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...

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We hypothesized that the muscle vasodilatation during mental stress and exercise would vary among humans who are polymorphic at alleles 16 and 27 of the β2-adrenoceptors. From 216 preselected volunteers, we studied 64 healthy, middle-aged normotensive women selected to represent three genotypes: homozygous for the alleles Arg16 and Gln27 (Arg16/Gln27, n = 34), Gly16 and Gln27 (Gly16/Gln27, n = 20), and Gly16 and Glu27 (Gly16/Glu27, n = 10). Forearm blood flow (plethysmography) and muscle sympathetic nerve activity (microneurography) were recorded during 3-min Stroop color-word test and 3-min handgrip isometric exercise (30% maximal voluntary contraction). Baseline muscle sympathetic nerve activity, forearm vascular conductance, mean blood pressure, and heart rate were not different among groups. During mental stress, the peak forearm vascular conductance responses were greater in Gly16/Glu27 group than in Gly16/Gln27 and Arg16/Gln27 groups (1.79 ± 0.66 vs. 0.70 ± 0.11 and 0.58 ± 0.12 units, P = 0.03). Similar results were found during exercise (0.80 ± 0.25 vs. 0.28 ± 0.08 and 0.31 ± 0.08 units, P = 0.02). Further analysis in a subset of subjects showed that brachial intra-arterial propranolol infusion abolished the difference in vasodilatory response between Gly16/Glu27 ( n = 6) and Arg16/Gln27 ( n = 7) groups during mental stress (0.33 ± 0.20 vs. 0.46 ± 0.21 units, P = 0.50) and exercise (0.08 ± 0.06 vs. 0.03 ± 0.03 units, P = 0.21). Plasma epinephrine concentration in Arg16/Gln27 and Gly16/Glu27 groups was similar. In conclusion, women who are homozygous for Gly16/Glu27 of the β2-adrenoceptors have augmented muscle vasodilatory responsiveness to mental stress and exercise.

BackgroundMetabolic syndrome (MetS) is associated with structural and functional vascular abnormalities, which may lead to increased arterial stiffness, more frequent cardiovascular events and higher mortality. However, the role played by clustering of risk factors and the combining pattern of MetS risk factors and their association with the arterial stiffness have yet to be fully understood. Age, hypertension and diabetes mellitus seem to be strongly associated with increased pulse wave velocity (PWV). This study aimed at determining the clustering and combining pattern of MetS risk factors and their association with the arterial stiffness in non-diabetic and non-hypertensive patients.MethodsRecently diagnosed and untreated patients with MetS (n = 64, 49 ± 8 year, 32 ± 4 kg/m2) were selected, according to ATP III criteria and compared to a control group (Control, n = 17, 49 ± 6 year, 27 ± 2 kg/m2). Arterial stiffness was evaluated by PWV in the carotid-femoral segment. Patients were categorized and analyzed according MetS risk factors clustering (3, 4 and 5 factors) and its combinations.ResultsPatients with MetS had increased PWV when compared to Control (7.8 ± 1.1 vs. 7.0 ± 0.5 m/s, p < 0.001). In multivariate analysis, the variables that remained as predictors of PWV were age (β = 0.450, p < 0.001), systolic blood pressure (β = 0.211, p = 0.023) and triglycerides (β = 0.212, p = 0.037). The increased number of risk factors reflected in a progressive increase in PWV. When adjusted to systolic blood pressure, PWV was greater in the group with 5 risk factors when compared to the group with 3 risk factors and Control (8.5 ± 0.4 vs. 7.5 ± 0.2, p = 0.011 and 7.2 ± 0.3 m/s, p = 0.012). Similarly, the 4 risk factors group had higher PWV than the Control (7.9 ± 0.2 vs. 7.2 ± 0.3, p = 0.047).ConclusionsThe number of risk factors seems to increase arterial stiffness. Notably, besides age and increased systolic blood pressure, alterations in the triglycerides worsened the stiffness of large vessels, emphasizing the importance in addressing this risk factor in MetS patients.

