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Dive into the research topics where Wladimir Musetti Medeiros is active.

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Featured researches published by Wladimir Musetti Medeiros.


Respiratory Physiology & Neurobiology | 2016

Effects of heart failure on cerebral blood flow in COPD: Rest and exercise

Mayron F. Oliveira; Maria Clara Alencar; Flavio Arbex; Aline Souza; Priscila A. Sperandio; Luiz Medina; Wladimir Musetti Medeiros; Daniel M. Hirai; Denis E. O'Donnell; J. Alberto Neder

Cerebral blood flow (CBF) and oxygenation (COx) are generally well-preserved in COPD. It is unknown whether prevalent cardiovascular co-morbidities, such as heart failure, may impair CBF and COx responses to exertion. Eighteen males with moderate-to-severe COPD (8 with and 10 without overlapping heart failure) underwent a progressive exercise test with pre-frontal CBF and COx measurements (indocyanine green and near-infrared spectroscopy). Mean arterial pressure and cardiac output were lower from rest to exercise in overlap. Only COPD patients demonstrated an increase in arterialized PCO2 towards the end of progressive exercise. CBF index was consistently higher and increased further by ∼40% during exercise in COPD whereas a ∼10% reduction was observed in overlap. COx was lower in overlap despite preserved arterial oxygenation. In conclusion, heart failure introduces pronounced negative effects on CBF and COx in COPD which may be associated with clinically relevant outcomes, including dyspnea, exercise intolerance, cerebrovascular disease and cognitive impairment.


American Journal of Physiology-regulatory Integrative and Comparative Physiology | 2015

Oxygen delivery-utilization mismatch in contracting locomotor muscle in COPD: peripheral factors

Wladimir Musetti Medeiros; Mari C. T. Fernandes; Diogo P. Azevedo; Flávia F Manfredi de Freitas; Beatriz C. Amorim; Luciana Dias Chiavegato; Daniel M. Hirai; Denis E. O'Donnell; J. Alberto Neder

Central cardiorespiratory and gas exchange limitations imposed by chronic obstructive pulmonary disease (COPD) impair ambulatory skeletal muscle oxygenation during whole body exercise. This investigation tested the hypothesis that peripheral factors per se contribute to impaired contracting lower limb muscle oxygenation in COPD patients. Submaximal neuromuscular electrical stimulation (NMES; 30, 40, and 50 mA at 50 Hz) of the quadriceps femoris was employed to evaluate contracting skeletal muscle oxygenation while minimizing the influence of COPD-related central cardiorespiratory constraints. Fractional O₂ extraction was estimated by near-infrared spectroscopy (deoxyhemoglobin/myoglobin concentration; deoxy-[Hb/Mb]), and torque output was measured by isokinetic dynamometry in 15 nonhypoxemic patients with moderate-to-severe COPD (SpO2 = 94 ± 2%; FEV₁ = 46.4 ± 10.1%; GOLD II and III) and in 10 age- and gender-matched sedentary controls. COPD patients had lower leg muscle mass than controls (LMM = 8.0 ± 0.7 kg vs. 8.9 ± 1.0 kg, respectively; P < 0.05) and produced relatively lower absolute and LMM-normalized torque across the range of NMES intensities (P < 0.05 for all). Despite producing less torque, COPD patients had similar deoxy-[Hb/Mb] amplitudes at 30 and 40 mA (P > 0.05 for both) and higher deoxy-[Hb/Mb] amplitude at 50 mA (P < 0.05). Further analysis indicated that COPD patients required greater fractional O₂ extraction to produce torque (i.e., ↑Δdeoxy-[Hb/Mb]/torque) relative to controls (P < 0.05 for 40 and 50 mA) and as a function of NMES intensity (P < 0.05 for all). The present data obtained during submaximal NMES of small muscle mass indicate that peripheral abnormalities contribute mechanistically to impaired contracting skeletal muscle oxygenation in nonhypoxemic, moderate-to-severe COPD patients.


