LIGIA DE MORAES ANTUNES CORREA
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conferenceObject Effects of Aerobic and Inspiratory Training on Skeletal Muscle Microrna-1 and Downstream-Associated Pathways in Patients With Systolic Heart Failure(2019) ANTUNES-CORREA, Ligia M.; TREVIZAN, Patricia; BACURAU, Aline V.; FERREIRA-SANTOS, Larissa; GOMES, Joao L.; URIAS, Ursula; OLIVEIRA, Patricia; ALVES, Maria-Janieire N.; ALMEIDA, Dirceu R.; BRUM, Patricia C.; OLIVEIRA, Edilamar M.; HAJJAR, Ludhmila; KALIL FILHO, Roberto; NEGRAO, Carlos E.- Exercise training prevents the deterioration in the arterial baroreflex control of sympathetic nerve activity in chronic heart failure patients(2015) GROEHS, Raphaela V.; TOSCHI-DIAS, Edgar; ANTUNES-CORREA, Ligia M.; TREVIZAN, Patricia F.; RONDON, Maria Urbana P. B.; OLIVEIRA, Patricia; ALVES, Maria J. N. N.; ALMEIDA, Dirceu R.; MIDDLEKAUFF, Holly R.; NEGRAO, Carlos E.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 (V) over dot O-2 <= 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.
- Effects of exercise training on neurovascular control and skeletal myopathy in systolic heart failure(2015) NEGRAO, Carlos E.; MIDDLEKAUFF, Holly R.; GOMES-SANTOS, Igor L.; ANTUNES-CORREA, Ligia M.Neurohormonal excitation and dyspnea are the hallmarks of heart failure (HF) and have long been associated with poor prognosis in HF patients. Sympathetic nerve activity (SNA) and ventilatory equivalent of carbon dioxide (VE/VO2) are elevated in moderate HF patients and increased even further in severe HF patients. The increase in SNA in HF patients is present regardless of age, sex, and etiology of systolic dysfunction. Neurohormonal activation is the major mediator of the peripheral vasoconstriction characteristic of HF patients. In addition, reduction in peripheral blood flow increases muscle inflammation, oxidative stress, and protein degradation, which is the essence of the skeletal myopathy and exercise intolerance in HF. Here we discuss the beneficial effects of exercise training on resting SNA in patients with systolic HF and its central and peripheral mechanisms of control. Furthermore, we discuss the exercise-mediated improvement in peripheral vasoconstriction in patients with HF. We will also focus on the effects of exercise training on ventilatory responses. Finally, we review the effects of exercise training on features of the skeletal myopathy in HF. In summary, exercise training plays an important role in HF, working synergistically with pharmacological therapies to ameliorate these abnormalities in clinical practice.
- Muscle electrical stimulation improves neurovascular control and exercise tolerance in hospitalised advanced heart failure patients(2016) GROEHS, Raphaela V.; ANTUNES-CORREA, Ligia M.; NOBRE, Thais S.; ALVES, Maria-Janieire N. N.; RONDON, Maria Urbana P. B.; BARRETO, Antonio Carlos Pereira; NEGRAO, Carlos E.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 fraction30% were consecutively randomly assigned into two groups: functional electrical stimulation (n=15; 542 years) and control (n=15; 492 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 10Hz frequency, 150ms pulse width and 70 mA intensity for 60minutes/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.
