Evidence map›Paper›PMID 36781881›Full record

ArticleScientific reports2023

Resistance training restores skeletal muscle atrophy and satellite cell content in an animal model of Alzheimer's disease.

Masoud Rahmati, Mohammad Shariatzadeh Joneydi, Ai Koyanagi, Guang Yang, Bingzhou Ji, Seung Won Lee, Dong Keon Yon, Lee Smith, Jae Il Shin, Yusheng Li

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 1 pooled it
6.1field-weighted citation impact, top 3% 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.

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

19 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.

  1. Pooled it
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  11. Research on Alzheimer's Disease (AD) Involving the Use ofCentral nervous system agents in medicinal chemistry · 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

10 authors at 9 institutions in 5 countries.

Masoud RahmatiDepartment of Physical Education and Sport Sciences, Faculty of Literature and Human Sciences, Lorestan University, Khorramabad, Iran. rahmati.mas@lu.ac.ir.
Mohammad Shariatzadeh JoneydiSport Sciences Research Institute of Iran, Tehran, Iran. shariatzade221@yahoo.com.
Ai KoyanagiParc Sanitari Sant Joan de Deu/CIBERSAM, ISCIII, Universitat de Barcelona, Fundacio Sant Joan de Deu, Sant Boi de Llobregat, Barcelona, Spain.
Guang YangDeparment of Orthopedics, Xiangya Hospital, Central South University, Changsha, Hunan, China.
Bingzhou JiDeparment of Orthopedics, Xiangya Hospital, Central South University, Changsha, Hunan, China.
Seung Won LeeSungkyunkwan University School of Medicine, Suwon, Republic of Korea.
Dong Keon YonMedical Science Research Institute, Kyung Hee University College of Medicine, Seoul, Republic of Korea.
Lee SmithCentre for Health, Performance, and Wellbeing, Anglia Ruskin University, Cambridge, UK.
Jae Il ShinDepartment of Pediatrics, Yonsei University College of Medicine, Seoul, Republic of Korea.
Yusheng LiDeparment of Orthopedics, Xiangya Hospital, Central South University, Changsha, Hunan, China. liyusheng@csu.edu.cn.
Xiangya Hospital Central South University · CNAnglia Ruskin University · GBCentral South University · CNKyung Hee University Medical Center · KRLorestan University · IRShariati Hospital · IRSungkyunkwan University · KRUniversitat de Barcelona · ESYonsei University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is the most common neurodegenerative disease, and numerous recent findings suggest that several pathologic signs, including loss of muscle strength and mass, are also detected in these patients. In the present study, we evaluated muscle cross-sectional area (CSA), myonuclear number, satellite cell (SC) content, and myosin heavy chain (MyHC) types in an animal model of AD and examined the possible role of resistance training in controlling skeletal muscle size in this disease. Fifty-eight male rats were randomly divided into four groups: healthy-control (H-C), healthy-exercise (H-Ex), Alzheimer-control (A-C), and Alzheimer-exercise (A-Ex). AD was induced by the single injection of 1-42 amyloid into the CA1 region of the hippocampus (1 μl/site). The rats in H-Ex and A-Ex groups performed a 5-week resistance training period (17 sessions). The results indicated that AD induces significant skeletal muscle atrophy and reduces the myonuclear number and SC content in gastrocnemius muscle in both whole muscle cross-sections and isolated myofibers. Interestingly, we did not find any significant differences in the different MyHC distributions of AD animals compared with controls, while resistance training significantly increased the CSA of MyHC IIb fibers in both AD and healthy animals. Altogether, these observations suggest that the skeletal muscle of AD animals are more prone to atrophy and loss of myonuclear number and satellite cell content, while resistance training successfully restores these impairments.

Indexed as

Alzheimer DiseaseMuscle, SkeletalMuscular AtrophyResistance TrainingSatellite Cells, Skeletal MuscleAnimalsMaleModels, AnimalMuscle Fibers, SkeletalMyosin Heavy ChainsNeurodegenerative DiseasesRatsMyosin Heavy Chains

Identifiers

PMID36781881
PMCPMC9925431
OpenAlexW4320497817

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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.