Training improves the oxidative phenotype of muscle during the transition from cardiac hypertrophy to heart failure without altering MyoD and myogenin.

What is the central question of this study? We investigated the effects of physical training on phenotypic (fibre-type content) and myogenic features (MyoD and myogenin expression) in skeletal muscle during the transition from cardiac hypertrophy to heart failure. What is the main finding and its importance? We provide new insight into skeletal muscle adaptations by showing that physical training increases the type I fibre content during the transition from cardiac hypertrophy to heart failure, without altering MyoD and myogenin expression. These results have important clinical implications for patients with heart failure, because this population has reduced muscle oxidative capacity.

Aerobic training attenuates nicotinic acethylcholine receptor changes in the diaphragm muscle during heart failure.

Introduction: Heart failure (HF) is a progressive myopathy, with clinical signs of fatigue and limb weakness that can damage the nerve-muscle interaction, altering synaptic transmission and nicotinic acetylcholine receptors (nAChR) in neuromuscular junctions (NMJs). The diaphragm is composed of a mixed proportion of muscle fibres, and during HF, this muscle becomes slower and can alter its function. As exercise training is an accepted practice to minimise abnormalities of skeletal muscle during HF, in this study, we evaluated the hypothesis that aerobic training attenuates alterations in the expression of nAChR subunits in NMJs diaphragm during heart failure.

Creatine does not promote hypertrophy in skeletal muscle in supplemented compared with nonsupplemented rats subjected to a similar workload.

The purpose of this study was to test the hypothesis that creatine (Cr) supplementation may promote an additional hypertrophic effect on skeletal muscle independent of a higher workload on Cr-supplemented trained muscle compared with Cr-nonsupplemented trained muscle. Male Wistar rats (2-3 months old, 250-300 g) were divided randomly into 4 groups (n = 8 per group): nontrained without Cr supplementation (CO), nontrained with Cr supplementation (CR), trained without Cr supplementation (TR), and trained with Cr supplementation (TRCR). Creatine supplementation was given at 0.

High-intensity resistance training with insufficient recovery time between bouts induce atrophy and alterations in myosin heavy chain content in rat skeletal muscle.

The aim of this study was to test whether high-intensity resistance training with insufficient recovery time between bouts, could result in a decrease of muscle fiber cross-sectional area (CSA), alter fiber-type frequencies and myosin heavy chain (MHC) isoform content in rat skeletal muscle. Wistar rats were divided into two groups: trained (Tr) and control (Co). Tr group were subjected to a high-intensity resistance training program (5 days/week) for 12 weeks, involving jump bouts into water, carrying progressive overloads based on percentage body weight.

Nandrolone stimulates MyoD expression during muscle regeneration in the condition of myonecrosis induced by Bothrops jararacussu venom poisoning.

Myonecrosis with permanent loss of muscle mass is a relevant local toxic effect following envenomation with Bothrops jararacussu snake venom. Regeneration of adult skeletal muscle involves the activation of satellite cells, a process regulated by myogenic regulatory factors (MRF). MyoD is an MRF involved in both proliferation and differentiation of satellite cells.

Heart failure increases atrogin-1 and MuRF1 gene expression in skeletal muscle with fiber type-specific atrophy.

Heart failure (HF) is characterized by a reduced tolerance to exercise due to early fatigue and dyspnea; this may be due in part to skeletal muscle myopathy with a shift from slow to fast fibers and loss of muscle mass. Muscle wasting does not occur similarly in all types of muscle fiber, thus we tested the hypothesis that HF induces skeletal muscle atrophy in a fiber type-specific manner altering the expression of atrogin-1 and MuRF1 in a fast muscle of rats with monocrotaline-induced heart failure. We studied extensor digitorum longus (EDL) muscle from both HF and control Wistar rats.