Improved skeletal muscle fatigue resistance in experimental autoimmune myositis mice following high-intensity interval training

Background Muscle weakness and decreased fatigue resistance are key manifestations of systemic autoimmune myopathies (SAMs). We here examined whether high-intensity interval training (HIIT) improves fatigue resistance in the skeletal muscle of experimental autoimmune myositis (EAM) mice, a widely us...

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Published in:Arthritis research & therapy 2022-06, Vol.24 (1), p.1-156, Article 156
Main Authors: Yamada, Takashi, Ashida, Yuki, Tamai, Katsuyuki, Kimura, Iori, Yamauchi, Nao, Naito, Azuma, Tokuda, Nao, Westerblad, Håkan, Andersson, Daniel C, Himori, Koichi
Format: Article
Language:English
Subjects:
Analysis
Arthritis
Autoimmune diseases
Diagnosis
Enzymes
Exercise
Experiments
Fatigue
Fitness training programs
Gene expression
Inflammation
Inflammatory diseases
Interval training
Kinases
Maximum oxygen consumption
Medicin och hälsovetenskap
Muscle function
Muscle strength
Muscles
Musculoskeletal diseases
Musculoskeletal system
Phosphorylation
Physiological aspects
Physiology
Proteins
Risk factors
Rodents
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Summary:Background Muscle weakness and decreased fatigue resistance are key manifestations of systemic autoimmune myopathies (SAMs). We here examined whether high-intensity interval training (HIIT) improves fatigue resistance in the skeletal muscle of experimental autoimmune myositis (EAM) mice, a widely used animal model for SAM. Methods Female BALB/c mice were randomly assigned to control (CNT) or EAM groups (n = 28 in each group). EAM was induced by immunization with three injections of myosin emulsified in complete Freund's adjuvant. The plantar flexor (PF) muscles of mice with EAM were exposed to either an acute bout or 4 weeks of HIIT (a total of 14 sessions). Results The fatigue resistance of PF muscles was lower in the EAM than in the CNT group (P < 0.05). These changes were associated with decreased activities of citrate synthase and cytochrome c oxidase and increased expression levels of the endoplasmic reticulum stress proteins (glucose-regulated protein 78 and 94, and PKR-like ER kinase) (P < 0.05). HIIT restored all these alterations and increased the peroxisome proliferator-activated receptor [gamma] coactivator-1[alpha] (PGC-1[alpha]) and the mitochondrial electron transport chain complexes (I, III, and IV) in the muscles of EAM mice (P < 0.05). Conclusions HIIT improves fatigue resistance in a SAM mouse model, and this can be explained by the restoration of mitochondria oxidative capacity via inhibition of the ER stress pathway and PGC-1[alpha]-mediated mitochondrial biogenesis.
ISSN:1478-6362
1478-6354
1478-6362
DOI:10.1186/s13075-022-02846-2