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Aerobic exercise induces selective changes in skeletal muscle protein quality control markers in rats with heart failure

Year: 2026

Type: article

Abstract: The objective of this study was to determine whether aerobic exercise could aid in the preservation of the autophagy lysosomal system and mitigate oxidative stress in skeletal muscle during heart failure (HF) progression. Exercise tolerance was lower in HF groups compared to Control (C) groups ( p < 0.05). In skeletal muscle, HF induced type II fiber atrophy (type IIa: p = 0.0007; type IIx/b: p < 0.0001) and impaired all five oxidative phosphorylation complexes ( p < 0.05). Exercise reduced protein carbonyls ( p = 0.0043), while HF decreased antioxidant enzymes (manganese-superoxide dismutase: p = 0.0077; glutathione peroxidase: p = 0.0497) compared to C groups. HF elevated LC3B-II/I ratio compared to C ( p = 0.0246) and reduced cathepsin B ( p = 0.0484), consistent with altered autophagy, although autophagic flux was not assessed. Exercise lowered p62 expression ( p = 0.0449). WGCNA analysis identified an inverse correlation between MEbrown genes and autophagy-lysosomal markers. HF reduced aerobic capacity, likely due to mitochondrial impairments and reduced antioxidant defenses. Autophagy-related pathways remained partially responsive to exercise and may represent an adaptable component of muscle remodeling during HF progression.

Source: Scientific Reports

DOI: 10.1038/s41598-026-72488-w

Authors: Quinten W. Pigg, Daniela S. Inoue, Dillon R. Harris, Dongmei Zhang, Devon J. Boland, Mariana Janini Gomes

Institution: Texas A&M University

Language: English

Topic: Muscle Physiology and Disorders

Subfield: Molecular Biology

Field: Biochemistry, Genetics and Molecular Biology

Domain: Life Sciences

SDG: Good health and well-being

Open Access status: gold

Estimated APC paid: $2,690