RESUMO
BACKGROUND: Spontaneous arousals are relatively common during sleep, and induce hemodynamic responses. We sought to investigate the frequency and magnitude of blood pressure (BP) increases triggered by spontaneous arousals in patients with primary hypertension. METHODS: We conducted a study in which we divided 18 nonobese, sedentary adults without sleep-disordered breathing into two groups, consisting of: (i) hypertensive (HT, n = 8) patients; and (ii) normotensive (NT, n = 10) controls. The groups were matched for age and body mass index. All subjects underwent full polysomnography with simultaneous monitoring of heart rate (HR) and beat-by-beat BP. Each subject's BP and HR were analyzed immediately before BP peaks triggered by spontaneous arousals during stage 2 of nonrapid eye movement sleep. RESULTS: The total sleep time, sleep efficiency, and sleep structure in the two study groups were similar. In contrast, the number of arousals was significantly higher in the HT than in the NT group, at 25 ± 5 vs. 12 ± 3 events/h, respectively (P < 0.05). The HR of the HT and NT groups was similar before arousal (65 ± 3 bpm vs. 67 ± 3 bpm, respectively, P < 0.01) and increased significantly and similarly in the two groups upon arousal (to 79 ± 6 bpm vs. 74 ± 4 bpm, respectively, P < 0.01). Systolic and diastolic BPs were significantly higher throughout sleep in the HT than in the NT group. During spontaneous arousals, BP increased in both groups (P < 0.05). However, the magnitude of the increase in systolic BP was significantly greater in the HT than in the NT group (22 ± 3 mm Hg vs. 15 ± 3 mm Hg, P < 0.05). CONCLUSIONS: Patients with hypertension who do not have sleep-disordered breathing have an increased cardiovascular burden during sleep, which may be due to the greater number of arousals and exacerbated systolic BP response that they experience during sleep. These novel findings may have cardiovascular implications in patients with hypertension.
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Pressão Sanguínea/fisiologia , Hipertensão/fisiopatologia , Transtornos do Despertar do Sono/epidemiologia , Adulto , Estudos de Casos e Controles , Feminino , Hemodinâmica/fisiologia , Humanos , Incidência , Masculino , Polissonografia , Sono/fisiologiaRESUMO
BACKGROUND: Exercise training is a non-pharmacological strategy for treatment of heart failure. Exercise training improves functional capacity and quality of life in patients. Moreover, exercise training reduces muscle sympathetic nerve activity (MSNA) and peripheral vasoconstriction. However, most of these studies have been conducted in middle-aged patients. Thus, the effects of exercise training in older patients are much less understood. The present study was undertaken to investigate whether exercise training improves functional capacity, muscular sympathetic activation and muscular blood flow in older heart failure patients, as it does in middle-aged heart failure patients. DESIGN: Fifty-two consecutive outpatients with heart failure from the database of the Unit of Cardiovascular Rehabilitation and Physiology Exercise were divided by age (middle-aged, defined as 45-59 years, and older, defined as 60-75 years) and exercise status (trained and untrained). METHODS: MSNA was recorded directly from the peroneal nerve using the microneurography technique. Forearm blood flow (FBF) was measured by venous occlusion plethysmography. Functional capacity was evaluated by cardiopulmonary exercise test. RESULTS: Exercise training significantly and similarly increased FBF and peak VO(2) in middle-aged and older heart failure patients. In addition, exercise training significantly and similarly reduced MSNA and forearm vascular resistance in these patients. No significant changes were found in untrained patients. CONCLUSION: Exercise training improves neurovascular control and functional capacity in heart failure patients regardless of age.
