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J Cardiovasc Electrophysiol ; 30(11): 2591-2598, 2019 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-31544272


INTRODUCTION: The muscular metaboreflex, whose activation regulates blood flow during isometric and aerobic exercise, is blunted in patients with heart failure (HF), and cardiac resynchronization therapy (CRT) may restore this regulatory reflex. OBJECTIVE: To evaluate metaboreflex responses after CRT. METHODS: Thirteen HF patients and 12 age-matched healthy control subjects underwent the following evaluations (pre- and post-CRT implantation in the patient group): (a) heart rate, blood pressure, and forearm blood flow measurements; (b) muscle sympathetic nerve activity (MSNA) evaluation; and (c) peak oxygen consumption (VO2peak ). Examinations were performed at rest, during moderate isometric exercise (IE), and during forearm ischemia (metaboreflex activation). The primary outcome was the increment in MSNA during limb ischemia compared to the rest moment (ΔMSNA rest to metaboreflex activation). RESULTS: After CRT, rest MSNA decreased in the HF participants: 50.4 ± 9.2 bursts/min pre-CRT vs 34.0 ± 14.4 bursts/min post-CRT, P = .001, accompanied by an improvement in systolic blood pressure and in rate-pressure product. MSNA during limb ischemia decreased: 56.6 ± 11.5 bursts/min pre-CRT vs 43.6 ± 12.7 bursts/min post-CRT, P = .001, and the ΔMSNA rest to metaboreflex activation increased: 0% (interquartile range [IQR)], -7 to 9) vs 13% (IQR, 5-30), P = .03. An augmentation of mean blood pressure during limb ischemia post-CRT was noticed: 94 mmHg (IQR, 81-104) vs 110 mmHg (IQR, 100-117), P = .04. CRT improved VO2peak , and this improvement was correlated with diminution in ΔMSNA pre- to post-CRT at rest moment (rs = -0.74, P = .006). CONCLUSION: CRT provides metaboreflex sensitization and MSNA enhancement. The restoration of sympathetic responsiveness correlates with the improvement in functional capacity.

Am J Physiol Heart Circ Physiol ; 311(5): H1180-H1188, 2016 11 01.
Artigo em Inglês | MEDLINE | ID: mdl-27591218


Heart failure (HF) is characterized by decreased exercise capacity, attributable to neurocirculatory and skeletal muscle factors. Cardiac resynchronization therapy (CRT) and exercise training have each been shown to decrease muscle sympathetic nerve activity (MSNA) and increase exercise capacity in patients with HF. We hypothesized that exercise training in the setting of CRT would further reduce MSNA and vasoconstriction and would increase Ca2+-handling gene expression in skeletal muscle in patients with chronic systolic HF. Thirty patients with HF, ejection fraction <35% and CRT for 1 mo, were randomized into two groups: exercise-trained (ET, n = 14) and untrained (NoET, n = 16) groups. The following parameters were compared at baseline and after 4 mo in each group: V̇o2 peak, MSNA (microneurography), forearm blood flow, and Ca2+-handling gene expression in vastus lateralis muscle. After 4 mo, exercise duration and V̇o2 peak were significantly increased in the ET group (P = 0.04 and P = 0.01, respectively), but not in the NoET group. MSNA was significantly reduced in the ET (P = 0.001), but not in NoET, group. Similarly, forearm vascular conductance significantly increased in the ET (P = 0.0004), but not in the NoET, group. The expression of the Na+/Ca2+ exchanger (P = 0.01) was increased, and ryanodine receptor expression was preserved in ET compared with NoET. In conclusion, the exercise training in the setting of CRT improves exercise tolerance and neurovascular control and alters Ca2+-handling gene expression in the skeletal muscle of patients with systolic HF. These findings highlight the importance of including exercise training in the treatment of patients with HF even following CRT.

