ArticleApplied biochemistry and biotechnology2026
Epicardial Adipose Tissue Metabolic Changes Associated with Different Intensities Interval Exercise Preconditioning in Myocardial I/R Injury.
Article in Applied biochemistry and biotechnology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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.
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.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
Myocardial ischemia-reperfusion (I/R) injury remains a critical challenge in cardiovascular therapeutics, with exercise preconditioning emerging as a promising cardioprotective strategy. This study investigates the metabolic plasticity of epicardial adipose tissue (EAT)-a key paracrine regulator of myocardial injury-in response to graded intensities of interval exercise preconditioning during I/R injury. Male C57BL/6 mice underwent 6 weeks of low-, moderate-, or high-intensity interval treadmill training followed by I/R surgery. Untargeted metabolomics of EAT revealed intensity-dependent metabolic reprogramming. Moderate-intensity exercise preconditioning uniquely restored I/R-induced metabolic disturbances, reversing dysregulation in bile acid biosynthesis, xenobiotic detoxification, and cholesterol metabolism. In contrast, low- and high-intensity protocols incompletely normalized lipid homeostasis, with persistent suppression of glycerophospholipid metabolism and failure to rescue oxidative stress pathways (L + I/R vs. I/R, P = 0.01; H + I/R vs. I/R, P = 0.04). Multivariate analysis identified 51 overlapping metabolites in the moderate-intensity group showing full reversal of I/R-induced alterations, while the low- and high-intensity groups each showed partial recovery of 27 overlapping metabolites. Metabolic normalization by moderate-intensity exercise involved restoration of bile acid biosynthesis (I/R vs. SHAM: DA Score = -0.375, P = 0.001; M + I/R vs. I/R: DA Score = 0.25, P = 0.028) and xenobiotic detoxification (I/R vs. SHAM: DA Score = -0.4, P = 0.01; M + I/R vs. I/R: DA Score = 0.4, P = 0.01) pathways critical to mitochondrial function. These findings identify metabolic changes in EAT that are associated with exercise-induced cardioprotection, and indicate that moderate-intensity interval exercise is most strongly associated with restoration of EAT metabolic profiles after I/R. These associations warrant further mechanistic investigation to determine causality.
Indexed as
Identifiers
42138775What OpenQuestion holds
Registered trials
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.