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Related Concept Videos

Cross-bridge Cycle01:26

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As muscle contracts, the overlap between the thin and thick filaments increases, decreasing the length of the sarcomere—the contractile unit of the muscle—using energy in the form of ATP. At the molecular level, this is a cyclic, multistep process that involves binding and hydrolysis of ATP, and movement of actin by myosin.
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Muscle fatigue refers to the decline in a muscle's ability to maintain the force of contraction after prolonged activity. It primarily stems from changes within muscle fibers. Even before experiencing muscle fatigue, one may feel tired and have the urge to stop the activity. This response, known as central fatigue, occurs due to changes in the central nervous system, namely the brain and spinal cord. While there is no single mechanism that induces fatigue, it may serve as a protective...
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Related Experiment Video

Updated: Mar 28, 2026

Anterior Cruciate Ligament Transection and Synovial Fluid Lavage in a Rodent Model to Study Joint Inflammation and Posttraumatic Osteoarthritis
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Muscle atrophy after ACL reconstruction involves molecular mechanisms beyond unloading.

Alexander R Keeble1,2, Sara Gonzalez-Velez1,2,3, Nicholas T Thomas1,3

  • 1Center for Muscle Biology, University of Kentucky, Lexington, Kentucky, United States.

Journal of Applied Physiology (Bethesda, Md. : 1985)
|March 26, 2026
PubMed
Summary

Anterior cruciate ligament reconstruction (ACLR) causes muscle atrophy, but disuse alone doesn't explain it. ACLR triggers unique gene expression changes beyond simple unloading, revealing specific molecular pathways involved in post-surgery muscle loss.

Keywords:
ACLRRNA-sequencingdisusequadricepsskeletal muscle

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Area of Science:

  • Muscle physiology
  • Molecular biology
  • Bioinformatics

Background:

  • Anterior cruciate ligament reconstruction (ACLR) often results in significant muscle atrophy and weakness that hinders rehabilitation.
  • The precise contribution of disuse (limb unloading) to early muscle pathology following ACLR is not fully understood.

Purpose of the Study:

  • To compare the early transcriptional responses to disuse versus ACLR in skeletal muscle.
  • To differentiate between genes affected by unloading alone and those specifically altered by ACLR.

Main Methods:

  • Analysis of publicly available RNA-sequencing datasets from vastus lateralis muscle biopsies.
  • Comparison of gene expression profiles from limbs after ACLR and unilateral lower limb suspension (ULLS) against matched control limbs.
  • Bioinformatic analyses (intersection and interaction) to identify differentially expressed genes (DEGs).

Main Results:

  • Substantial divergence in transcriptomic responses between ACLR and ULLS, despite similar unloading periods.
  • Only 16% of DEGs were common to both conditions; ACLR induced over 1,000 more DEGs than ULLS.
  • ACLR uniquely showed reduced extracellular matrix (ECM) remodeling and increased expression of denervation-responsive genes.

Conclusions:

  • Limb unloading contributes only modestly to the early muscle transcriptomic changes after ACLR.
  • ACLR elicits distinct molecular responses beyond disuse, including altered ECM remodeling and denervation signaling.
  • Identifying ACLR-specific molecular pathways is crucial for understanding muscle atrophy pathophysiology and improving functional recovery.