Abstract
Increased contractile acitivity induces autophagy in skeletal muscle
The FASEB journal, Vol.24(S1), pp.lb646-lb646
04/2010
DOI: 10.1096/fasebj.24.1_supplement.lb646
Abstract
Contractile activity is essential in maintaining and promoting the oxidative phenotype of fatigue resistance, metabolic flexibility, insulin sensitivity and resistance to oxidative stress in skeletal muscle. This requires constant remodeling of structural proteins and organelles (e.g. mitochondria). We therefore hypothesized that autophagy, a catabolic process involved in the degradation of long‐lived proteins and organelles, is enhanced by increased contractile activity (i.e. endurance exercise). We submitted adult mice (12‐wk old, C57BL6) to 28 days of voluntary wheel running and used sedentary mice as controls (n=10/group). The expression of proteins associated with autophagosome formation (Beclin 1, LC3‐I+LC3‐II), mitochondrial autophagy (Bnip3), and aggregate protein degradation (p62/SQSTM1) were measured in the exercise‐recruited plantaris muscles. Consistent with our hypothesis, exercise training resulted in significant induction of Beclin1 (33%), Bnip3 (41.5%), LC3‐I+LC3‐II (43%) and LC3‐II‐to‐LC3‐I ratio (210%), and reduction of p62 (24%). The same directional changes were observed when tonic, oxidative soleus muscles were compared with phasic, glycolytic white vastus muscles in sedentary mice. Our findings suggest a role for autophagy in contractile activity‐mediated maintenance and promotion of oxidative phenotype in skeletal muscle.
This study was funded by NIH Grant AR050429 (Zhen Yan).
Details
- Title: Subtitle
- Increased contractile acitivity induces autophagy in skeletal muscle
- Creators
- Vitor A. Lira - University of VirginiaMitsuharu Okutsu - University of VirginiaMei Zhang - University of VirginiaZhen Yan - University of Virginia
- Resource Type
- Abstract
- Publication Details
- The FASEB journal, Vol.24(S1), pp.lb646-lb646
- Publisher
- Federation of American Societies for Experimental Biology
- DOI
- 10.1096/fasebj.24.1_supplement.lb646
- ISSN
- 0892-6638
- eISSN
- 1530-6860
- Number of pages
- 1
- Grant note
- NIH (AR050429)
- Language
- English
- Date published
- 04/2010
- Academic Unit
- Health and Human Physiology
- Record Identifier
- 9984267154202771
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