Evidence map›Paper›PMID 40950865›Full record

ArticleJournal of thoracic disease2025

Effect of aerobic exercise on the susceptibility of atrial fibrillation among aged mice.

Cheng Zhao, Zhaoyi Wang, Yichen Zhao, Philip Y K Pang, Magdalena Rufa, Sebastian Feickert, Qing Ye, Kemin Liu, Jingyuan Gu, Junhui Sun and 1 more

Abstract read
In one paragraph

Article in Journal of thoracic disease, 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. Fto-mediated m6A demethylation of Lox drives atrial fibrosis and promotes atrial fibrillation in a murine model of hyperthyroidism.Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology · 2026
    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

11 authors.

Cheng Zhao *Department of Cardiac Surgery, Beijing Anzhen Hospital, Capital Medical University, Beijing, China.
Zhaoyi Wang *School of Traditional Chinese Medicine, Beijing University of Chinese Medicine, Beijing, China.
Yichen ZhaoDepartment of Cardiac Surgery, Beijing Anzhen Hospital, Capital Medical University, Beijing, China.
Philip Y K PangDepartment of Cardiothoracic Surgery, National Heart Centre Singapore, Singapore, Singapore.
Magdalena RufaDepartment of Cardiovascular Surgery, Robert Bosch Hospital, Stuttgart, Germany.
Sebastian FeickertDepartment of Cardiology and Internal Intensive Care Unit, Berlin Heartrhythm Center, Vivantes Clinic Am Urban, Berlin, Germany.
Qing YeDepartment of Cardiac Surgery, Beijing Anzhen Hospital, Capital Medical University, Beijing, China.
Kemin LiuDepartment of Cardiac Surgery, Beijing Anzhen Hospital, Capital Medical University, Beijing, China.
Jingyuan GuDepartment of Cardiac Surgery, Beijing Anzhen Hospital, Capital Medical University, Beijing, China.
Junhui SunDepartment of Cardiac Surgery, Beijing Anzhen Hospital, Capital Medical University, Beijing, China.
Jiangang WangDepartment of Cardiac Surgery, Beijing Anzhen Hospital, Capital Medical University, Beijing, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Regular aerobic exercise has been shown to improve mitochondrial function and delay mitochondrial aging. Mitochondria play a crucial role in maintaining cardiac function and metabolism in myocardial cells. However, the effect of aerobic exercise on the incidence of atrial fibrillation (AF) is unclear. The aim of this study was to investigate the effects of aerobic exercise of different intensities on the susceptibility of aged mice to AF, and the relationship between altered mitochondrial structure and function and susceptibility to AF. Methods: Thirty-two 18-month-old C57BL/6N aged mice were selected and divided into low-, medium-, and high-speed aerobic exercise groups, and a no-exercise control group. Electrophysiological characteristics, susceptibility to AF, mitochondrial morphology and structure, mitochondrial membrane potential, adenosine triphosphate (ATP)ase activity, cytosolic calcium ion concentration, and mitochondrial function were assessed in each group of aged mice using the intracardiac catheterization technique, transmission electron microscopy, cellular flow technique, and Seahorse mitochondrial stress test. Results: A negative correlation was found between the success rate of AF induction/AF duration and the speed of exercise, such that the success rate of AF induction/AF duration was significantly lower in the high-speed group than the no-exercise group (P=0.01/P=0.02). Transmission electron microscopy revealed that the number and density of mitochondria in mouse atrial myocytes were positively correlated with exercise velocity. The basal oxygen consumption, mitochondrial energy supply, and maximum mitochondrial energy supply potential of atrial myocytes increased as exercise speed increased (P<0.001). Conclusions: Both moderate- and vigorous-intensity aerobic exercise significantly reduced the susceptibility of the aged mice to develop AF while concurrently enhancing mitochondrial morphology and structural integrity, ultimately leading to improved mitochondrial bioenergetic function.

Indexed as

aerobic exerciseAgingatrial fibrillation (AF)mitochondria

Identifiers

PMID40950865
PMCPMC12433064

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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.