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Terapia por Exercício , Insuficiência Cardíaca/reabilitação , Hemodinâmica , Músculo Esquelético/irrigação sanguínea , Músculo Esquelético/inervação , Nervo Fibular/fisiopatologia , Adulto , Fatores Etários , Idoso , Brasil , Tolerância ao Exercício , Feminino , Antebraço , Insuficiência Cardíaca/fisiopatologia , Humanos , Modelos Logísticos , Masculino , Pessoa de Meia-Idade , Análise Multivariada , Consumo de Oxigênio , Pletismografia , Recuperação de Função Fisiológica , Fluxo Sanguíneo Regional , Resultado do TratamentoRESUMO
INTRODUCTION: Among patients with congestive heart failure (CHF) both obstructive and central sleep apnea (SA) are associated with increased sympathetic activity. However, the day-night pattern of cardiac autonomic nervous system modulation in CHF patients with and without sleep apnea is unknown. MATERIAL AND METHODS: Twenty-five CHF patients underwent polysomnography with simultaneous beat-to-beat blood pressure (Portapres), respiration and electrocardiogram monitoring. Patients were divided according to the presence (SA, n=17) and absence of SA (NoSA, n=8). Power spectral analyses of heart rate variability (HRV) and spontaneous baroreflex sensitivity (BRS) were determined in periods with stable breathing while awake at 6 am, 10 am, 10 pm, as well as during stage 2 sleep. In addition, muscle sympathetic nerve activity (MSNA) was evaluated at 10 am. RESULTS: RR variance, low-frequency (LF), high-frequency (HF) powers of HRV, and BRS were significantly lower in patients with SA compared with NoSA in all periods. HF power, a marker of vagal activity, increased during sleep in patients with NoSA but in contrast did not change across the 24-hour period in patients with SA. MSNA was significantly higher in patients with SA compared with NoSA. RR variance, LF and HF powers correlated inversely with simultaneous MSNA (r=-0.64, -0.61, and -0.61 respectively; P<0.01). CONCLUSIONS: Patients with CHF and SA present a reduced and blunted cardiac autonomic modulation across the 24-hour period. These findings may help to explain the increased cardiovascular risk in patients with CHF and SA.
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Sistema Nervoso Autônomo/fisiologia , Ritmo Circadiano/fisiologia , Insuficiência Cardíaca/fisiopatologia , Síndromes da Apneia do Sono/fisiopatologia , Adulto , Idoso , Eletrocardiografia/métodos , Feminino , Insuficiência Cardíaca/complicações , Humanos , Masculino , Pessoa de Meia-Idade , Polissonografia/métodos , Síndromes da Apneia do Sono/complicaçõesRESUMO
AIMS: We compared the effects of exercise training on neurovascular control and functional capacity in men and women with chronic heart failure (HF). METHODS AND RESULTS: Forty consecutive HF outpatients from the Heart Institute, University of Sao Paulo, Brazil were divided into the following four groups matched by age: men exercise-trained (n = 12), men untrained (n = 10), women exercise-trained (n = 9), women untrained (n = 9). Maximal exercise capacity was determined from a maximal progressive exercise test on a cycle ergometer. Forearm blood flow was measured by venous occlusion plethysmography. Muscle sympathetic nerve activity (MSNA) was recorded directly using the technique of microneurography. There were no differences between groups in any baseline parameters. Exercise training produced a similar reduction in resting MSNA (P = 0.000002) and forearm vascular resistance (P = 0.0003), in men and women with HF. Peak VO(2) was similarly increased in men and women with HF (P = 0.0003) and VE/VCO(2) slope was significantly decreased in men and women with HF (P = 0.0007). There were no significant changes in left-ventricular ejection fraction in men and women with HF. CONCLUSION: The benefits of exercise training on neurovascular control and functional capacity in patients with HF are independent of gender.
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Exercício Físico/fisiologia , Insuficiência Cardíaca/fisiopatologia , Músculo Esquelético/irrigação sanguínea , Sistema Nervoso Simpático/fisiologia , Adulto , Idoso , Pressão Sanguínea/fisiologia , Feminino , Frequência Cardíaca/fisiologia , Humanos , Masculino , Pessoa de Meia-Idade , Fluxo Sanguíneo Regional , Fatores Sexuais , Volume Sistólico/fisiologia , Sistema Nervoso Simpático/fisiopatologia , Resultado do TratamentoRESUMO
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.