Introduction/Purpose We demonstrated that patients with obstructive sleep apnea (OSA) have reduced muscle metaboreflex control of muscle sympathetic nerve activity (MSNA). In addition, exercise training increased muscle metaboreflex control in heart failure patients. Objective We tested the hypothesis that exercise training would increase muscle metaboreflex control of MSNA in patients with OSA. Methods Forty-one patients with OSA were randomized into the following two groups: 1) nontrained (OSANT, n = 21) and 2) trained (OSAT, n = 20). Muscle sympathetic nerve activity was assessed by microneurography technique, muscle blood flow (FBF) by venous occlusion plethysmography, heart rate by electrocardiography, and blood pressure with an automated oscillometric device. All physiological variables were simultaneously assessed at rest, during isometric handgrip exercise at 30% of the maximal voluntary contraction, and during posthandgrip muscle ischemia (PHMI). Muscle metaboreflex sensitivity was calculated as the difference in MSNA between PHMI and the rest period. Patients in the OSAT group underwent 72 sessions of moderate exercise training, whereas patients in the OSANT group were clinical follow-up for 6 months. Results The OSANT and OSAT groups were similar in anthropometric, neurovascular, hemodynamic and sleep parameters. Exercise training reduced the baseline MSNA (34 ± 2 bursts per minute vs 25 ± 2 bursts per minute; P < 0.05) and increased the baseline FBF (2.1 ± 0.2 mL·min−1 per 100 g vs 2.4 ± 0.2 mL·min−1 per 100 g; P < 0.05). Exercise training significantly reduced MSNA levels and increased FBF responses during isometric exercise. Exercise training significantly increased MSNA responses during PHMI (Δ6.5 ± 1 vs −1.7 ± 1 bursts per minute, P < 0.01). No significant changes in FBF or hemodynamic parameters in OSANT patients were found. Conclusions Exercise training increases muscle metaboreflex sensitivity in patients with OSA. This autonomic change associated with increased muscle blood flow may contribute to the increase in exercise performance in this set of patients.

Background Resting sympathetic hyperactivity and impaired parasympathetic reactivation after exercise have been described in patients with heart failure (HF). However, the association of these autonomic changes in patients with HF and sarcopenia is unknown. Objective The aim of this study was to evaluate the impact of autonomic modulation on sarcopenia in male patients with HF. Methods We enrolled 116 male patients with HF and left ventricular ejection fraction < 40%. All patients underwent a maximal cardiopulmonary exercise testing. Maximal heart rate was recorded and delta heart rate recovery (∆HRR) was assessed at 1 st and 2 nd minutes after exercise. Muscle sympathetic nerve activity (MSNA) was recorded by microneurography. Dual-energy X-ray absorptiometry was used to measure body composition and sarcopenia was defined by the sum of appendicular lean muscle mass (ALM) divided by height in meters squared and handgrip strength. Results Sarcopenia was identified in 33 patients (28%). Patients with sarcopenia had higher MSNA than those without (47 [41-52] vs. 40 [34-48] bursts/min, p = 0.028). Sarcopenic patients showed lower ∆HRR at 1 st (15 [10-21] vs. 22 [16-30] beats/min, p < 0.001) and 2 nd min (25 [19-39] vs. 35 [24-48] beats/min, p = 0.017) than non-sarcopenic. There was a positive correlation between ALM and ∆HRR at 1 st (r = 0.26, p = 0.008) and 2 nd min (r = 0.25, p = 0.012). We observed a negative correlation between ALM and MSNA (r = -0.29, p = 0.003). Conclusion Sympatho-vagal imbalance seems to be associated with sarcopenia in male patients with HF. These results highlight the importance of a therapeutic approach in patients with muscle wasting and increased peripheral sympathetic outflow.