COPD: Journal of Chronic Obstructive Pulmonary Disease | 2016

Heart Failure Impairs Muscle Blood Flow and Endurance Exercise Tolerance in COPD

Mayron F. Oliveira; Flavio Arbex; Maria Clara Alencar; Aline Souza; Sperandio Pa; Wladimir Musetti Medeiros; Adriana Mazzuco; Audrey Borghi-Silva; Luiz Medina; Santos R; Daniel M. Hirai; Frederico José Neves Mancuso; Dirceu R. Almeida; Denis E. O'Donnell; José Alberto Neder

Abstract Heart failure, a prevalent and disabling co-morbidity of COPD, may impair cardiac output and muscle blood flow thereby contributing to exercise intolerance. To investigate the role of impaired central and peripheral hemodynamics in limiting exercise tolerance in COPD-heart failure overlap, cycle ergometer exercise tests at 20% and 80% peak work rate were performed by overlap (FEV1 = 56.9 ± 15.9% predicted, ejection fraction = 32.5 ± 6.9%; N = 16), FEV1-matched COPD (N = 16), ejection fraction-matched heart failure patients (N = 15) and controls (N = 12). Differences (Δ) in cardiac output (impedance cardiography) and vastus lateralis blood flow (indocyanine green) and deoxygenation (near-infrared spectroscopy) between work rates were expressed relative to concurrent changes in muscle metabolic demands (ΔO2 uptake). Overlap patients had approximately 30% lower endurance exercise tolerance than COPD and heart failure (p < 0.05). ΔBlood flow was closely proportional to Δcardiac output in all groups (r = 0.89–0.98; p < 0.01). Overlap showed the largest impairments in Δcardiac output/ΔO2 uptake and Δblood flow/ΔO2 uptake (p < 0.05). Systemic arterial oxygenation, however, was preserved in overlap compared to COPD. Blunted limb perfusion was related to greater muscle deoxygenation and lactate concentration in overlap (r = 0.78 and r = 0.73, respectively; p < 0.05). ΔBlood flow/ΔO2 uptake was related to time to exercise intolerance only in overlap and heart failure (p < 0.01). In conclusion, COPD and heart failure add to decrease exercising cardiac output and skeletal muscle perfusion to a greater extent than that expected by heart failure alone. Treatment strategies that increase muscle O2 delivery and/or decrease O2 demand may be particularly helpful to improve exercise tolerance in COPD patients presenting heart failure as co-morbidity.


International Journal of Chronic Obstructive Pulmonary Disease | 2015

Relationship between linear and nonlinear dynamics of heart rate and impairment of lung function in COPD patients

Adriana Mazzuco; Wladimir Musetti Medeiros; Milena Pelosi Sperling; Aline Souza; Maria Clara Alencar; Flavio Arbex; José Alberto Neder; Ross Arena; Audrey Borghi-Silva

Background In chronic obstructive pulmonary disease (COPD), functional and structural impairment of lung function can negatively impact heart rate variability (HRV); however, it is unknown if static lung volumes and lung diffusion capacity negatively impacts HRV responses. We investigated whether impairment of static lung volumes and lung diffusion capacity could be related to HRV indices in patients with moderate to severe COPD. Methods Sixteen sedentary males with COPD were enrolled in this study. Resting blood gases, static lung volumes, and lung diffusion capacity for carbon monoxide (DLCO) were measured. The RR interval (RRi) was registered in the supine, standing, and seated positions (10 minutes each) and during 4 minutes of a respiratory sinus arrhythmia maneuver (M-RSA). Delta changes (Δsupine-standing and Δsupine-M-RSA) of the standard deviation of normal RRi, low frequency (LF, normalized units [nu]) and high frequency (HF [nu]), SD1, SD2, alpha1, alpha2, and approximate entropy (ApEn) indices were calculated. Results HF, LF, SD1, SD2, and alpha1 deltas significantly correlated with forced expiratory volume in 1 second, DLCO, airway resistance, residual volume, inspiratory capacity/total lung capacity ratio, and residual volume/total lung capacity ratio. Significant and moderate associations were also observed between LF/HF ratio versus total gas volume (%), r=0.53; LF/HF ratio versus residual volume, %, r=0.52; and HF versus total gas volume (%), r=−0.53 (P<0.05). Linear regression analysis revealed that ΔRRi supine-M-RSA was independently related to DLCO (r=−0.77, r2=0.43, P<0.05). Conclusion Responses of HRV indices were more prominent during M-RSA in moderate to severe COPD. Moreover, greater lung function impairment was related to poorer heart rate dynamics. Finally, impaired lung diffusion capacity was related to an altered parasympathetic response in these patients.


