Cited by 248Muscle Physiology and DisordersNutrition and Health in AgingNerve injury and regeneration

Neural control of aging skeletal muscle

Open access
Delbono, Osvaldo·2003·Aging Cell

Abstract

Summary: Functional and structural decline in the neuromuscular system with aging has been recognized as a cause of impairment in physical performance and loss of independence in the elderly. Alterations in spinal cord motor neurones and at the neuromuscular junction have been identified as evidence of denervation in skeletal muscles from aging mammals, including humans. However, the reciprocal influences of neurones on gene expression in muscle and of muscle on age‐related neurodegeneration are poorly understood, and, as a result, interventions aimed at delaying or preventing degeneration of the neural component in aging muscle have been largely unsuccessful. The present article discusses the evidence for neural influence on age‐related impairments of skeletal muscle, including a role in excitation–contraction uncoupling. The role of nerves in regulating the trophic actions of insulin‐like growth factor‐1 (IGF‐1) and other neurotrophic factors is considered as a novel influence on the effects of aging on the neuromuscular junction. A better understanding of nerve–muscle interactions will allow for more rational interventions in the aging neuromuscular system.

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1046/j.1474-9728.2003.00011.x

Cites

96 of 96 references verified0 citation errors · 0 not checkable

Statistics

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • Possible mechanisms for reduced muscle mass and strength in sarcopenic obesity include type II fibre atrophy, motor neuron loss, collagen deposition and fibre necrosis.

    “A number of mechanisms might explain the reduction of muscle mass and strength in sarcopenic obesity, including type II muscle fibre atrophy, reduction in motor neurons, collagen deposition and fibre necrosis67–70.”

    From Sarcopenic obesity in older adults: aetiology, epidemiology and treatment strategies (2018) · cites this paper as [69]

    The Introduction links age-related muscle-mass loss to fibre atrophy, and ‘Neural influences on aging skeletal muscle’ describes motor-unit loss and denervation of fast fibres. The Conclusions also discuss possible motor-neurone loss and reduced muscle force. These passages concern aging muscle, not specifically sarcopenic obesity; they do not establish type II fibre atrophy, collagen deposition, or fibre necrosis. Page numbers are unavailable in our copy. (LLM, conf=0.88)

    Experimental — accuracy not yet measured

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Cites

Flagged first, then by citations

1 of the 97 references couldn’t be matched to a known paper.

Cited by

Sorted by citations

Authors
Delbono, O.
Affiliations
Wake Forest University Health Sciences (US)
Corresponding author
Delbono, Osvaldo
Venue
Aging Cell
Publisher
Wiley
Published
2003-01-28
Volume
2
Issue
1
Pages
21-29
ISSN
  • 1474-9718 (ISSN-L)
  • 1474-9726
OpenAlex
W2046854924
Cited by
248
References
97
Citations by year
2026: 6 · 2025: 3 · 2024: 6 · 2023: 8 · 2022: 5 · 2021: 18 · 2020: 16 · 2019: 12 · 2018: 11 · 2017: 9 · 2016: 20 · 2015: 11 · 2014: 9 · 2013: 9 · 2012: 16
FWCI
0.88
Type
journal article
Language
en
Open access
Locations
  • Aging Cell (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • Muscular Dystrophy Association
  • National Institutes of Health (AG13934)
  • National Institute on Aging (AG/AR 18755, AG 15820, AG-13934, R01AG015820)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
  • Health Sciences › Medicine › Physiology › Nutrition and Health in Aging
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nerve injury and regeneration
Keywords
skeletal muscle aging, neuromuscular junction, spinal motoneurons, denervation, excitation-contraction uncoupling, insulin-like growth factor I, neurotrophic factors, nerve-muscle interaction, age-related neurodegeneration, muscle gene expression
MeSH terms
Aging, Animals, Humans, Insulin-Like Growth Factor I, Motor Neurons, Nerve Growth Factors, Neuromuscular Junction, Muscle, Skeletal

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review