- Personalized Preventive Medicine: Genetics and the Response to Regular Exercise in Preventive Interventionse(2015) BOUCHARD, Claude; ANTUNES-CORREA, Ligia M.; ASHLEY, Euan A.; FRANKLIN, Nina; HWANG, Paul M.; MATTSSON, C. Mikael; NEGRAO, Carlos E.; PHILLIPS, Shane A.; SARZYNSKI, Mark A.; WANG, Ping-yuan; WHEELER, Matthew T.Regular exercise and a physically active lifestyle have favorable effects on health. Several issues related to this theme are addressed in this report. A comment on the requirements of personalized exercise medicine and in-depth biological profiling along with the opportunities that they offer is presented. This is followed by a brief overview of the evidence for the contributions of genetic differences to the ability to benefit from regular exercise. Subsequently, studies showing that mutations in TP53 influence exercise capacity in mice and humans are succinctly described. The evidence for effects of exercise on endothelial function in health and disease also is covered. Finally, changes in cardiac and skeletal muscle in response to exercise and their implications for patients with cardiac disease are summarized. Innovative research strategies are needed to define the molecular mechanisms involved in adaptation to exercise and to translate them into useful clinical and public health applications.
- The influence of aetiology on the benefits of exercise training in patients with heart failure(2017) ANTUNES-CORREA, Ligia M.; UENO-PARDI, Linda M.; TREVIZAN, Patricia F.; SANTOS, Marcelo R.; SILVA, Carlos Henrique P. da; FRANCO, Fabio G. M.; ALVES, Maria Janieire N. N.; RONDON, Maria Urbana P. B.; NEGRAO, Carlos E.Background: Exercise training improves neurovascular control and functional capacity in heart failure (HF) patients. However, the influence of the aetiology on these benefits is unknown. We compared the effects of exercise training on neurovascular control and functional capacity in idiopathic, ischaemic and hypertensive HF patients. Design: Subjects consisted of 45 exercise-trained HF patients from our database (2000-2015), aged 40-70 years old, functional class II/ III and ejection fraction <= 40%, and they were divided into three groups: idiopathic (n = 11), ischaemic (n = 18) and hypertensive (n = 16). Methods: Functional capacity was determined by cardiopulmonary exercise testing. Muscle sympathetic nerve activity (MSNA) was recorded by microneurography. Forearm blood flow (FBF) was measured by venous occlusion plethysmography. Results: Four months of exercise training significantly reduced MSNA and significantly increased FBF in all groups. However, the relative reduction in MSNA was greater in hypertensive patients compared with that in idiopathic patients (frequency: -34% vs. -15%, p -0.01; incidence: -31% vs. -12%, p -0.02). No differences were found between hypertensive patients and ischaemic patients. The relative increase in FBF was greater in hypertensive patients than in ischaemic and idiopathic patients (42% vs. 15% and 17%, respectively, p = 0.02). The relative increase in forearm vascular conductance was greater in hypertensive patients compared with those in ischaemic and idiopathic patients (57% vs. 13% and 26%, respectively, p = 0.001). Exercise training significantly and similarly increased peak oxygen consumption in all groups. Conclusion: The exercise-induced improvement in neurovascular control is more pronounced in hypertensive HF patients than in idiopathic and ischaemic HF patients. The increase in functional capacity is independent of aetiology.
- Effects of exercise training on neurovascular responses during handgrip exercise in heart failure patients(2011) SOARES-MIRANDA, Luisa; FRANCO, Fabio G. M.; ROVEDA, Fabiana; MARTINEZ, Daniel G.; RONDON, Maria U. P. B.; MOTA, Jorge; BRUM, Patricia C.; ANTUNES-CORREA, Ligia M.; NOBRE, Thais S.; BARRETTO, Antonio C. P.; MIDDLEKAUFF, Holly R.; NEGRAO, Carlos E.
- Exercise training improves neurovascular control and functional capacity in heart failure patients regardless of age(2012) ANTUNES-CORREA, Ligia M.; KANAMURA, Bianca Y.; MELO, Ruth C.; NOBRE, Thais S.; UENO, Linda M.; FRANCO, Fabio G. M.; ROVEDA, Fabiana; BRAGA, Ana Maria; RONDON, Maria U. P. B.; BRUM, Patricia C.; BARRETTO, Antonio C. P.; MIDDLEKAUFF, Holly R.; NEGRAO, Carlos E.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 VO2 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.