Cardiology in The Young | 2016

Abnormal heart rate recovery and deficient chronotropic response after submaximal exercise in young Marfan syndrome patients.

Paulo Peres; Antonio Carlos Campos de Carvalho; Ana Beatriz Alvarez Perez; Wladimir Musetti Medeiros

BACKGROUND Marfan syndrome patients present important cardiac structural changes, ventricular dysfunction, and electrocardiographic changes. An abnormal heart rate response during or after exercise is an independent predictor of mortality and autonomic dysfunction. The aim of the present study was to compare heart rate recovery and chronotropic response obtained by cardiac reserve in patients with Marfan syndrome subjected to submaximal exercise. METHODS A total of 12 patients on β-blocker therapy and 13 off β-blocker therapy were compared with 12 healthy controls. They were subjected to submaximal exercise with lactate measurements. The heart rate recovery was obtained in the first minute of recovery and corrected for cardiac reserve and peak lactate concentration. RESULTS Peak heart rate (141±16 versus 155±17 versus 174±8 bpm; p=0.001), heart rate reserve (58.7±9.4 versus 67.6±14.3 versus 82.6±4.8 bpm; p=0.001), heart rate recovery (22±6 versus 22±8 versus 34±9 bpm; p=0.001), and heart rate recovery/lactate (3±1 versus 3±1 versus 5±1 bpm/mmol/L; p=0.003) were different between Marfan groups and controls, respectively. All the patients with Marfan syndrome had heart rate recovery values below the mean observed in the control group. The absolute values of heart rate recovery were strongly correlated with the heart rate reserve (r=0.76; p=0.001). CONCLUSION Marfan syndrome patients have reduced heart rate recovery and chronotropic deficit after submaximal exercise, and the chronotropic deficit is a strong determinant of heart rate recovery. These changes are suggestive of autonomic dysfunction.


Revista Brasileira De Reumatologia | 2007

Reabilitação em artrite idiopática juvenil

Vanessa C. Bueno; Império Lombardi Júnior; Wladimir Musetti Medeiros; Mariana Moreira Alckmin Azevedo; Claudio Arnaldo Len; Maria Teresa Terreri; Jamil Natour; Maria Odete Esteves Hilário

INTRODUCTION AND AIMS: juvenile idiopathic arthritis (JIA) may cause permanent physical disabilities in children and adolescents. This study aimed to describe the several kinds of rehabilitation procedures, ranging from evaluation to prescription of exercises, as well as the elaboration of a practical rehabilitation guide for JIA patients. SOURCES OF DATA: the research was based on data from Medline and Lilacs. The opinion of experts working on the Pediatric Rheumatology service from Lar Escola Sao Francisco and Universidade Federal de Sao Paulo was considered on the debate of several topics. SUMMARY: JIA patients may present pain and limitation of joint movement thereby leading to decrease in physical capacity, affecting both aerobic and anaerobic activities. In addition to the joint compromise, cardiac and autonomic dysfunctions collaborate on this process, impairing sport and everyday activities. The American College of Rheumatology recommends 30-minute activity with moderate intensity, two to three times weekly. Hydrotherapy is associated to treatment adherence, besides helping in decreasing pain perception and adding to cope with daily activities. Other rehabilitation modalities, such as massage, education, joint protection, energy conservation, and splints are also considered in the present review. CONCLUSION: there are few studies in the literature focusing on rehabilitation in children with JIA. Particularly, there is a lack of studies concerning aspects of adequate prescription of exercises, weight-bearing, number of series and repetitions, as well as the best choice regarding ground or water activity. We believe that additional information is needed in order to improve the physical care to these patients.


