Evidence map›Paper›PMID 33678425›Full record

ArticleNeurobiology of aging2021

Voluntary wheel running with and without follistatin overexpression improves NMJ transmission but not motor unit loss in late life of C57BL/6J mice.

Deepti Chugh, Chitra C Iyer, Prameela Bobbili, Anton J Blatnik, Brian K Kaspar, Kathrin Meyer, Arthur Hm Burghes, Brian C Clark, W David Arnold

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Neurobiology of aging, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
–field-weighted citation impact
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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

11 citing papers in PubMed.

  1. Article
  2. The Neuromuscular Junction: A Shared Vulnerability in Aging and Disease.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025
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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

9 authors.

Deepti ChughDepartment of Neurology, Neuromuscular Division, The Ohio State University Wexner Medical Center, Columbus, OH, USA.
Chitra C IyerDepartment of Neurology, Neuromuscular Division, The Ohio State University Wexner Medical Center, Columbus, OH, USA.
Prameela BobbiliDepartment of Neurology, Neuromuscular Division, The Ohio State University Wexner Medical Center, Columbus, OH, USA.
Anton J BlatnikDepartment of Biological Chemistry and Pharmacology, The Ohio State University Wexner Medical Center, Columbus, OH, USA.
Brian K KasparThe Research Institute, Nationwide Children's Hospital, Columbus, OH, USA.
Kathrin MeyerThe Research Institute, Nationwide Children's Hospital, Columbus, OH, USA; Department of Pediatrics, The Ohio State University, Columbus, OH, USA.
Arthur Hm BurghesDepartment of Biological Chemistry and Pharmacology, The Ohio State University Wexner Medical Center, Columbus, OH, USA.
Brian C ClarkOhio Musculoskeletal and Neurological Institute & the Department of Biomedical Sciences, Athens, OH, USA.
W David ArnoldDepartment of Neurology, Neuromuscular Division, The Ohio State University Wexner Medical Center, Columbus, OH, USA; Department of Physical Medicine and Rehabilitation, The Ohio State University Wexner Medical Center, Columbus, OH, USA; Department of Neuroscience, The Ohio State University Wexner Medical Center, Columbus, OH, USA; Department of Physiology and Cell Biology, The Ohio State University Wexner Medical Center, Columbus, OH, USA. Electronic address: William.arnold@osumc.edu.

Funding

Sarcopenia and the motor neuronR03AG050877 · NIA · OHIO STATE UNIVERSITY · PI ARNOLD, WILLIAM DAVID · 2016 to 2017
$231k
Social Isolation and Loss of Physical Function: Defining a Novel Neuromuscular PhenotypeR03AG067387 · NIA · OHIO STATE UNIVERSITY · PI ARNOLD, WILLIAM DAVID · 2020 to 2021
$156k
NIA NIH HHS R03 AG050877NIA NIH HHS R03 AG067387
6 · The paper itself

Abstract

Sarcopenia, or pathological loss of muscle mass and strength during aging, is an important contributor to loss of physical function in older adults. Sarcopenia is a multifactorial syndrome associated with intrinsic muscle and upstream neurological dysfunction. Exercise is well-established as an effective intervention for sarcopenia, but less is known about the long-term neurobiological impact of exercise. The goals of this study were to investigate the effects of exercise, alone or in combination with follistatin (FST) overexpression (antagonist of myostatin), on neuromuscular junction transmission and motor unit numbers in mice between the age of 22 and 27 months, ages at which prior studies have demonstrated that some motor unit loss is already evident. C57BL/6J mice underwent baseline assessment and were randomized to housing with or without voluntary running wheels and injection with adeno-associated virus to overexpress FST or vehicle. Groups for comparison included sedentary and running with and without FST. Longitudinal assessments showed significantly increased muscle mass and contractility in the 'running plus FST' group, but running, with and without FST, showed no effect on motor unit degeneration. In contrast, running, with and without FST, demonstrated marked improvement of neuromuscular junction transmission stability.

Indexed as

AgingAnimalsFemaleFollistatinGene ExpressionMaleMiceMice, Inbred C57BLMotor NeuronsNeuromuscular JunctionRunningSarcopeniaSynaptic TransmissionFollistatinAgingExerciseFollistatinMotor UnitNeuromuscular Junction

Identifiers

PMID33678425
PMCPMC8122043

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Registered trials

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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.