Agonist muscle adaptation accompanied by antagonist muscle atrophy in the hindlimb of mice following stretch-shortening contraction training
Advanced Search
Select up to three search categories and corresponding keywords using the fields to the right. Refer to the Help section for more detailed instructions.

Search our Collections & Repository

For very narrow results

When looking for a specific result

Best used for discovery & interchangable words

Recommended to be used in conjunction with other fields

Dates

to

Document Data
Library
People
Clear All
Clear All

For additional assistance using the Custom Query please check out our Help Page

CDC STACKS serves as an archival repository of CDC-published products including scientific findings, journal articles, guidelines, recommendations, or other public health information authored or co-authored by CDC or funded partners. As a repository, CDC STACKS retains documents in their original published format to ensure public access to scientific information.
i

Agonist muscle adaptation accompanied by antagonist muscle atrophy in the hindlimb of mice following stretch-shortening contraction training

Filetype[PDF-5.35 MB]


Select the Download button to view the document
This document is over 5mb in size and cannot be previewed
English
Details Supporting Files You May Also Like

Details:

  • Alternative Title:
    BMC Musculoskelet Disord
  • Personal Author:
  • Description:
    Background

    The vast majority of dynamometer-based animal models for investigation of the response to chronic muscle contraction exposure has been limited to analysis of isometric, lengthening, or shortening contractions in isolation. An exception to this has been the utilization of a rat model to study stretch-shortening contractions (SSCs), a sequence of consecutive isometric, lengthening, and shortening contractions common during daily activity and resistance-type exercise. However, the availability of diverse genetic strains of rats is limited. Therefore, the purpose of the present study was to develop a dynamometer-based SSC training protocol to induce increased muscle mass and performance in plantarflexor muscles of mice.

    Methods

    Young (3 months old) C57BL/6 mice were subjected to 1 month of plantarflexion SSC training. Hindlimb muscles were analyzed for muscle mass, quantitative morphology, myogenesis/myopathy relevant gene expression, and fiber type distribution.

    Results

    The main aim of the research was achieved when training induced a 2-fold increase in plantarflexion peak torque output and a 19% increase in muscle mass for the agonist plantaris (PLT) muscle. In establishing this model, several outcomes emerged which raised the value of the model past that of being a mere recapitulation of the rat model. An increase in the number of muscle fibers per transverse muscle section accounted for the PLT muscle mass gain while the antagonist tibialis anterior (TA) muscle atrophied by 30% with preferential atrophy of type IIb and IIx fibers. These alterations were accompanied by distinct gene expression profiles.

    Conclusions

    The findings confirm the development of a stretch-shortening contraction training model for the PLT muscle of mice and demonstrate that increased cross-sectional fiber number can occur following high-intensity SSC training. Furthermore, the TA muscle atrophy provides direct evidence for the concept of muscle imbalance in phasic non-weight bearing muscles, a concept largely characterized based on clinical observation of patients. The susceptibility to this imbalance is demonstrated to be selective for the type IIb and IIx muscle fiber types. Overall, the study highlights the importance of considering muscle fiber number modulation and the effect of training on surrounding muscles in exercise comprised of SSCs.

    Electronic supplementary material

    The online version of this article (doi:10.1186/s12891-017-1397-4) contains supplementary material, which is available to authorized users.

  • Subjects:
  • Source:
    BMC Musculoskelet Disord. 18.
  • Pubmed ID:
    28148306
  • Pubmed Central ID:
    PMC5288976
  • Document Type:
    Journal Article
  • Volume:
    18
  • Collection(s):
  • Main Document Checksum:
  • Download URL:
  • File Type:

You May Also Like

Checkout today's featured content at stacks.cdc.gov