European Journal of Preventive Cardiology | 2014

The dysfunction of ammonia in heart failure increases with an increase in the intensity of resistance exercise, even with the use of appropriate drug therapy:

Wladimir Musetti Medeiros; Antonio Carlos Carvalho; Paulo Peres; Fábio Augusto De Luca; Carlos Gun

Background: Hyperammonemia during rest periods is a dysfunction in heart failure (HF). The low formation of ammonia during exercise reflects an inefficiency of purine metabolism. Hyperkalemia in response to physical exercise is common in HF and may contribute to a contractile inefficiency in type II fibers, leading to early fatigue. We tested the hypothesis that during resistance exercise of high intensity and low volume, this disorder of ammonia metabolism would be more intense, due to the hyperkalemia present in HF. Methods: Alternating resistance exercise (RE) of low intensity and high volume, and high intensity and low volume, were applied to 18 patients with an interval of 7 days between them (functional class II-III New York Heart Association, FE = 33.5 ± 4%) and compared with 22 healthy controls matched for age and gender. Ammonia, potassium and lactate levels were assessed before and immediately after the RE. Results: Significant differences: Deltas (control vs. HF) in 40% RE: lactate (mg/dl) 26.3 ± 10 vs. 37.7 ± 7; p < 0,001, ammonia (ug/dl) 92.5 ± 18 vs. 48.9 ± 9; p < 0.001. Deltas (control vs. HF) in 80%RE: lactate(mg/dl) 45.0 ± 12 vs. 54.1 ± 11; p < 0.05, ammonia(ug/dl) 133.5 ± 22 vs. 32.2 ± 7; p < 0.001, potassium (mEq/L) 1.6 ± 0.4 vs. 2.0 ± 0.8; p < 0.05. A negative correlation was found between the deltas of ammonia and potassium (r = −0.74, p < 0.001) in the HF group. Conclusions: We conclude that in HF, there is an inefficiency of purine metabolism that increases with increasing exercise intensity, but not with an increase of total volume. These findings suggest that hyperkalemia may play an important role in the disorders of purine metabolism.


Arquivos Brasileiros De Cardiologia | 2012

Efeito de um programa de exercício físico em portador da Síndrome Marfan com disfunção ventricular

Wladimir Musetti Medeiros; Paulo Peres; Antonio Carlos Carvalho; Carlos Gun; Fábio Augusto De Luca

Marfan syndrome (MS) is an autosomal dominant disorder that affects multiple organs and systems. Several cardiac alterations are present, with the main ones being aortic root and ascending aorta dilatation, mitral valve prolapse and left ventricle (LV) dilatation. Aerobic exercise has not shown to be a non-drug therapy that promotes anti-remodeling effect in patients with heart failure. This case report describes the echocardiographic changes in a patient with Marfan syndrome during four years of cardiovascular physical therapy.El Sindrome de Marfan (SM) es un desorden autosomico dominante que afecta multiples organos y sistemas. Diversas alteraciones cardiacas estan presentes, siendo las principales la dilatacion de la raiz de la aorta y de la aorta ascendente, el Prolapso de Valvula Mitral y la dilatacion del Ventriculo Izquierdo (VI). El ejercicio aerobico ha mostrado ser un recurso terapeutico no medicamentoso, por promover efecto de antirremodelado en pacientes con insuficiencia cardiaca. Este relato de caso describe las alteraciones ecocardiograficas de un paciente con Sindrome de Marfan durante cuatro anos de un programa de fisioterapia cardiovascular.


