Respiratory Muscle Training Improves Diaphragm Citrate Synthase Activity and Hemodynamic Function in Rats with Heart Failure.

Rodrigo Boemo Jaenisch,Audrey Borghi-Silva,Ross Arena,Mariane Bertagnolli,Pedro Dal Lago

doi:10.21470/1678-9741-2017-0002

Abstract

Introduction Enhanced respiratory muscle strength in patients with heart failure positively alters the clinical trajectory of heart failure. In an experimental model, respiratory muscle training in rats with heart failure has been shown to improve cardiopulmonary function through mechanisms yet to be entirely elucidated.ObjectiveThe present report aimed to evaluate the respiratory muscle training effects in diaphragm citrate synthase activity and hemodynamic function in rats with heart failure.MethodsWistar rats were divided into four experimental groups: sedentary sham (Sed-Sham, n=8), trained sham (RMT-Sham, n=8), sedentary heart failure (Sed-HF, n=7) and trained heart failure (RMT-HF, n=7). The animals were submitted to a RMT protocol performed 30 minutes a day, 5 days/week, for 6 weeks.ResultsIn rats with heart failure, respiratory muscle training decreased pulmonary congestion and right ventricular hypertrophy. Deleterious alterations in left ventricular pressures, as well as left ventricular contractility and relaxation, were assuaged by respiratory muscle training in heart failure rats. Citrate synthase activity, which was significantly reduced in heart failure rats, was preserved by respiratory muscle training. Additionally, a negative correlation was found between citrate synthase and left ventricular end diastolic pressure and positive correlation was found between citrate synthase and left ventricular systolic pressure.ConclusionRespiratory muscle training produces beneficial adaptations in the diaphragmatic musculature, which is linked to improvements in left ventricular hemodynamics and blood pressure in heart failure rats. The RMT-induced improvements in cardiac architecture and the oxidative capacity of the diaphragm may improve the clinical trajectory of patients with heart failure.

Highlights

Enhanced respiratory muscle strength in patients with heart failure positively alters the clinical trajectory of heart failure
Respiratory muscle training produces beneficial adaptations in the diaphragmatic musculature, which is linked to improvements in left ventricular hemodynamics and blood pressure in heart failure rats
The respiratory muscle training (RMT)-induced improvements in cardiac architecture and the oxidative capacity of the diaphragm may improve the clinical trajectory of patients with heart failure

Summary

Introduction

Enhanced respiratory muscle strength in patients with heart failure positively alters the clinical trajectory of heart failure. Heart failure (HF) is related to reduced cardiac output as well as blood flow to the skeletal muscle, which impairs cell aerobic metabolism, during physical exertion[1]. The inability of the heart to supply adequate amounts of blood to meet the metabolic needs of peripheral tissues[2], including the diaphragm muscle, is likely a key pathophysiological mechanism of HF. Patients with HF often present with inspiratory muscle weakness[4] and peripheral skeletal muscle dysfunction[5], which are important contributors to exercise intolerance and culminate in poor prognosis[4,5]. Peripheral muscle abnormalities in HF, such as impaired skeletal muscle energy metabolism, mitochondrial dysfunction, fiber-type transition and atrophy, play an important role in exercise intolerance[1], which seems to be associated with the genesis of the pathophysiological mechanism. Alterations in muscle energy metabolism related to mitochondrial dysfunction has been assessed through measurement of citrate synthase (CS) activity, one of the first enzymes participating in the citric acid cycle and cellular oxidative metabolism, reflecting mitochondrial content in muscle tissue[2,6]

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