Cálcio/metabolismo , Terapia de Ressincronização Cardíaca , Terapia por Exercício , Exercício , Insuficiência Cardíaca/terapia , Acoplamento Neurovascular , Músculo Quadríceps/metabolismo , Sistema Nervoso Simpático/metabolismo , Ecocardiografia , Teste de Esforço , Tolerância ao Exercício , Feminino , Antebraço/irrigação sanguínea , Expressão Gênica , Insuficiência Cardíaca/genética , Humanos , Masculino , Pessoa de Meia-Idade , Músculo Esquelético/inervação , Músculo Esquelético/metabolismo , Consumo de Oxigênio , Músculo Quadríceps/inervação , RNA Mensageiro/metabolismo , Fluxo Sanguíneo Regional , Canal de Liberação de Cálcio do Receptor de Rianodina/genética , Trocador de Sódio e Cálcio/genética
Eur J Prev Cardiol ; 23(15): 1599-608, 2016 10.
Artigo em Inglês | MEDLINE | ID: mdl-27271264


BACKGROUND: We investigated the effects of muscle functional electrical stimulation on muscle sympathetic nerve activity and muscle blood flow, and, in addition, exercise tolerance in hospitalised patients for stabilisation of heart failure. METHODS: Thirty patients hospitalised for treatment of decompensated heart failure, class IV New York Heart Association and ejection fraction ≤ 30% were consecutively randomly assigned into two groups: functional electrical stimulation (n = 15; 54 ± 2 years) and control (n = 15; 49 ± 2 years). Muscle sympathetic nerve activity was directly recorded via microneurography and blood flow by venous occlusion plethysmography. Heart rate and blood pressure were evaluated on a beat-to-beat basis (Finometer), exercise tolerance by 6-minute walk test, quadriceps muscle strength by a dynamometer and quality of life by Minnesota questionnaire. Functional electrical stimulation consisted of stimulating the lower limbs at 10 Hz frequency, 150 ms pulse width and 70 mA intensity for 60 minutes/day for 8-10 consecutive days. The control group underwent electrical stimulation at an intensity of < 20 mA. RESULTS: Baseline characteristics were similar between groups, except age that was higher and C-reactive protein and forearm blood flow that were smaller in the functional electrical stimulation group. Functional electrical stimulation significantly decreased muscle sympathetic nerve activity and increased muscle blood flow and muscle strength. No changes were found in the control group. Walking distance and quality of life increased in both groups. However, these changes were greater in the functional electrical stimulation group. CONCLUSION: Functional electrical stimulation improves muscle sympathetic nerve activity and vasoconstriction and increases exercise tolerance, muscle strength and quality of life in hospitalised heart failure patients. These findings suggest that functional electrical stimulation may be useful to hospitalised patients with decompensated chronic heart failure.

Estimulação Elétrica/métodos , Tolerância ao Exercício/fisiologia , Insuficiência Cardíaca/terapia , Pacientes Internados , Força Muscular/fisiologia , Músculo Esquelético/fisiopatologia , Sistema Nervoso Simpático/fisiologia , Adolescente , Adulto , Idoso , Feminino , Antebraço/irrigação sanguínea , Insuficiência Cardíaca/fisiopatologia , Frequência Cardíaca/fisiologia , Humanos , Masculino , Pessoa de Meia-Idade , Pletismografia , Qualidade de Vida , Fluxo Sanguíneo Regional/fisiologia , Adulto Jovem
Am J Physiol Heart Circ Physiol ; 308(9): H1096-102, 2015 May 01.
Artigo em Inglês | MEDLINE | ID: mdl-25747752


Arterial baroreflex control of muscle sympathetic nerve activity (ABRMSNA) is impaired in chronic systolic heart failure (CHF). The purpose of the study was to test the hypothesis that exercise training would improve the gain and reduce the time delay of ABRMSNA in CHF patients. Twenty-six CHF patients, New York Heart Association Functional Class II-III, EF ≤ 40%, peak V̇o2 ≤ 20 ml·kg(-1)·min(-1) were divided into two groups: untrained (UT, n = 13, 57 ± 3 years) and exercise trained (ET, n = 13, 49 ± 3 years). Muscle sympathetic nerve activity (MSNA) was directly recorded by microneurography technique. Arterial pressure was measured on a beat-to-beat basis. Time series of MSNA and systolic arterial pressure were analyzed by autoregressive spectral analysis. The gain and time delay of ABRMSNA was obtained by bivariate autoregressive analysis. Exercise training was performed on a cycle ergometer at moderate intensity, three 60-min sessions per week for 16 wk. Baseline MSNA, gain and time delay of ABRMSNA, and low frequency of MSNA (LFMSNA) to high-frequency ratio (HFMSNA) (LFMSNA/HFMSNA) were similar between groups. ET significantly decreased MSNA. MSNA was unchanged in the UT patients. The gain and time delay of ABRMSNA were unchanged in the ET patients. In contrast, the gain of ABRMSNA was significantly reduced [3.5 ± 0.7 vs. 1.8 ± 0.2, arbitrary units (au)/mmHg, P = 0.04] and the time delay of ABRMSNA was significantly increased (4.6 ± 0.8 vs. 7.9 ± 1.0 s, P = 0.05) in the UT patients. LFMSNA-to-HFMSNA ratio tended to be lower in the ET patients (P < 0.08). Exercise training prevents the deterioration of ABRMSNA in CHF patients.