Journal of Applied Physiology | 2018

Hyperadditive Ventilatory Response Arising from Interaction between the Carotid Chemoreflex and the Muscle Mechanoreflex in Healthy Humans

Talita M. Silva; Liliane Cunha Aranda; Marcelle Paula-Ribeiro; Diogo Machado Oliveira; Wladimir Musetti Medeiros; Lauro C. Vianna; Luiz Eduardo Nery; Bruno M. Silva

Physical exercise potentiates the carotid chemoreflex control of ventilation (VE). Hyperadditive neural interactions may partially mediate the potentiation. However, some neural interactions remain incompletely explored. As the potentiation occurs even during low-intensity exercise, we tested the hypothesis that the carotid chemoreflex and the muscle mechanoreflex could interact in a hyperadditive fashion. Fourteen young healthy subjects inhaled randomly, in separate visits, 12% O2 to stimulate the carotid chemoreflex and 21% O2 as control. A rebreathing circuit maintained isocapnia. During gases administration, subjects either remained at rest (i.e., normoxic and hypoxic rest) or the muscle mechanoreflex was stimulated via passive knee movement (i.e., normoxic and hypoxic movement). Surface muscle electrical activity did not increase during the passive movement, confirming the absence of active contractions. Hypoxic rest and normoxic movement similarly increased VE [change (mean ± SE) = 1.24 ± 0.72 vs. 0.73 ± 0.43 l/min, respectively; P = 0.46], but hypoxic rest only increased tidal volume (Vt), and normoxic movement only increased breathing frequency (BF). Hypoxic movement induced greater VE and mean inspiratory flow (Vt/Ti) increase than the sum of hypoxic rest and normoxic movement isolated responses (VE change: hypoxic movement = 3.72 ± 0.81 l/min vs. sum = 1.96 ± 0.83 l/min, P = 0.01; Vt/Ti change: hypoxic movement = 0.13 ± 0.03 l/s vs. sum = 0.06 ± 0.03 l/s, P = 0.02). Moreover, hypoxic movement increased both Vt and BF. Collectively, the results indicate that the carotid chemoreflex and the muscle mechanoreflex interacted, mediating a hyperadditive ventilatory response in healthy humans. NEW & NOTEWORTHY The main finding of this study was that concomitant carotid chemoreflex and muscle mechanoreflex stimulation provoked greater ventilation increase than the sum of ventilation increase induced by stimulation of each reflex in isolation, which, consequently, supports that the carotid chemoreflex and the muscle mechanoreflex interacted, mediating a hyperadditive ventilatory response in healthy humans.


Arquivos Brasileiros De Cardiologia | 2012

Effect of a physical exercise program in a patient with Marfan Syndrome and ventricular dysfunction

Wladimir Musetti Medeiros; Paulo Peres; Antonio Carlos Carvalho; Carlos Gun; Fábio Augusto De Luca

Marfan syndrome (MS) is an autosomal dominant disorder that affects multiple organs and systems. Several cardiac alterations are present, with the main ones being aortic root and ascending aorta dilatation, mitral valve prolapse and left ventricle (LV) dilatation. Aerobic exercise has not shown to be a non-drug therapy that promotes anti-remodeling effect in patients with heart failure. This case report describes the echocardiographic changes in a patient with Marfan syndrome during four years of cardiovascular physical therapy.El Sindrome de Marfan (SM) es un desorden autosomico dominante que afecta multiples organos y sistemas. Diversas alteraciones cardiacas estan presentes, siendo las principales la dilatacion de la raiz de la aorta y de la aorta ascendente, el Prolapso de Valvula Mitral y la dilatacion del Ventriculo Izquierdo (VI). El ejercicio aerobico ha mostrado ser un recurso terapeutico no medicamentoso, por promover efecto de antirremodelado en pacientes con insuficiencia cardiaca. Este relato de caso describe las alteraciones ecocardiograficas de un paciente con Sindrome de Marfan durante cuatro anos de un programa de fisioterapia cardiovascular.

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Flavio Arbex

Federal University of São Paulo

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Maria Clara Alencar

Federal University of São Paulo

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Paulo Peres

Federal University of São Paulo

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Antonio Carlos Carvalho

Federal University of São Paulo

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J. Alberto Neder

Federal University of São Paulo

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Aline Souza

Federal University of São Paulo

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Luciana Dias Chiavegato

Federal University of São Paulo

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Mari C. T. Fernandes

Federal University of São Paulo

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