High- versus moderate-intensity aerobic exercise training effects on skeletal muscle of infarcted rats

Abstract

Moreira JB, Bechara LR, Bozi LH, Jannig PR, Monteiro AW, Dourado PM, Wisløff U, Brum PC. High-versus moderate-intensity aerobic exercise training effects on skeletal muscle of infarcted rats. J Appl Physiol 114: 1029 -1041, 2013. First published February 21, 2013 doi:10.1152/japplphysiol.00760.2012.-Poor skeletal muscle performance was shown to strongly predict mortality and long-term prognosis in a variety of diseases, including heart failure (HF). Despite the known benefits of aerobic exercise training (AET) in improving the skeletal muscle phenotype in HF, the optimal exercise intensity to elicit maximal outcomes is still under debate. Therefore, the aim of the present study was to compare the effects of highintensity AET with those of a moderate-intensity protocol on skeletal muscle of infarcted rats. Wistar rats underwent myocardial infarction (MI) or sham surgery. MI groups were submitted either to an untrained (MI-UNT); moderate-intensity (MI-CMT, 60% V O2 max); or matched volume, high-intensity AET (MI-HIT, intervals at 85% V O2 max) protocol. High-intensity AET (HIT) was superior to moderate-intensity AET (CMT) in improving aerobic capacity, assessed by treadmill running tests. Cardiac contractile function, measured by echocardiography, was equally improved by both AET protocols. CMT and HIT prevented the MI-induced decay of skeletal muscle citrate synthase and hexokinase maximal activities, and increased glycogen content, without significant differences between protocols. Similar improvements in skeletal muscle redox balance and deactivation of the ubiquitin-proteasome system were also observed after CMT and HIT. Such intracellular findings were accompanied by prevented skeletal muscle atrophy in both MI-CMT and MI-HIT groups, whereas no major differences were observed between protocols. Taken together, our data suggest that despite superior effects of HIT in improving functional capacity, skeletal muscle adaptations were remarkably similar among protocols, leading to the conclusion that skeletal myopathy in infarcted rats was equally prevented by either moderate-intensity or high-intensity AET. atrophy; heart failure; proteasome; oxidative stress SKELETAL MUSCLE ABNORMALITIES in systemic diseases have been described for decades (9, 14, 29, 52), including in heart failure (HF). Capillary rarefaction, switch from type I (oxidative) to type II (glycolytic) fibers, impaired metabolism, and skeletal muscle atrophy have been shown in human and experimental models of HF (14,21,29,43,49,52). This maladaptation seems to impair skeletal muscle performance, which was proposed as the main determinant of exercise capacity in patients with HF (21,32,40). Additionally, skeletal muscle loss was shown to be an independent predictor of mortality in HF (3).Recent efforts by researchers have identified possible intracellular mechanisms underlying the skeletal muscle abnormalities in cardiovascular diseases, and promising targets such as metabolic enzymes, calcium handling-related proteins, antioxidant scavengers, and in...

Impact of Inspiratory Muscle Training Versus Resistance Training on Ventricular Dysfunction in Patients With Dilated Cardiomyopathy: A Randomized Controlled Trial

“…Current evidence demonstrates that regular physical training not only improves exercise capacity and oxygen uptake in patients with heart failure, but also attenuates left-ventricular dilatation and abnormal cardiac remodeling [6]. In addition, training is associated with improved endothelial function and left-ventricular ejection fraction and reduced hospital readmissions in patients with heart failure [7] .Consistently, studies on different models of cardiac injury have indicated that exercise promotes a broad range of effects beneficial to the heart, such as the attenuation of calcium imbalance, renin-angiotensin and sympathetic nervous system activation, mitochondrial dysfunction, and oxidative stress [8,9]. In recent years, inspiratory muscle training has demonstrated a positive impact on ventilatory efficiency, respiratory muscle strength, peak oxygen consumption, and functional capacity in different types of cardiac dysfunction [10].…”

Atuação do sistema proteolítico lisossomal/autofágico no músculo esquelético de animais com insuficiência cardíaca

“…Atrogin-1/MAFbx também está aumentada na musculatura esquelética de animais com IC, refletindo em maior atividade do proteassoma, o que pode ter contribuído para atrofia muscular (Cunha et al, 2012;Moreira et al, 2013).…”

“…A disfunção cardíaca associada aos sintomas de edema pulmonar e intolerância ao esforço físico são indicativos da presença de IC nos animais infartados (Lucas et al, 2000). Todas essas alterações corroboram com resultados anteriores do nosso e de outros laboratórios (Ferreira et al, 2011;Moreira et al, 2013;Schulze et al, 2003;Tsutsui et al, 2001), e indicam que a cirurgia de IM em ratos é eficaz em promover IC e mimetizar sintomas presentes em humanos com esta doença.…”

“…O envolvimento do sistema ubiquitina/proteassoma na atrofia muscular induzida por doenças crônicas já foi demonstrado (Acharyya et al, 2004;Cunha et al, 2012;Lecker et al, 2004;Moreira et al, 2013). Nosso grupo recentemente observou que a atrofia muscular tanto de modelos experimentais como de humanos com IC, também está associada à maior ativação do sistema ubiquitina/proteassoma (Bechara, 2012;Cunha et al, 2012;Moreira et al, 2013).…”

“…Nosso grupo recentemente observou que a atrofia muscular tanto de modelos experimentais como de humanos com IC, também está associada à maior ativação do sistema ubiquitina/proteassoma (Bechara, 2012;Cunha et al, 2012;Moreira et al, 2013). Por outro lado, o envolvimento do sistema lisossomal/autofágico na miopatia esquelética induzida pela IC ainda não foi investigado, apesar do seu importante papel em outras condições atróficas.…”