RESUMO
Skeletal muscle is the major deposit of protein molecules. As for any cell or tissue, total muscle protein reflects a dynamic turnover between net protein synthesis and degradation. Noninvasive and invasive techniques have been applied to determine amino acid catabolism and muscle protein building at rest, during exercise and during the recovery period after a single experiment or training sessions. Stable isotopic tracers (13C-lysine, 15N-glycine, ²H5-phenylalanine) and arteriovenous differences have been used in studies of skeletal muscle and collagen tissues under resting and exercise conditions. There are different fractional synthesis rates in skeletal muscle and tendon tissues, but there is no major difference between collagen and myofibrillar protein synthesis. Strenuous exercise provokes increased proteolysis and decreased protein synthesis, the opposite occurring during the recovery period. Individuals who exercise respond differently when resistance and endurance types of contractions are compared. Endurance exercise induces a greater oxidative capacity (enzymes) compared to resistance exercise, which induces fiber hypertrophy (myofibrils). Nitrogen balance (difference between protein intake and protein degradation) for athletes is usually balanced when the intake of protein reaches 1.2 g·kg-1·day-1 compared to 0.8 g·kg-1·day-1 in resting individuals. Muscular activities promote a cascade of signals leading to the stimulation of eukaryotic initiation of myofibrillar protein synthesis. As suggested in several publications, a bolus of 15-20 g protein (from skimmed milk or whey proteins) and carbohydrate (± 30 g maltodextrine) drinks is needed immediately after stopping exercise to stimulate muscle protein and tendon collagen turnover within 1 h.
Assuntos
Humanos , Atletas , Aminoácidos Essenciais/administração & dosagem , Proteínas Alimentares/administração & dosagem , Exercício Físico/fisiologia , Proteínas Musculares/metabolismo , Músculo Esquelético/metabolismo , Recomendações Nutricionais , Aminoácidos Essenciais/farmacocinética , Metabolismo Energético/fisiologia , Proteínas do Leite/administração & dosagem , Proteínas Musculares/fisiologia , Músculo Esquelético/fisiologia , Resistência Física/fisiologia , Biossíntese de Proteínas/fisiologiaRESUMO
Skeletal muscle is the major deposit of protein molecules. As for any cell or tissue, total muscle protein reflects a dynamic turnover between net protein synthesis and degradation. Noninvasive and invasive techniques have been applied to determine amino acid catabolism and muscle protein building at rest, during exercise and during the recovery period after a single experiment or training sessions. Stable isotopic tracers ((13)C-lysine, (15)N-glycine, ²H5-phenylalanine) and arteriovenous differences have been used in studies of skeletal muscle and collagen tissues under resting and exercise conditions. There are different fractional synthesis rates in skeletal muscle and tendon tissues, but there is no major difference between collagen and myofibrillar protein synthesis. Strenuous exercise provokes increased proteolysis and decreased protein synthesis, the opposite occurring during the recovery period. Individuals who exercise respond differently when resistance and endurance types of contractions are compared. Endurance exercise induces a greater oxidative capacity (enzymes) compared to resistance exercise, which induces fiber hypertrophy (myofibrils). Nitrogen balance (difference between protein intake and protein degradation) for athletes is usually balanced when the intake of protein reaches 1.2 g · kg(-1) · day(-1) compared to 0.8 g · kg(-1) · day(-1) in resting individuals. Muscular activities promote a cascade of signals leading to the stimulation of eukaryotic initiation of myofibrillar protein synthesis. As suggested in several publications, a bolus of 15-20 g protein (from skimmed milk or whey proteins) and carbohydrate (± 30 g maltodextrine) drinks is needed immediately after stopping exercise to stimulate muscle protein and tendon collagen turnover within 1 h.