- Exercise training improves neurovascular control and calcium cycling gene expression in patients with heart failure with cardiac resynchronization therapy(2016) NOBRE, Thais S.; ANTUNES-CORREA, Ligia M.; GROEHS, Raphaela V.; ALVES, Maria Janieire N. N.; SARMENTO, Adriana O.; BACURAU, Aline V.; URIAS, Ursula; ALVES, Guilherme B.; RONDON, Maria Urbana P. B.; BRUM, Patricia C.; MARTINELLI, Martino; MIDDLEKAUFF, Holly R.; NEGRAO, Carlos E.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: (V) over dotO(2peak), MSNA (microneurography), forearm blood flow, and Ca2+ -handling gene expression in vastus lateralis muscle. After 4 mo, exercise duration and (V) over dotO(2peak) 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.
- Oscillatory Pattern of Sympathetic Nerve Bursts Is Associated With Baroreflex Function in Heart Failure Patients With Reduced Ejection Fraction(2021) TOSCHI-DIAS, Edgar; MONTANO, Nicola; TOBALDINI, Eleonora; TREVIZAN, Patricia F.; V, Raphaela Groehs; ANTUNES-CORREA, Ligia M.; NOBRE, Thais S.; LOBO, Denise M.; SALES, Allan R. K.; UENO-PARDI, Linda M.; MATOS, Luciana D. N. J. de; OLIVEIRA, Patricia A.; BRAGA, Ana Maria F. W.; ALVES, Maria Janieire N. N.; NEGRAO, Carlos E.; RONDON, Maria Urbana P. B.Sympathetic hyperactivation and baroreflex dysfunction are hallmarks of heart failure with reduced ejection fraction (HFrEF). However, it is unknown whether the progressive loss of phasic activity of sympathetic nerve bursts is associated with baroreflex dysfunction in HFrEF patients. Therefore, we investigated the association between the oscillatory pattern of muscle sympathetic nerve activity (LFMSNA/HFMSNA) and the gain and coupling of the sympathetic baroreflex function in HFrEF patients. In a sample of 139 HFrEF patients, two groups were selected according to the level of LFMSNA/HFMSNA index: (1) Lower LFMSNA/HFMSNA (lower terciles, n = 46, aged 53 +/- 1 y) and (2) Higher LFMSNA/HFMSNA (upper terciles, n = 47, aged 52 +/- 2 y). Heart rate (ECG), arterial pressure (oscillometric method), and muscle sympathetic nerve activity (microneurography) were recorded for 10 min in patients while resting. Spectral analysis of muscle sympathetic nerve activity was conducted to assess the LFMSNA/HFMSNA, and cross-spectral analysis between diastolic arterial pressure, and muscle sympathetic nerve activity was conducted to assess the sympathetic baroreflex function. HFrEF patients with lower LFMSNA/HFMSNA had reduced left ventricular ejection fraction (26 +/- 1 vs. 29 +/- 1%, P = 0.03), gain (0.15 +/- 0.03 vs. 0.30 +/- 0.04 a.u./mmHg, P < 0.001) and coupling of sympathetic baroreflex function (0.26 +/- 0.03 vs. 0.56 +/- 0.04%, P < 0.001) and increased muscle sympathetic nerve activity (48 +/- 2 vs. 41 +/- 2 bursts/min, P < 0.01) and heart rate (71 +/- 2 vs. 61 & PLUSMN; 2 bpm, P < 0.001) compared with HFrEF patients with higher LFMSNA/HFMSNA. Further analysis showed an association between the LFMSNA/HFMSNA with coupling of sympathetic baroreflex function (R = 0.56, P < 0.001) and left ventricular ejection fraction (R = 0.23, P = 0.02). In conclusion, there is a direct association between LFMSNA/HFMSNA and sympathetic baroreflex function and muscle sympathetic nerve activity in HFrEF patients. This finding has clinical implications, because left ventricular ejection fraction is less in the HFrEF patients with lower LFMSNA/HFMSNA.