Proceedings of The Physiological Society

Europhysiology 2018 (London, UK) (2018) Proc Physiol Soc 41, PCA196

Poster Communications

Effects of eccentric exercise on myofibrillar function and amount of αB-crystallin binding to myofibrils in skeletal muscle from adjuvant-induced arthritis rats

K. Himori1, D. Tatebayashi1, Y. Ashida1, R. Yamada1, T. Yamada1

1. Graduate School of Health Sciences, Sapporo Medical University, Sapporo, Hokkaido, Japan.

Patients with rheumatoid arthritis (RA) suffer from muscle weakness. We have previously demonstrated that this abnormality is attributed to oxidative stress-induced myofibrillar dysfunction in adjuvant-induced arthritis (AIA) rats, a widely used animal model for RA (Yamada et al, 2015). In response to eccentric (ECC) contractions, but not concentric contractions, the small heat shock protein αB-crystallin binds to myofibrils and protect them from degeneration (Frankenberg et al, 2014). The aim of this study was to determine whether ECC exercise prevents myofibrillar dysfunction in skeletal muscles from AIA rats. All experimental procedures were approved by the Committee on Animal Experiments of Sapporo Medical University (No. 15-083). Wistar rats (10 week old, n=18) were assigned into control (CNT) (n=6), AIA (n=6), and AIA+ECC (n=6) groups. Under 2% isoflurane anesthesia, AIA was induced in the knees of rats by an injection of complete Freund's adjuvant. Throughout the ECC exercise, rats were anesthetized by isoflurane inhalation. To induce ECC contractions, planter flexors were electrically stimulated via surface electrodes (45 V, 30 Hz, and 2 s /4 s duty cycle) while the ankle was forcibly dorsiflexed by servomotor (20 deg s-1). ECC exercise was applied every other day for 3 weeks and consisted of 4 sets of 5 contractions. After the intervention period, rats were killed by cervical dislocation under isoflurane anesthesia and gastrocnemius muscles were excised for mechanical and biochemical analyses. Data are presented as mean ± SEM. One-way ANOVA followed by Bonferroni post hoc test was used to examine the statistical significance. ECC exercise prevented the AIA-induced decreases in maximum Ca2+-activated force in skinned fibers (CNT: 362 ± 8, AIA: 239 ± 11, AIA+ECC: 344 ± 11 mN/mm2 [n=40-51]; p < 0.05: AIA vs AIA+ECC) and myosin heavy chain (MyHC) and actin expression ([n=9]; AIA vs AIA+ECC, p < 0.05). Moreover, AIA muscles showed increased expression levels of malondialdehyde-protein adducts, NADPH oxidase, and neuronal nitric oxide synthase ([n=5-6]; CNT vs AIA, p < 0.05). ECC exercise markedly increased the steady-state levels of αB-crystallin and its binding to the myofibrils in AIA muscles ([n=6-9]; AIA vs AIA+ECC, p < 0.05). In conclusion, ECC exercise preserves myofibrillar function by preventing the loss of MyHC and actin in AIA rats. These beneficial effects can be ascribed to the protective effect of αB-crystallin on the myofibrils against oxidative stress-mediated protein degradation.

Where applicable, experiments conform with Society ethical requirements