Pressão Arterial , Barorreflexo , Sistema Cardiovascular/inervação , Terapia por Exercício , Insuficiência Cardíaca/terapia , Músculo Esquelético/inervação , Sistema Nervoso Simpático/fisiopatologia , Adulto , Idoso , Ciclismo , Brasil , Doença Crônica , Terapia por Exercício/métodos , Feminino , Insuficiência Cardíaca/diagnóstico , Insuficiência Cardíaca/fisiopatologia , Humanos , Masculino , Pessoa de Meia-Idade , Fatores de Tempo , Resultado do Tratamento
Am J Physiol Heart Circ Physiol ; 307(11): H1655-66, 2014 Dec 01.
Artigo em Inglês | MEDLINE | ID: mdl-25305179


Previous studies have demonstrated that muscle mechanoreflex and metaboreflex controls are altered in heart failure (HF), which seems to be due to changes in cyclooxygenase (COX) pathway and changes in receptors on afferent neurons, including transient receptor potential vanilloid type-1 (TRPV1) and cannabinoid receptor type-1 (CB1). The purpose of the present study was to test the hypotheses: 1) exercise training (ET) alters the muscle metaboreflex and mechanoreflex control of muscle sympathetic nerve activity (MSNA) in HF patients. 2) The alteration in metaboreflex control is accompanied by increased expression of TRPV1 and CB1 receptors in skeletal muscle. 3) The alteration in mechanoreflex control is accompanied by COX-2 pathway in skeletal muscle. Thirty-four consecutive HF patients with ejection fractions <40% were randomized to untrained (n = 17; 54 ± 2 yr) or exercise-trained (n = 17; 56 ± 2 yr) groups. MSNA was recorded by microneurography. Mechanoreceptors were activated by passive exercise and metaboreceptors by postexercise circulatory arrest (PECA). COX-2 pathway, TRPV1, and CB1 receptors were measured in muscle biopsies. Following ET, resting MSNA was decreased compared with untrained group. During PECA (metaboreflex), MSNA responses were increased, which was accompanied by the expression of TRPV1 and CB1 receptors. During passive exercise (mechanoreflex), MSNA responses were decreased, which was accompanied by decreased expression of COX-2, prostaglandin-E2 receptor-4, and thromboxane-A2 receptor and by decreased in muscle inflammation, as indicated by increased miRNA-146 levels and the stable NF-κB/IκB-α ratio. In conclusion, ET alters muscle metaboreflex and mechanoreflex control of MSNA in HF patients. This alteration with ET is accompanied by alteration in TRPV1 and CB1 expression and COX-2 pathway and inflammation in skeletal muscle.

Terapia por Exercício , Insuficiência Cardíaca/metabolismo , Insuficiência Cardíaca/terapia , Músculo Esquelético/metabolismo , Músculo Esquelético/fisiopatologia , Reflexo/fisiologia , Adulto , Idoso , Doença Crônica , Ciclo-Oxigenase 2/fisiologia , Teste de Esforço , Feminino , Insuficiência Cardíaca/fisiopatologia , Humanos , Masculino , Pessoa de Meia-Idade , Receptor CB1 de Canabinoide/biossíntese , Transdução de Sinais/fisiologia , Volume Sistólico/fisiologia , Sistema Nervoso Simpático/fisiopatologia , Canais de Cátion TRPV/biossíntese