Abstract
IntroductionPhysical inactivity significantly contributes to loss of muscle mass and performance in bed-bound patients. Loss of skeletal muscle mitochondrial content has been well-established in muscle unloading models, but the underlying molecular mechanism remains unclear. We hypothesized that apparent unloading-induced loss of muscle mitochondrial content is preceded by increased mitophagy- and decreased mitochondrial biogenesis-signaling during the early stages of unloading.
MethodsWe analyzed a comprehensive set of molecular markers involved in mitochondrial-autophagy, -biogenesis, -dynamics, and -content, in the gastrocnemius muscle of C57BL/6J mice subjected to 0- and 3-days hind limb suspension, and in biopsies from human vastus lateralis muscle obtained before and after 7days of one-leg immobilization.
ResultsIn both mice and men, short-term skeletal muscle unloading results in molecular marker patterns indicative of increased receptor-mediated mitophagy and decreased mitochondrial biogenesis regulation, before apparent loss of mitochondrial content.
DiscussionThese results emphasize the early-onset of skeletal muscle disuse-induced mitochondrial remodeling.
Original language | English |
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Pages (from-to) | 769-778 |
Number of pages | 10 |
Journal | Muscle & Nerve |
Volume | 60 |
Issue number | 6 |
Early online date | 23 Oct 2019 |
DOIs | |
Publication status | Published - Dec 2019 |
Keywords
- inactivity
- mitochondria
- mitochondrial biogenesis
- mitophagy
- muscle unloading
- skeletal muscle
- LEG IMMOBILIZATION
- OVER-EXPRESSION
- SOLEUS MUSCLE
- DYNAMICS
- ATROPHY
- FUNDC1
- ACTIVATION
- PATHWAYS
- GENES
- YOUNG