Evidence map›Paper›PMID 26503074›Full record

ReviewThe Journal of physiology2016

Beneficial effects of exercise on age-related mitochondrial dysfunction and oxidative stress in skeletal muscle.

Anna-Maria Joseph, Peter J Adhihetty, Christiaan Leeuwenburgh

Abstract readReview
In one paragraph

Review in The Journal of physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 103 papers.

0numbers the graph read from it
0cells of the map it votes in
103citing 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

103 citing papers in PubMed.

  1. Trial
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  9. Inhibitory effect of standardizedJournal of traditional and complementary medicine · 2026
    Article
  10. Sarcopenia Risk is Associated With Decreased Swallow Safety in Patients With Dysphagia.Otolaryngology--head and neck surgery : official journal of American Academy of Otolaryngology-Head and Neck Surgery · 2026
    Article
  11. Article
  12. Review
  13. Review
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  15. Article
  16. Exercise, Exerkines, and Sarcopenia.Diabetes & metabolism journal · 2026
    Review
  17. Article
  18. Article
  19. Article
  20. Review

43 more citing papers are in PubMed but not listed here.

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

3 authors.

Anna-Maria JosephDepartment of Aging and Geriatric Research, Division of Biology of Aging, University of Florida, Gainesville, FL, 32611, USA. amjoseph@ufl.edu.
Peter J AdhihettyDepartment of Applied Physiology and Kinesiology, University of Florida, Gainesville, FL, 32611, USA.
Christiaan LeeuwenburghDepartment of Aging and Geriatric Research, Division of Biology of Aging, University of Florida, Gainesville, FL, 32611, USA.

Funding

University of Florida Older Americans Independence Center (OAIC)P30AG028740 · NIA · UNIVERSITY OF FLORIDA · PI Peihua Qiu · 2007 to 2026
$22.8M
PICS: A New Horizon for Surgical Critical CareP50GM111152 · NIGMS · UNIVERSITY OF FLORIDA · PI MOORE, FREDERICK A · 2014 to 2018
$10.7M
NIA NIH HHS P30 AG028740NIGMS NIH HHS P50 GM111152
6 · The paper itself

Abstract

Mitochondria are negatively affected by ageing leading to their inability to adapt to higher levels of oxidative stress and this ultimately contributes to the systemic loss of muscle mass and function termed sarcopenia. Since mitochondria are central mediators of muscle health, they have become highly sought-after targets of physiological and pharmacological interventions. Exercise is the only known strategy to combat sarcopenia and this is largely mediated through improvements in mitochondrial plasticity. More recently a critical role for mitochondrial turnover in preserving muscle has been postulated. Specifically, cellular pathways responsible for the regulation of mitochondrial turnover including biogenesis, dynamics and autophagy may become dysregulated during ageing resulting in the reduced clearance and accumulation of damaged organelles within the cell. When mitochondrial quality is compromised and homeostasis is not re-established, myonuclear cell death is activated and muscle atrophy ensues. In contrast, acute and chronic exercise attenuates these deficits, restoring mitochondrial turnover and promoting a healthier mitochondrial pool that leads to the preservation of muscle. Additionally, the magnitude of these exercise-induced mitochondrial adaptations is currently debated with several studies reporting a lower adaptability of old muscle relative to young, but the processes responsible for this diminished training response are unclear. Based on these observations, understanding the molecular details of how advancing age and exercise influence mitochondria in older muscle will provide invaluable insight into the development of exercise protocols that will maximize beneficial adaptations in the elderly. This information will also be imperative for future research exploring pharmacological targets of mitochondrial plasticity.

Indexed as

AgingAnimalsExerciseHumansMitochondria, MuscleMuscle, SkeletalMuscular AtrophyOxidative Stress

Identifiers

PMID26503074
PMCPMC5023701

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.