BDNF contributes to the skeletal muscle anti-atrophic effect of exercise training through AMPK-PGC1α signaling in heart failure mice.

Exercise training is a coadjuvant therapy in preventive cardiology, and it delays cardiac dysfunction and exercise intolerance in heart failure (HF). However, the mechanisms underlying muscle function improvement and cardioprotection are poorly understood. In this study, we tested whether exercise training would counteract skeletal muscle atrophy via activation of the BDNF pathway in myocardial infarction (MI)-induced HF mice. A cohort of male Sham-operated and MI mice were assigned into 8-week moderate exercise training, and untrained counterparters were used as control. Exercise capacity, plasma norepinephrine (NE) level, heart rate (HR), fractional shortening (FS) and ejection fraction (EF) were measured. The protein expression of BDNF, p-TrkB, p-AMPK and PGC1α were analyzed by Western blot. Compared with the Sham-operated mice, MI mice displayed reduced total distance run and elevated plasma NE level (both Taken together, our data provide evidence for exercise training may counteract HF-induced muscle atrophy through induced activation of BDNF pathway.

Déclaration de conflit d'intérêts

The authors declare no conflict of interest.