Evidence map›Paper›PMID 32179050›Full record

ReviewRedox biology2020

Intramuscular mechanisms of overtraining.

Arthur J Cheng, Baptiste Jude, Johanna T Lanner

Open access · goldAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Redox biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
72citing papers in PubMed, 3 pooled it
8.1field-weighted citation impact, top 2% 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

72 citing papers in PubMed, 3 syntheses or guidelines pooled it, 142 citations in OpenAlex.

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12 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 at 2 institutions in 2 countries.

Arthur J ChengYork University, Faculty of Health/ School of Kinesiology and Health Sciences, Muscle Health Research Centre/ Muscle Calcium Dynamics Lab, 351 Farquharson Life Sciences Building, Toronto, M3J 1P3, Canada.
Baptiste JudeKarolinska Institutet, Department of Physiology and Pharmacology, Molecular Muscle Physiology and Pathophysiology laboratory, Biomedicum C5, 17177, Stockholm, Sweden.
Johanna T LannerKarolinska Institutet, Department of Physiology and Pharmacology, Molecular Muscle Physiology and Pathophysiology laboratory, Biomedicum C5, 17177, Stockholm, Sweden. Electronic address: johanna.lanner@ki.se.
Karolinska Institutet · SEYork University · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Strenuous exercise is a potent stimulus to induce beneficial skeletal muscle adaptations, ranging from increased endurance due to mitochondrial biogenesis and angiogenesis, to increased strength from hypertrophy. While exercise is necessary to trigger and stimulate muscle adaptations, the post-exercise recovery period is equally critical in providing sufficient time for metabolic and structural adaptations to occur within skeletal muscle. These cyclical periods between exhausting exercise and recovery form the basis of any effective exercise training prescription to improve muscle endurance and strength. However, imbalance between the fatigue induced from intense training/competitions, and inadequate post-exercise/competition recovery periods can lead to a decline in physical performance. In fact, prolonged periods of this imbalance may eventually lead to extended periods of performance impairment, referred to as the state of overreaching that may progress into overtraining syndrome (OTS). OTS may have devastating implications on an athlete's career and the purpose of this review is to discuss potential underlying mechanisms that may contribute to exercise-induced OTS in skeletal muscle. First, we discuss the conditions that lead to OTS, and their potential contributions to impaired skeletal muscle function. Then we assess the evidence to support or refute the major proposed mechanisms underlying skeletal muscle weakness in OTS: 1) glycogen depletion hypothesis, 2) muscle damage hypothesis, 3) inflammation hypothesis, and 4) the oxidative stress hypothesis. Current data implicates reactive oxygen and nitrogen species (ROS) and inflammatory pathways as the most likely mechanisms contributing to OTS in skeletal muscle. Finally, we allude to potential interventions that can mitigate OTS in skeletal muscle.

Indexed as

ExerciseMuscle, SkeletalAdaptation, PhysiologicalHumansOxidative Stress

Identifiers

PMID32179050
PMCPMC7284919
OpenAlexW3009029087

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.