Assuntos
Exercício Físico , Insuficiência Cardíaca/reabilitação , Apneia do Sono Tipo Central/reabilitação , Apneia Obstrutiva do Sono/reabilitação , Adulto , Idoso , Velocidade do Fluxo Sanguíneo/fisiologia , Exercício Físico/fisiologia , Feminino , Antebraço/irrigação sanguínea , Insuficiência Cardíaca/fisiopatologia , Humanos , Masculino , Pessoa de Meia-Idade , Músculo Esquelético/inervação , Oxigênio/sangue , Pletismografia , Polissonografia , Estudos Prospectivos , Qualidade de Vida , Apneia do Sono Tipo Central/fisiopatologia , Apneia Obstrutiva do Sono/fisiopatologia , Sistema Nervoso Simpático/fisiopatologiaRESUMO
OBJECTIVES: The present study investigates the hemodynamic and autonomic regulation during sleep-awake transitions and across different sleep cycles in patients with essential hypertension. METHODS: Nineteen individuals free of sleep apnea (10 normotensive and nine hypertensive matched for age, sex, and body mass index) underwent a standard polysomnography, with simultaneous electrocardiography and beat-to-beat blood pressure monitoring (Portapres). All measurements were determined while awake (before and after sleep), as well as in the beginning and at end of the sleep cycle (first/last cycle of nonrapid and rapid eye movement stages). RESULTS: Systolic blood pressure was higher in hypertensives and exhibited a similar reduction to the normotensives ones in initial nonrapid eye movement sleep. This reduction was because of different mechanisms: a significant fall in cardiac output in normotensives, whereas in hypertensives was also dependent of a decrease in peripheral vascular resistance. Hypertensive patients presented lower heart rate variation and attenuated baroreflex sensitivity during sleep but not immediately before and after sleep. Spectral analysis suggested a higher sympathetic activity in the sleep stages in hypertension. Additionally, a progressive sympathetic predominance (final rapid eye movement > initial rapid eye movement and awake period postsleep > awake period presleep) was observed in both groups. CONCLUSION: Hypertension is associated with depressed baroreflex sensitivity and increased sympathetic activation during sleep. The greater sympathetic predominance at the end of night (preceding the morning surge of sympathetic activity) could be implicated in the occurrence of cardiovascular events.
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Hemodinâmica , Hipertensão/fisiopatologia , Sono/fisiologia , Sistema Nervoso Simpático/fisiopatologia , Adulto , Barorreflexo/fisiologia , Feminino , Humanos , Masculino , Sono REM/fisiologiaRESUMO
Chemoreflex control of sympathetic nerve activity is exaggerated in heart failure (HF) patients. However, the vascular implications of the augmented sympathetic activity during chemoreceptor activation in patients with HF are unknown. We tested the hypothesis that the muscle blood flow responses during peripheral and central chemoreflex stimulation would be blunted in patients with HF. Sixteen patients with HF (49 +/- 3 years old, Functional Class II-III, New York Heart Association) and 11 age-paired normal controls were studied. The peripheral chemoreflex control was evaluated by inhalation of 10% O(2) and 90% N(2) for 3 min. The central chemoreflex control was evaluated by inhalation of 7% CO(2) and 93% O(2) for 3 min. Muscle sympathetic nerve activity (MSNA) was directly evaluated by microneurography. Forearm blood flow was evaluated by venous occlusion plethysmography. Baseline MSNA were significantly greater in HF patients (33 +/- 3 vs. 20 +/- 2 bursts/min, P = 0.001). Forearm vascular conductance (FVC) was not different between the groups. During hypoxia, the increase in MSNA was significantly greater in HF patients than in normal controls (9.0 +/- 1.6 vs. 0.8 +/- 2.0 bursts/min, P = 0.001). The increase in FVC was significantly lower in HF patients (0.00 +/- 0.10 vs. 0.76 +/- 0.25 units, P = 0.001). During hypercapnia, MSNA responses were significantly greater in HF patients than in normal controls (13.9 +/- 3.2 vs. 2.1 +/- 1.9 bursts/min, P = 0.001). FVC responses were significantly lower in HF patients (-0.29 +/- 0.10 vs. 0.37 +/- 0.18 units, P = 0.001). In conclusion, muscle vasodilatation during peripheral and central chemoreceptor stimulation is blunted in HF patients. This vascular response seems to be explained, at least in part, by the exaggerated MSNA responses during hypoxia and hypercapnia.