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Long‐term endurance exercise coactivates autophagy/mitophagy and anabolic signaling
Abstract   Peer reviewed

Long‐term endurance exercise coactivates autophagy/mitophagy and anabolic signaling

Stephan Quintin, Yongchul Jang, Insu Kwon, Wankeun Song, Ludmila M. Cosio-Lima and Youngil Lee
The FASEB journal, Vol.32(Supplement 1), p.452
04/2018
DOI: https://doi.org/10.1096/fasebj.2018.32.1_supplement.lb452

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Abstract

Growing evidence has identified that autophagy plays an important role in sustaining normal cellular function. Endurance exercise (EE) is a potent inducer of autophagy in multiple tissues. However, the exact underlying signaling pathways responsible for exercise‐induced autophagy in brain has not been fully understood yet. In this study, we investigated potential signaling pathways involved in EE‐induced autophagy and mitochondrial dynamics in the cortex of the brain. C57BL/6 male mice were randomly assigned to a control group (CON, n=12) and an endurance exercise group (EXE, n=12). Our data demonstrated that EE‐induced autophagy evidenced by upregulation of autophagy‐related proteins (e.g., LC3 II, BECLIN1, ATG7, LAMP2, CATHEPSIN L and TFEB) coincides with increased anabolic signaling state (p‐AKT, p‐mTOR and p‐p70S6K). Furthermore, we revealed that EE promoted mitophagy evidenced by increases in LC3 II, p62, BNIP3, PINK, DRP1 in isolated mitochondrial fraction). We attempted to examine if low degree of oxidative stress would be a potential factor involved in EE‐induced autophagy. As opposed to our postulation, oxidative stress was not the case since EE did not increase protein oxidation, but rather enhanced antioxidative capacity (CATALASE and PRX III). Taken together, our results indicate that EE‐induced autophagy/mitophagy concomitant with anabolic signaling activation may be a novel protective signaling that mediates facilitation of healthy brain.

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