RESUMEN
Here, we report the acute effects of aerobic (AER), resistance (RES), and combined (COM) exercises on blood pressure, central blood pressure and augmentation index, hemodynamic parameters, and autonomic modulation of resistant (RH) and nonresistant hypertensive (NON-RH) subjects. Twenty participants (10 RH and 10 NON-RH) performed three exercise sessions (i.e., AER, RES, and COM) and a control session. Hemodynamic (Finometer®, Beatscope), office blood pressure (BP), and autonomic variables (accessed through spectral analysis of the pulse-to-pulse BP signal, in the time and frequency domain-Fast Fourrier Transform) were assessed before (T0), one-hour (T1), and twenty-four (T2) hours after each experimental session. There were no changes in office BP, pulse wave behavior, and hemodynamic parameters after (T0 and T1) exercise sessions. However, AER and COM exercises significantly reduced sympathetic modulation in RH patients. It is worth mentioning that more significant changes in sympathetic modulation were observed after AER as compared to COM exercise. These findings suggest that office blood pressure, arterial stiffness, and hemodynamic parameters returned to baseline levels in the first hour and remained stable in the 24 hours after the all-exercise sessions. Notably, our findings bring new light to the effects of exercise on RH, indicating that RH patients show different autonomic responses to exercise compared to NON-RH patients. This trial is registered with trial registration number NCT02987452.
Asunto(s)
Sistema Cardiovascular , Hipertensión , Entrenamiento de Fuerza , Sistema Nervioso Autónomo/fisiología , Presión Sanguínea/fisiología , Humanos , Hipertensión/terapiaRESUMEN
Abstract Background: There is evidence that subclinical systemic inflammation is present in resistant hypertension (RHTN). Objective: The aim of the study was to develop an integrated measure of circulating cytokines/adipokines involved in the pathophysiology of RHTN. Methods: RHTN (n = 112) and mild to moderate hypertensive (HTN) subjects (n=112) were studied in a cross-sectional design. Plasma cytokines/adipokines (TNF-alpha, interleukins [IL]-6, -8, -10, leptin and adiponectin) values were divided into tertiles, to which a score ranging from 1 (lowest tertile) to 3 (highest tertile) was assigned. The inflammatory score (IS) of each subject was the sum of each pro-inflammatory cytokine scores from which anti-inflammatory cytokines (adiponectin and IL-10) scores were subtracted. The level of significance accepted was alpha = 0.05. Results: IS was higher in RHTN subjects compared with HTN subjects [4 (2-6) vs. 3 (2-5); p = 0.02, respectively]. IS positively correlated with body fat parameters, such as body mass index (r = 0.40; p < 0.001), waist circumference (r = 0.30; p < 0.001) and fat mass assessed by bioelectrical impedance analysis (r = 0.31; p < 0.001) in all hypertensive subjects. Logistic regression analyses revealed that IS was an independent predictor of RHTN (OR = 1.20; p = 0.02), independent of age, gender and race, although it did not remain significant after adjustment for body fat parameters. Conclusion: A state of subclinical inflammation defined by an IS including TNF-alpha, IL-6, IL-8, IL-10, leptin and adiponectin is associated with obese RHTN. In addition, this score correlates with obesity parameters, independently of hypertensive status. The IS may be used for the evaluation of conditions involving low-grade inflammation, such as obesity-related RHTN. Indeed, it also highlights the strong relationship between obesity and inflammatory process.
