Abstract

The consequences of two-week hindlimb suspension (HS) on skeletal muscle atrophy were investigated in balanced diet-fed Fat-1 transgenic and C57BL/6 wild-type mice. Body composition and gastrocnemius fatty acid composition were measured. Skeletal muscle force, cross-sectional area (CSA), and signaling pathways associated with protein synthesis (protein kinase B, Akt; ribosomal protein S6, S6, eukaryotic translation initiation factor 4E-binding protein 1, 4EBP1; glycogen synthase kinase3-beta, GSK3-beta; and extracellular-signal-regulated kinases 1/2, ERK 1/2) and protein degradation (atrophy gene-1/muscle atrophy F-box, atrogin-1/MAFbx and muscle RING finger 1, MuRF1) were evaluated in the soleus muscle. HS decreased soleus muscle wet and dry weights (by 43% and 26%, respectively), muscle isotonic and tetanic force (by 29% and 18%, respectively), CSA of the soleus muscle (by 36%), and soleus muscle fibers (by 45%). Fat-1 transgenic mice had a decrease in the ω-6/ω-3 polyunsaturated fatty acids (PUFAs) ratio as compared with C57BL/6 wild-type mice (56%, p < 0.001). Fat-1 mice had lower soleus muscle dry mass loss (by 10%) and preserved absolute isotonic force (by 17%) and CSA of the soleus muscle (by 28%) after HS as compared with C57BL/6 wild-type mice. p-GSK3B/GSK3B ratio was increased (by 70%) and MuRF-1 content decreased (by 50%) in the soleus muscle of Fat-1 mice after HS. Balanced diet-fed Fat-1 mice are able to preserve in part the soleus muscle mass, absolute isotonic force and CSA of the soleus muscle in a disuse condition.

Highlights

  • Skeletal muscle disuse-induced atrophy is associated with decreases in skeletal muscle mass, cross-sectional area, contractile force, and protein synthesis signaling activity [1,2,3,4]

  • Skeletal muscle signaling pathways associated with protein synthesis (Akt, S6, 4EBP1, GSK3B and ERK 1/2 content) and protein degradation were measured

  • The slides obtained from sections of the central portion of the soleus muscle were stained with hematoxylin and eosin (HE)

Read more

Summary

Introduction

Skeletal muscle disuse-induced atrophy is associated with decreases in skeletal muscle mass, cross-sectional area, contractile force, and protein synthesis signaling activity [1,2,3,4]. We recently reported [1] the effects of oral supplementation of “high dose” of either eicosapentaenoic (EPA)- or docosahexaenoic (DHA)-rich fish oil on protein synthesis/degradation signaling pathways in skeletal muscle mass loss induced by two weeks of hindlimb suspension (HS). The purpose was to investigate whether small changes in the ω-6/ω-3 PUFAs ratio, in “long term”, would be able to attenuate skeletal muscle disuse-induced atrophy. For this purpose, the following measurements were performed: body weight gain, hindlimb skeletal muscle wet and dry mass, soleus muscle and soleus muscle fibers CSA and force production by the soleus muscle. Skeletal muscle signaling pathways associated with protein synthesis (Akt, S6, 4EBP1, GSK3B and ERK 1/2 content) and protein degradation (cathepsin L and 26S proteasome activities and contents of atrogin-1/MAFbx and MuRF1) were measured

Animals
Experimental Design
Gastrocnemius Fatty Acid Composition
In Vivo Soleus Muscle Electrical Stimulation
Analysis of Soleus Muscle Force and Contractile Properties
Analysis of Soleus Muscle Resistance to Fatigue
Histological Analysis of the Soleus Muscle
Determination of Cathepsin L Activity in the Gastrocnemius Muscle
2.11. Statistical Analysis
Body Weight Gain
Gastrocnemius Muscle Fatty Acid Composition
CSA of the Soleus Muscle and of Soleus Muscle Fibers
Protein
Discussion
Conclusions
Methods

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.