Evidence map›Paper›PMID 41412496›Full record

ArticleJournal of sport and health science2025

Exercise attenuates stress-related signaling as sensed by higher phosphorylation of small heat shock proteins in skeletal muscle from older individuals.

Noni T Frankenberg, Victoria L Wyckelsma, Dion Ellul, Aaron C Petersen, Itamar Levinger, Michael J McKenna, Robyn M Murphy

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of sport and health science, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Article
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

7 authors.

Noni T FrankenbergDepartment of Biochemistry and Chemistry, La Trobe Institute for Molecular Science, School of Agriculture, Biomedicine and Environment, La Trobe University, Melbourne, VIC 3086, Australia.
Victoria L WyckelsmaDepartment of Biochemistry and Chemistry, La Trobe Institute for Molecular Science, School of Agriculture, Biomedicine and Environment, La Trobe University, Melbourne, VIC 3086, Australia; Institute for Health and Sport (IHES), Victoria University, Melbourne, VIC 8001, Australia.
Dion EllulDepartment of Biochemistry and Chemistry, La Trobe Institute for Molecular Science, School of Agriculture, Biomedicine and Environment, La Trobe University, Melbourne, VIC 3086, Australia.
Aaron C PetersenInstitute for Health and Sport (IHES), Victoria University, Melbourne, VIC 8001, Australia.
Itamar LevingerInstitute for Health and Sport (IHES), Victoria University, Melbourne, VIC 8001, Australia; Australian Institute for Musculoskeletal Science (AIMSS), Westen Health, St Albans, VIC 3021, Australia.
Michael J McKennaInstitute for Health and Sport (IHES), Victoria University, Melbourne, VIC 8001, Australia; College of Physical Education, Southwest University, Chongqing 400715, China; College of Sport Science, Zhuhai College of Science and Technology, Zhuhai 519041, China.
Robyn M MurphyDepartment of Biochemistry and Chemistry, La Trobe Institute for Molecular Science, School of Agriculture, Biomedicine and Environment, La Trobe University, Melbourne, VIC 3086, Australia. Electronic address: r.murphy@latrobe.edu.au.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundHeat shock proteins (HSPs) are key molecular chaperones that help maintain protein homeostasis by stabilizing or removing damaged proteins during cellular stress. Aging weakens these stress-response systems, disrupting proteostasis and increasing vulnerability to sarcopenia. High-intensity training (HIT) can counteract these declines by activating protective pathways such as the HSP response. HSPs are highly responsive to stress, examining their regulation during aging is important, as altered HSP activity is linked to the progressive loss of muscle mass.

methodsThis study investigated the abundance and phosphorylation of HSPs in skeletal muscle from healthy, active young and older adults (n = 7 per group), assessed at baseline and again in the older group following 12 weeks of HIT. Using calibrated Western blotting on both whole-muscle homogenates and pooled single muscle fibres, we quantified HSP content and phosphorylation to determine how aging and exercise influence stress-responsive protein regulation at both the tissue and cellular levels.

resultsIn whole muscle homogenates, HSPs (HSP72, HSP27, and αB-crystallin) did not differ between young and older adults, while higher phosphorylation of small HSPs (sHSPs): phospho-HSP27 at Serine15 (pHSP27 Ser15) and phospho-αB-crystallin at Serine59 (pαB-crystallin Ser59) (∼1.8-fold and ∼2.9-fold, respectively) were found in muscle from older adults, indicating higher cellular stress associated with aging. A 12-week HIT intervention in older adults reduced homogenate pHSP27 Ser15 and pαB-crystallin Ser59 abundances to similar levels found in young adults. Total HSPs typically displayed a distinct fiber-type profile in both age groups, with more in type I compared to type II fibers, distinguished by the presence of myosin heavy chain I (MHCI) or MHCII. Phosphorylation at pHSP27 Ser15 and pαB-crystallin Ser59 was not different between type I and type II fibers. The HIT in older adults decreased total and phosphorylated sHSPs in both type I and type II fibers but increased HSP72 in type I fibers.

conclusionHIT has the potential to mitigate age-related cellular stress and modulate protein expression patterns in aging skeletal muscle and, perhaps, has the potential to delay age-related muscle decline, thereby improving muscle health in older adults.

Indexed as

AgingFiber typeHigh-intensity training (HIT)HSPSingle muscle fibers

Identifiers

PMID41412496
PMCPMC12828604

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.