baroreceptors located in the carotid sinus and aortic arch causes reflex bradycardia and tachycardia, respectively. At the vascular level, stimulation of the arterial baroreceptors results in sympathetic inhibition and, in consequence, reflex vasodilation. In contrast, the deactivation of the arterial baroreceptors elicits sympathetic-mediated vasoconstriction. 1 All of these responses work in concert to maintain the BP levels in the reference range. 1It has been described that arterial baroreflex sensitivity can be profoundly altered in some cardiovascular diseases. 2,3 In hypertension, some investigators, 4 -6 but not all, 7-9 observed that baroreflex control of heart rate (HR) and sympathetic nerve activity is significantly reduced. This autonomic dysfunction seems to correlate with an increase in sympathetic outflow and in BP levels. 10 On the other hand, previous studies have demonstrated that regular exercise causes significant changes in baroreflex control of HR in experimental hypertension. Exercise training improves baroreflex control of HR during the increase and decrease of BP in spontaneously hypertensive rats. 11,12 Furthermore, these studies indicate that the improvement in baroreflex sensitivity is, in part, mediated by the enhancement of the aortic depressor nerve sensitivity. In humans with hypertension, little information exists regarding the effects of exercise training on the baroreflex sensitivity. One of the few studies showed that exercise training caused a modest improvement in baroreflex bradycardia. 13 Thus, the effects of regular exercise on the baroreflex control of sympathetic nerve activity in humans with hypertension are unknown.It has been consistently shown that exercise training is a powerful nonpharmacological strategy to reduce BP levels in humans with hypertension. 14 -16 However, the mechanisms involved in the BP reduction after exercise training are still a matter of discussion. In the present study, we investigated the
Home-based IMT represents an important strategy to improve cardiac and peripheral autonomic controls, functional capacity, and quality of life in patients with CHF.
Abstract-Autonomic dysfunction, including baroreceptor attenuation and sympathetic activation, has been reported in patients with myocardial infarction (MI) and has been associated with increased mortality. We tested the hypotheses that exercise training (ET) in post-MI patients would normalize arterial baroreflex sensitivity (BRS) and muscle sympathetic nerve activity (MSNA), and long-term ET would maintain the benefits in BRS and MSNA. Twenty-eight patients after 1 month of uncomplicated MI were randomly assigned to 2 groups, ET (MI-ET) and untrained. A normal control group was also studied. ET consisted of three 60-minute exercise sessions per week for 6 months. We evaluated MSNA (microneurography), blood pressure (automatic oscillometric method), heart rate (ECG), and spectral analysis of RR interval, systolic arterial pressure (SAP), and MSNA. Baroreflex gain of SAP-RR interval and SAP-MSNA were calculated using the ␣-index. At 3 to 5 days and 1 month after MI, MSNA and low-frequency SAP were significantly higher and BRS significantly lower in MI patients when compared with the normal control group. ET significantly decreased MSNA (bursts per 100 heartbeats) and the low-frequency component of SAP and significantly increased the low-frequency component of MSNA and BRS of the RR interval and MSNA. These changes were so marked that the differences between patients with MI and the normal control group were no longer observed after ET. MSNA and BRS in the MI-untrained group did not change from baseline over the same time period. ET normalizes BRS, low-frequency SAP, and MSNA in patients with MI. These improvements in autonomic control are maintained by long-term ET. Key Words: myocardial infarction Ⅲ sympathetic nerve activity Ⅲ exercise training Ⅲ autonomic control Ⅲ baroreflex control P revious studies show that myocardial infarction (MI) is linked to increased sympathetic nervous activity 1,2 and impaired arterial baroreflex sensitivity (BRS). 3 These findings of autonomic dysfunction have been associated with increased mortality in patients after MI. 4 -10 La Rovere et al 7 demonstrated that decreased BRS is associated with cardiac mortality risk. A follow-up of 61 months in uncomplicated post-MI patients with preserved left ventricular function showed that depressed BRS discriminated a subgroup at long-term high risk for cardiovascular mortality. 10 Increased muscle sympathetic nerve activity (MSNA) is an independent predictor of poor prognosis in patients with chronic heart failure, including patients with chronic heart failure after MI. 11 Thus, a therapeutic strategy targeted to the improvement in autonomic control in patients with MI represents an important clinical goal.In patients with cardiovascular disease, studies have shown that physical exercise is an important strategy to improve autonomic function. Exercise training has been shown to decrease MSNA 12 and improve BRS 12-14 in patients with MI. It remains unknown whether the magnitude of change in autonomic control actually normalizes BRS and sy...
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
customersupport@researchsolutions.com
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
This site is protected by reCAPTCHA and the Google Privacy Policy and Terms of Service apply.
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.