Evidence map›Paper›PMID 32866081›Full record

ReviewSports health

Muscle Atrophy After ACL Injury: Implications for Clinical Practice.

Lindsey K Lepley, Steven M Davi, Julie P Burland, Adam S Lepley

Registry-linked trialOpen access · greenAbstract readReview
In one paragraph

Review in Sports health. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06341868 (Dynamic Gait-Synchronous Neuromuscular Electrical Stimulation Following Anterior Cruciate Ligament Reconstruction), which is not on this map. Cited by 54 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed, 1 pooled it
7.6field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

NCT06341868 narecruitingnot on this map

Dynamic Gait-Synchronous Neuromuscular Electrical Stimulation Following Anterior Cruciate Ligament Reconstruction

TypeinterventionalSponsorKeller Army Community HospitalRan2024 to 2026Enrolled60ConditionsAnterior Cruciate Ligament InjuriesArmsKneeStim
3 · Its place in the literature

Who cites it

54 citing papers in PubMed, 1 synthesis or guideline pooled it, 103 citations in OpenAlex.

  1. Pooled it
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  7. Muscle atrophy after ACL reconstruction involves molecular mechanisms beyond unloading.Journal of applied physiology (Bethesda, Md. : 1985) · 2026
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 3 institutions in 1 country.

Lindsey K LepleySchool of Kinesiology, University of Michigan, Ann Arbor, Michigan.
Steven M DaviDepartment of Kinesiology, University of Connecticut, Storrs, Connecticut.
Julie P BurlandSpaulding National Running Center, Harvard Medical School, Boston, Massachusetts.
Adam S LepleySchool of Kinesiology, University of Michigan, Ann Arbor, Michigan.
University of Michigan–Ann Arbor · USHarvard University · USUniversity of Connecticut · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

contextDistinct from the muscle atrophy that develops from inactivity or disuse, atrophy that occurs after traumatic joint injury continues despite the patient being actively engaged in exercise. Recognizing the multitude of factors and cascade of events that are present and negatively influence the regulation of muscle mass after traumatic joint injury will likely enable clinicians to design more effective treatment strategies. To provide sports medicine practitioners with the best strategies to optimize muscle mass, the purpose of this clinical review is to discuss the predominant mechanisms that control muscle atrophy for disuse and posttraumatic scenarios, and to highlight how they differ. EVIDENCE ACQUISITION: Articles that reported on disuse atrophy and muscle atrophy after traumatic joint injury were collected from peer-reviewed sources available on PubMed (2000 through December 2019). Search terms included the following: STUDY

designClinical review. LEVEL OF EVIDENCE: Level 5.

resultsWe highlight that (1) muscle atrophy after traumatic joint injury is due to a broad range of atrophy-inducing factors that are resistant to standard resistance exercises and need to be effectively targeted with treatments and (2) neurological disruptions after traumatic joint injury uncouple the nervous system from muscle tissue, contributing to a more complex manifestation of muscle loss as well as degraded tissue quality.

conclusionAtrophy occurring after traumatic joint injury is distinctly different from the muscle atrophy that develops from disuse and is likely due to the broad range of atrophy-inducing factors that are present after injury. Clinicians must challenge the standard prescriptive approach to combating muscle atrophy from simply prescribing physical activity to targeting the neurophysiological origins of muscle atrophy after traumatic joint injury.

Indexed as

Anterior Cruciate Ligament InjuriesCytokinesExerciseHumansMuscle Fibers, SkeletalMuscle ProteinsMuscle, SkeletalMuscular AtrophyMyostatinProteolysisSatellite Cells, Skeletal MuscleCytokinesMSTN protein, humanMuscle ProteinsMyostatinACLdisusemuscle wastingneurophysiological

Identifiers

PMID32866081
PMCPMC7785904
OpenAlexW3081966746

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.