Evidence map›Paper›PMID 28213823›Full record

ArticleThe journal of physiological sciences : JPS2018

Long-term resistance exercise-induced muscular hypertrophy is associated with autophagy modulation in rats.

Insu Kwon, Yongchul Jang, Joon-Yong Cho, Young C Jang, Youngil Lee

Open access · goldAbstract read
In one paragraph

Article in The journal of physiological sciences : JPS, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 2 pooled it
2.6field-weighted citation impact, top 10% 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

21 citing papers in PubMed, 2 syntheses or guidelines pooled it, 44 citations in OpenAlex.

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  15. A novel voluntary weightlifting model in mice promotes muscle adaptation and insulin sensitivity with simultaneous enhancement of autophagy and mTOR pathway.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020
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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

5 authors at 3 institutions in 2 countries.

Insu KwonMolecular and Cellular Exercise Physiology Laboratory, Department of Exercise Science and Community Health, College of Health, University of West Florida, Pensacola, FL, USA.
Yongchul JangMolecular and Cellular Exercise Physiology Laboratory, Department of Exercise Science and Community Health, College of Health, University of West Florida, Pensacola, FL, USA.
Joon-Yong ChoExercise Biochemistry Laboratory, Korea National Sport University, Seoul, Korea.
Young C JangSchool of Applied Physiology and Parker H. Petit Institute for Bioengineering and Bioscience, Georgia Institute of Technology, Atlanta, GA, USA.
Youngil LeeMolecular and Cellular Exercise Physiology Laboratory, Department of Exercise Science and Community Health, College of Health, University of West Florida, Pensacola, FL, USA. ylee1@uwf.edu.
University of West Florida · USGeorgia Institute of Technology · USKorea National Sport University · KR

Funding

University of West Florida (US), RSP CF6672
6 · The paper itself

Abstract

Elevation of anabolism and concurrent suppression of catabolism are critical metabolic adaptations for muscular hypertrophy in response to resistance exercise (RE). Here, we investigated if RE-induced muscular hypertrophy is acquired by modulating a critical catabolic process autophagy. Male Wistar Hannover rats (14 weeks old) were randomly assigned to either sedentary control (SC, n = 10) or resistance exercise (RE, n = 10). RE elicited significant hypertrophy of flexor digitorum profundus (FDP) muscles in parallel with enhancement in anabolic signaling pathways (phosphorylation of AKT, mTOR, and p70S6K). Importantly, RE-treated FDP muscle exhibited a significant decline in autophagy evidenced by diminished phosphorylation levels of AMPK, a decrease in LC3-II/LC3-I ratio, an increase in p62 level, and a decline in active form of lysosomal protease CATHEPSIN L in the absence of alterations of key autophagy proteins: ULK1 phosphorylation, BECLIN1, and BNIP3. Our study suggests that RE-induced hypertrophy is achieved by potentiating anabolism and restricting autophagy-induced catabolism.

Indexed as

AnimalsAutophagyAutophagy-Related Protein-1 HomologBeclin-1HypertrophyMaleMembrane ProteinsMicrotubule-Associated ProteinsMuscle, SkeletalPhosphorylationPhysical Conditioning, AnimalRatsRats, WistarSignal TransductionAutophagy-Related Protein-1 HomologBeclin-1Membrane ProteinsMicrotubule-Associated ProteinsAutophagyHypertrophyResistance exerciseSkeletal muscle

Identifiers

PMID28213823
PMCPMC10718009
OpenAlexW2588459414

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.