Assuntos
Aminoácidos Essenciais/administração & dosagem , Atletas , Proteínas Alimentares/administração & dosagem , Exercício Físico/fisiologia , Proteínas Musculares/metabolismo , Músculo Esquelético/metabolismo , Recomendações Nutricionais , Aminoácidos Essenciais/farmacocinética , Metabolismo Energético/fisiologia , Humanos , Proteínas do Leite/administração & dosagem , Proteínas Musculares/fisiologia , Músculo Esquelético/fisiologia , Resistência Física/fisiologia , Biossíntese de Proteínas/fisiologia , Proteínas do Soro do LeiteRESUMO
The aim of our work was to study the hemodynamic effects of dynamic cardiomyoplasty on an acute animal model of atrial fibrillated heart failure. Eight anesthetized open chest dogs suffering from atrial fibrillation and heart failure, obtained by topic acetylcholine and propranolol, were treated by a cardiomyoplasty procedure performed with an electrostimulated latissimus dorsi muscle flap (LDMF). Values considered for analysis during LDMF stimulation were selected from cardiac cycles with R-R intervals similar to those when the LDMF was not stimulated (+/- 20 ms). Atrial fibrillated heart failure showed a significant increase of systemic vascular resistance, end diastolic left ventricular pressure (EDLVP) and right atrial pressure (p < 0.05), and a significant decrease in cardiac output, systolic left ventricular pressure (SLVP), and mean aortic pressure (p < 0.05) compared with control values. LDMF stimulation in atrial fibrillated heart failure resulted in a significant increase of SLVP, cardiac output, and mean aortic pressure (p < 0.05) and a significant decrease of systemic vascular resistance, EDLVP, and right atrial pressure (p < 0.05) compared with nonstimulated values. The highest LVP values were obtained with R-R intervals long enough to allow an adequate LV filling. We conclude that dynamic cardiomyoplasty provides an appropriate recovery in this animal model of atrial fibrillated heart failure. Cardiomyoplasty is an appropriate procedure for cardiac assist when R-R intervals allow an adequate LV filling.
Assuntos
Fibrilação Atrial/cirurgia , Pressão Sanguínea/fisiologia , Débito Cardíaco/fisiologia , Insuficiência Cardíaca/cirurgia , Resistência Vascular/fisiologia , Acetilcolina/toxicidade , Animais , Fibrilação Atrial/induzido quimicamente , Cardiomioplastia , Modelos Animais de Doenças , Cães , Estimulação Elétrica , Feminino , Insuficiência Cardíaca/induzido quimicamente , Masculino , Propranolol/toxicidade , Resultado do Tratamento , Função Ventricular Esquerda/fisiologiaRESUMO
BACKGROUND: Intraaortic and pulmonary artery counterpulsation are useful techniques to support circulation during either left or right ventricular dysfunction. Electrically stimulated skeletal muscles wrapped around the aorta, used as means of cardiac failure treatment, have proved to be an effective method of handling experimental left ventricular failure. In this article we report an induced cardiac failure model in acute open chest dogs and describe the hemodynamic improvement of simultaneous aortic and pulmonary artery counterpulsation. METHODS: This was achieved with a bilateral latissimus dorsi muscle flap, stimulated with a software written in C++ for Windows. Dynamic aortomyoplasty was performed using the left latissimus dorsi muscle flap around the descending aorta, and dynamic pulmonaromyoplasty was achieved wrapping the pulmonary trunk with the right latissimus dorsi muscle flap. In all animals blood pressures and cardiac output were measured after cardiac failure induced by a high-dose of propranolol hydrochloride (3 mg/kg intravenously) before and after latissimus dorsi muscle flap stimulation. RESULTS: Aortopulmonary counterpulsation resulted in a significant increase in mean aortic pressure, mean pulmonary pressure, and cardiac output. In addition, a significant decrease was observed in end-diastolic left ventricular pressure, systemic vascular resistance, and pulmonary vascular resistance. Subendocardial viability index (diastolic pressure-time index/systolic tension-time index) in aortomyoplasty and tension time index in pulmonaromyoplasty showed significant improvement when cardiac assistance was performed by electrical stimulation of both muscles (p = 0.037 and p = 0.001, respectively). CONCLUSIONS: Treatment of experimentally induced cardiac failure using aortopulmonary counterpulsation allows effective hemodynamic improvement in open-chest dogs.
Assuntos
Aorta , Baixo Débito Cardíaco/cirurgia , Cardiomioplastia , Contrapulsação/métodos , Artéria Pulmonar , Animais , Aorta/fisiologia , Débito Cardíaco , Cães , Hemodinâmica , Artéria Pulmonar/fisiologia , Resistência VascularRESUMO
We describe a technique for mechanical cardiac assistance in an acute model of severe cardiac failure. Cardiac dysfunction was induced by a high dose of halothane in 13 dogs. Seven served as controls. Following median sternotomy, a pneumatically driven device was implanted in the other six dogs in a para-aortic position, using a simple surgical technique without cardiopulmonary bypass. The aorta was cross-clamped during cardiac assistance. During hemodynamic studies, the seven control animals with induced cardiac failure showed high end-diastolic left ventricular and right atrial pressures with low cardiac index and systolic left ventricular and aortic pressures. All dogs in this group died within 30 minutes. Use of a monovalvular cardiac assist device in the experimental group of six dogs to pump blood from the aortic root to the descending aorta in a counterpulsation manner, confirmed good preservation of systemic hemodynamic parameters after induction of heart failure. All animals in this treated group survived more than 45 minutes. Hemodynamically, the device acts as a new ventricle and the impaired left ventricle functionally becomes a left atrium. This condition is clinically appropriate for recovery of left ventricular function in severe acute myocardial failure.