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

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Background-The aim of this study was to evaluate whether selective radiofrequency (RF) catheter ablation of the atrial sites in which high-frequency stimulation induces vagal reflexes prevents paroxysmal atrial fibrillation (AF). Methods and Results-Ten patients with episodes suggestive of vagal-induced paroxysmal AF and no heart disease were selected for percutaneous epicardial and endocardial mapping of the atria to search for sites in which high-frequency transcatheter stimulation (20 Hz,) induced vagal reflexes. A vagal response defined as AV block of Ͼ2 seconds was elicited in 7 of 10 patients (70%) with an average of 5Ϯ2.4 (range, 2 to 9) sites per patient, and RF pulses (21.0Ϯ12.0 per patient) were applied at those sites to eliminate all evoked vagal reflexes. The 3 patients in whom evoked vagal reflexes were not obtained underwent circumferential pulmonary vein ablation with an average of 58.0Ϯ13.9 RF pulses per patient (Pϭ0.022). Autonomic evaluation was performed before and 48 hours and 3 months after the procedure and was consistent with vagal withdrawal in all patients. Two of the 7 patients who underwent denervation remained asymptomatic without the use of antiarrhythmic medication at a mean follow-up of 8.3Ϯ2.8 months (range, 5 to 15 months); 4 had frequent recurrences and were referred for circumferential pulmonary vein ablation; and 1 had few AF episodes without antiarrhythmic medication. The 3 patients without evoked vagal reflexes who underwent circumferential pulmonary vein ablation remained asymptomatic without antiarrhythmic medication. One patient had acute delayed gastric emptying after atrial vagal denervation. Conclusions-RF

BackgroundObstructive Sleep Apnea (OSA) is tightly linked to some components of Metabolic Syndrome (MetS). However, most of the evidence evaluated individual components of the MetS or patients with a diagnosis of OSA that were referred for sleep studies due to sleep complaints. Therefore, it is not clear whether OSA exacerbates the metabolic abnormalities in a representative sample of patients with MetS.Methodology/Principal FindingsWe studied 152 consecutive patients (age 48±9 years, body mass index 32.3±3.4 Kg/m2) newly diagnosed with MetS (Adult Treatment Panel III). All participants underwent standard polysomnography irrespective of sleep complaints, and laboratory measurements (glucose, lipid profile, uric acid and C-reactive protein). The prevalence of OSA (apnea-hypopnea index ≥15 events per hour of sleep) was 60.5%. Patients with OSA exhibited significantly higher levels of blood pressure, glucose, triglycerides, cholesterol, LDL, cholesterol/HDL ratio, triglycerides/HDL ratio, uric acid and C-reactive protein than patients without OSA. OSA was independently associated with 2 MetS criteria: triglycerides: OR: 3.26 (1.47–7.21) and glucose: OR: 2.31 (1.12–4.80). OSA was also independently associated with increased cholesterol/HDL ratio: OR: 2.38 (1.08–5.24), uric acid: OR: 4.19 (1.70–10.35) and C-reactive protein: OR: 6.10 (2.64–14.11). Indices of sleep apnea severity, apnea-hypopnea index and minimum oxygen saturation, were independently associated with increased levels of triglycerides, glucose as well as cholesterol/HDL ratio, uric acid and C-reactive protein. Excessive daytime sleepiness had no effect on the metabolic and inflammatory parameters.Conclusions/SignificanceUnrecognized OSA is common in consecutive patients with MetS. OSA may contribute to metabolic dysregulation and systemic inflammation in patients with MetS, regardless of symptoms of daytime sleepiness.

Background-The effects of diet and diet plus exercise training on muscle vasodilatation during physiological maneuvers in obese children are unknown. We tested the hypothesis that (1) blood pressure (BP) and forearm vascular conductance (FVC) responses during handgrip exercise and mental stress would be altered in obese children and (2) diet plus exercise training would restore BP and FVC responses during exercise and mental stress in obese children. Methods and Results-Thirty-nine obese children (aged 10Ϯ0.2 years) were randomly divided into 2 groups: diet plus exercise training (nϭ21; body mass index [BMI]ϭ28Ϯ0.5 kg/m 2 ) and diet (nϭ18; BMIϭ30Ϯ0.4 kg/m 2 ). Ten age-matched lean control children (BMIϭ17Ϯ0.5 kg/m 2 ) were also studied. Forearm blood flow was measured by venous occlusion plethysmography. BP was monitored noninvasively. Handgrip exercise was performed at 30% maximal voluntary contraction for 3 minutes. Stroop color word test was performed for 4 minutes. Baseline BP was significantly higher and FVC was significantly lower in obese children. During exercise and mental stress, BP responses were significantly higher and FVC responses were significantly lower in obese children. Diet and diet plus exercise training significantly reduced body weight. Diet and diet plus exercise training significantly decreased BP levels during exercise and mental stress. Diet plus exercise training, in contrast to diet alone, significantly increased FVC responses during exercise

We studied the effects of a hypocaloric diet (D, n = 24, age: 32.2 +/- 1.4 yr, body mass index: 34.7 +/- 0.5 kg/m2) and a hypocaloric diet associated with exercise training (D + T, n = 25, age: 32.3 +/- 1.3 yr, body mass index: 32.9 +/- 0.4 kg/m2) on muscle metaboreflex control, muscle sympathetic nerve activity (MSNA, microneurography), blood pressure, and forearm blood flow (plethysmography) levels during handgrip exercise at 10% and 30% of maximal voluntary contraction in normotensive obese women. An additional 10 women matched by age and body mass index were studied as a nonadherent group. D or D + T significantly decreased body mass index. D or D + T significantly decreased resting MSNA (bursts/100 heartbeats). The absolute levels of MSNA were significantly lower throughout 10% and 30% exercise after D or D + T, although no change was found in the magnitude of response of MSNA. D + T, but not D, significantly increased resting forearm vascular conductance. D + T significantly increased the magnitude of the response of forearm vascular conductance during 30% exercise. D or D + T significantly increased MSNA levels during posthandgrip circulatory arrest when muscle metaboreflex is isolated. In conclusion, weight loss improves muscle metaboreflex control in obese women. Weight loss reduces MSNA, which seems to be centrally mediated. Weight loss by D + T increases forearm vascular conductance at rest and during exercise in obese individuals.

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Patients with MetSyn and comorbid OSA have higher BP, higher sympathetic drive, and diminished BRS, compared with patients with MetSyn without OSA. These adverse cardiovascular and autonomic consequences of OSA may be associated with poorer outcomes in these patients. Moreover, increased BP and sympathetic drive in patients with MetSyn+OSA may be linked, in part, to impairment of baroreflex gain.