Resumo Fundamento: Evidências indicam que a inflamação sistêmica subclínica está presente na hipertensão arterial resistente (HAR). Objetivo: Desenvolver uma medida que integra citocinas envolvidas na fisiopatologia da HAR. Métodos: Indivíduos com HAR (n = 112) e indivíduos com hipertensão leve a moderada (HT) (n = 112) foram estudados em delineamento transversal. Valores de citocinas/adipocinas plasmáticas [TNF-alfa, interleucinas (IL)-6, -8, -10, leptina e adiponectina] foram divididos em tercis, e lhes atribuído um escore variando de 1 (tercil mais baixo) a 3 (tercil mais alto). O escore inflamatório (EI) de cada participante foi calculado como a soma do escore de cada citocina pró-inflamatória da qual subtraiu-se o escore de cada citocina anti-inflamatória (adiponectina e IL-10). O nível de significância aceito foi alfa = 0,05. Resultados: O EI foi mais alto nos indivíduos com HAR em comparação a indivíduos com HT [4 (2-6) vs. 3 (2-5); p = 0,02, respectivamente]. O EI correlacionou-se positivamente com parâmetros de gordura corporal, tais como índice de massa corporal (r = 0,40; p < 0,001), circunferência da cintura (r = 0,30; p < 0,001) e massa gorda avaliada por bioimpedância (r = 0,31; p < 0,001) em todos os indivíduos hipertensos. Análises de regressão logística mostraram que o EI foi um preditor independente de HAR (OR = 1,20; p = 0,02), independentemente de idade, sexo e raça; porém, o modelo perdeu significância estatística após ajuste para os parâmetros de gordura corporal. Conclusão: Um estado de inflamação subclínica definida pelo EI incluindo TNF-alfa, IL-6, IL-8, IL-10, leptina e adiponectina está associado com indivíduos obesos com HAR. Além disso, o escore correlaciona-se com parâmetros de obesidade, independentemente do grau de hipertensão. O EI pode ser usado na avaliação de condições que envolvem inflamação subclínica, tal como HAR relacionada à obesidade. O estudo também destaca a forte relação entre obesidade e inflamação.
Asunto(s)
Humanos , Masculino , Femenino , Adulto , Persona de Mediana Edad , Anciano , Citocinas/sangre , Adipoquinas/sangre , Hipertensión/sangre , Estándares de Referencia , Índice de Severidad de la Enfermedad , Ensayo de Inmunoadsorción Enzimática , Índice de Masa Corporal , Modelos Logísticos , Tejido Adiposo , Estudios Transversales , Factores de Riesgo , Estadísticas no Paramétricas , Medición de Riesgo , Hipertensión/fisiopatología , Hipertensión/tratamiento farmacológico , Antihipertensivos/uso terapéutico , Obesidad/fisiopatología , Obesidad/sangreRESUMEN
BACKGROUND: There is evidence that subclinical systemic inflammation is present in resistant hypertension (RHTN). OBJECTIVE: The aim of the study was to develop an integrated measure of circulating cytokines/adipokines involved in the pathophysiology of RHTN. METHODS: RHTN (n = 112) and mild to moderate hypertensive (HTN) subjects (n=112) were studied in a cross-sectional design. Plasma cytokines/adipokines (TNF-alpha, interleukins [IL]-6, -8, -10, leptin and adiponectin) values were divided into tertiles, to which a score ranging from 1 (lowest tertile) to 3 (highest tertile) was assigned. The inflammatory score (IS) of each subject was the sum of each pro-inflammatory cytokine scores from which anti-inflammatory cytokines (adiponectin and IL-10) scores were subtracted. The level of significance accepted was alpha = 0.05. RESULTS: IS was higher in RHTN subjects compared with HTN subjects [4 (2-6) vs. 3 (2-5); p = 0.02, respectively]. IS positively correlated with body fat parameters, such as body mass index (r = 0.40; p < 0.001), waist circumference (r = 0.30; p < 0.001) and fat mass assessed by bioelectrical impedance analysis (r = 0.31; p < 0.001) in all hypertensive subjects. Logistic regression analyses revealed that IS was an independent predictor of RHTN (OR = 1.20; p = 0.02), independent of age, gender and race, although it did not remain significant after adjustment for body fat parameters. CONCLUSION: A state of subclinical inflammation defined by an IS including TNF-alpha, IL-6, IL-8, IL-10, leptin and adiponectin is associated with obese RHTN. In addition, this score correlates with obesity parameters, independently of hypertensive status. The IS may be used for the evaluation of conditions involving low-grade inflammation, such as obesity-related RHTN. Indeed, it also highlights the strong relationship between obesity and inflammatory process.