Heart failure (HF) is characterized by limited exercise tolerance, skeletal muscle
atrophy, a shift toward fast muscle fiber, and
myogenic regulatory factor (MRF) changes.
Reactive oxygen species (ROS) also contribute to target organ damage in this syndrome. In this study, we investigated and compared morphofunctional characteristics and gene expression in Soleus (
SOL--oxidative and slow twitching muscle) and in Extensor Digitorum Longus (EDL--glycolytic and fast twitching muscle) during HF. Two groups of rats were used: control (CT) and
heart failure (HF), induced by a single injection of
monocrotaline. MyoD and
myogenin gene expression were determined by RT-qPCR, and MHC
isoforms by SDS-PAGE; muscle fiber type frequency and cross sectional area (CSA) were analyzed by mATPase. A biochemical study was performed to determine
lipid hydroperoxide (LH),
glutathione peroxidase (GSH-Px), and
superoxide dismutase (SOD); myography was used to determine amplitude, rise time, fall time, and
fatigue resistance in both muscles. HF showed
SOL and EDL
muscle atrophy in all muscle fiber types; fiber frequency decreased in type IIC and muscle contraction fall time increased only in
SOL muscle.
Myogenin mRNA expression was lower in
SOL and myoD decreased in HF EDL muscle. LH increased, and SOD and GSH-Px activity decreased only in HF
SOL muscle. HF EDL muscle did not present changes in MHC distribution, contractile properties, HL concentration, and
antioxidant enzyme activity. In conclusion, our results indicate that
monocrotaline induced HF promoted more prominent biochemical, morphological and functional changes in
SOL (oxidative and slow twitching muscle). Although further experiments are required to better determine the mechanisms involved in HF pathophysiology, our results contribute to understanding the muscle-specific changes that occur in this syndrome.