Effects of exercise training in patients with chronic heart failure and sleep apnea.

STUDY OBJECTIVES: To test the effects of exercise training on sleep and neurovascular control in patients with systolic heart failure with and without sleep disordered breathing. DESIGN: Prospective interventional study. SETTING: Cardiac rehabilitation and exercise physiology unit and sleep laboratory. PATIENTS: Twenty-five patients with heart failure, aged 42 to 70 years, and New York Heart Association Functional Class I-III were divided into 1 of 3 groups: obstructive sleep apnea (n=8), central sleep apnea (n=9) and no sleep apnea (n=7). INTERVENTIONS Four months of no-training (control) followed by 4 months of an exercise training program (three 60-minute, supervised, exercise sessions per week). MEASURES AND RESULTS: Sleep (polysomnography), microneurography, forearm blood flow (plethysmography), peak VO2, and quality of life were evaluated at baseline and at the end of the control and trained periods. No significant changes occurred in the control period. Exercise training reduced muscle sympathetic nerve activity (P < 0.001) and increased forearm blood flow (P < 0.01), peak VO2( P < 0.01), and quality of life (P < 0.01) in all groups, independent of the presence of sleep apnea. Exercise training improved the apnea-hypopnea index, minimum 0O saturation, and amount stage 3-4 sleep (P < 0.05) in patients with obstructive sleep apnea but had no significant effects in patients with central sleep apnea. CONCLUSIONS: The beneficial effects of exercise training on neurovascular function, functional capacity, and quality of life in patients with systolic dysfunction and heart failure occurs independently of sleep disordered breathing. Exercise training lessens the severity of obstructive sleep apnea but does not affect central sleep apnea in patients with heart failure and sleep disordered breathing.

Muscle sympathetic nerve activity in patients with Chagas' disease.

BACKGROUND: The progression of heart failure in Chagas' disease has been explained by remodeling, leading to neurohumoral activation, or by the direct parasite damage to parasympathetic neurons during acute phase, leading to early sympathetic activation and progressive heart failure. To help distinguish between these hypotheses we studied muscle sympathetic nerve activity (MSNA) at rest and during handgrip exercise (30% of maximal voluntary contraction) in patients with Chagas' disease and normal ejection fraction vs. patients with heart failure. METHODS: A consecutive study of 72 eligible out-patients/subjects was conducted between July 1998 and November 2004. The participants were classified in three advanced heart failure groups (New York Heart Association Functional Classes II-III): Chagas' disease (n=15), ischemic (n=15) and idiopathic cardiomyopathy (n=15). Twelve Chagas' disease patients without heart failure and normal ejection fraction, and 15 normal controls were also studied. MSNA was recorded directly from the peroneal nerve by microneurography technique. RESULTS: MSNA was greater in heart failure patients when compared with Chagas' disease patients without heart failure (51+/-3 vs. 20+/-2 bursts/min P=0.0001). MSNA in Chagas' patients with normal ejection fraction and normal controls was not different. During exercise, MSNA was similar in all 3 heart failure groups. And, was lower in the Chagas' patients with normal ejection fraction than in patients with Chagas' disease and heart failure (28+/-1 vs. 63+/-5 bursts/min, respectively). CONCLUSION: MSNA is not elevated in patients with Chagas' disease with normal ejection fraction. These findings support the concept of remodeling and neurohumoral activation as a common pathway following significant cardiac injury.

Exercise training reduces sympathetic nerve activity in heart failure patients treated with carvedilol.

BACKGROUND: Evidence suggests that carvedilol decreases muscle sympathetic nerve activity (MSNA) in patients with heart failure (HF) but carvedilol fails to improve forearm vascular resistance and overall functional capacity. Exercise training in HF reduces MSNA and improves forearm vascular resistance and functional capacity. AIMS: To investigate whether the beneficial effects exercise training on MSNA are maintained in the presence of carvedilol. METHODS AND RESULTS: Twenty seven HF patients, NYHA Class II-III, EF <35%, peak VO(2) <20 ml/kg/min, treated with carvedilol were randomly divided into two groups: exercise training (n=15) and untrained (n=12). MSNA was recorded by microneurography. Forearm blood flow (FBF) was measured by venous occlusion plethysmography. The four-month training program consisted of three 60-min exercise/week on a cycloergometer. Baseline parameters were similar between groups. Exercise training reduced MSNA (-14+/-3.3 bursts/100 HB, p=0.001) and increased forearm blood flow (0.6+/-0.1 mL/min/100 g, p<0.001) in HF patients on carvedilol. In addition, exercise training improved peak VO(2) in HF patients (20+/-6%, p=0.002). MSNA, FBF and peak VO(2) were unchanged in untrained HF patients on carvedilol. CONCLUSION: Exercise training reduces MSNA in heart failure patients treated with carvedilol. In addition, the beneficial effects of exercise training on muscle blood flow and functional capacity are still realized in patients on carvedilol.

Relationships among exercise capacity, hypertrophy, and left ventricular diastolic function in nonobstructive hypertrophic cardiomyopathy.

AIM: The aim of this study was to analyze the relationships among exercise capacity (EC), hypertrophy, and diastolic function in nonobstructive hypertrophic cardiomyopathy (NOHCM). METHODS AND RESULTS: Twenty-seven patients with NOHCM were studied. Left ventricular hypertrophy (LVH) was determined by appropriate echocardiographic indexes. For diastolic function evaluation, the following were measured: the early (E) and late (A) waves, E/A, and deceleration time of E of the mitral flow; the systolic (S), diastolic (D), and atrial reversal (AR) waves, S/D, and the atrial systolic filling fraction of the pulmonary vein flow; and the early (Ea), late (Aa) waves, Ea/Aa, and E/Ea by tissue Doppler imaging. The difference between the duration of AR and A waves (DurAR - DurA), the peak VO2, and anaerobic threshold (AT) were also determined. In these patients, the E/Ea ratio was 8.9 +/- 3.2 and DurAR - DurA was 22.6 +/- 32.6 milliseconds. The peak VO2 and AT correlated with D (r = 0.55, P = .003 and .51, P = .007, respectively) and Ea/Aa (r = 0.56, P = .007 and .45, P = .03, respectively). There was no correlation between EC and LVH. CONCLUSIONS: Patients with NOHCM demonstrated evidences of elevated left ventricular (LV) end-diastolic pressure with normal filling pressure. EC compromise may be attributed to relaxation changes with inadequate filling of the left ventricle.