Fast twitch skeletal muscle remodeling by prolonged endurance exercise is associated with crosstalk between anabolic and catabolic signaling pathways in mice

Kwon, Insu; Jang, Yongchul; Song, Wankeun; Cosio-Lima, Ludmila M.; Lee, Youngil

doi:10.4172/2168-9652.1000228

Fast twitch skeletal muscle remodeling by prolonged endurance exercise is associated with crosstalk between anabolic and catabolic signaling pathways in mice

Primary tabs

Kwon, I., Jang, Y., Song, W., Cosio-Lima, L. M., & Lee, Y. (2018). Fast twitch skeletal muscle remodeling by prolonged endurance exercise is associated with crosstalk between anabolic and catabolic signaling pathways in mice. Biochemistry & Physiology, 7(1). doi:10.4172/2168-9652.1000228

Details

Title: Fast twitch skeletal muscle remodeling by prolonged endurance exercise is associated with crosstalk between anabolic and catabolic signaling pathways in mice
Contributor(s): Kwon, Insu (author)
Jang, Yongchul (author)
Song, Wankeun (author)
Cosio-Lima, Ludmila M. (author)
Lee, Youngil (author)
Located In: Biochemistry & Physiology
ISSN: 2168-9652
Date: 2018
DOI: 10.4172/2168-9652.1000228
Use/Reproduction: Kwon I, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution and reproduction in any medium, provided the original author and source are credited.
Abstract: Endurance exercise (EXE) is a potent inducer of both muscle fiber transformation as well as autophagy in skeletal muscles. However, it has remained unknown whether autophagy is associated with EXE-induced muscle fiber transformation. Thus, we examined autophagy responses in in fast muscle (tibialis anterior; TA) tissues after sixweek long term treadmill EXE by assessing a series of autophagy signaling pathways and muscle fiber transformation through Western blot analysis and fluorescence microscopy. First, we confirmed that EXE caused slow muscle phenotypes in TA muscle, evidenced by reduction in cross-sectional areas of muscle fibers, increases in type I and II fibers, and upregulation of mitochondrial proteins. Subsequently, our results showed that transformation of muscle fiber types concurred with autophagy upregulation (e.g., an increase in LC3-II, LC3-II/I ratio, and BNIP3); however, intriguingly, inductive signaling of autophagy (e.g., phosphorylation of AMPK and BCL2) were suppressed. Moreover, anabolic signaling (e.g., an increase in phosphorylation levels of AKT, mTOR, p70S6K, and FOXO3), which typically serves as anti-autophagy factor were significantly elevated. Our findings suggest that although autophagy levels were sustained higher in TA of EXE-trained mice compared to sedentary mice, concomitant potentiation of anabolic signaling by EXE may serve as a negative feedback to prevent excessive catabolism induced by autophagy. We also suggest that this anabolic response may be necessary for remodeling of anaerobic fast muscle fibers into aerobic muscle fibers and mitochondrial biogenesis.
Subject(s): Endurance exercise
Autophagy
Mitochondria
Skeletal muscle
Anabolic signalling