# Temporal Exercise Conditioning Confers Dual-Phase Cardioprotection Against Isoproterenol-Induced Injury in a Rat Model

**Authors:** Krisztina Kupai, Zsolt Murlasits, Hsu Lin Kang, Eszter Regős, Ákos Várkonyi, Csaba Lengyel, Imre Pávó, Zsolt Radák, Béla Juhász, Dániel Priksz, Anikó Pósa

PMC · DOI: 10.3390/antiox15020152 · Antioxidants · 2026-01-23

## TL;DR

Moderate exercise before and after heart damage in rats reduces injury and improves heart function by lowering oxidative stress.

## Contribution

The study demonstrates that timed moderate exercise provides dual-phase cardioprotection against isoproterenol-induced injury.

## Key findings

- Exercise before and after ISO reduced infarct size and improved left ventricular function.
- HO-1 levels increased and MPO activity decreased with exercise, indicating reduced oxidative stress.
- Echocardiography showed improved stroke volume and ejection fraction in exercised groups.

## Abstract

Exercise training has demonstrated potential benefits in addressing the adverse effects of cardiovascular diseases, particularly myocardial infarction (MI). This study analyzed the cardioprotective effects of moderate exercise before and after MI in rats subjected to isoproterenol (ISO)-induced heart damage. Wistar rats were assigned to five groups: controls (CTRL), isoproterenol-treated (ISO), swimming before ISO (PRE + ISO), swimming after ISO (ISO + POST), and swimming both before and after ISO (PRE + ISO + POST). Cardiac function was assessed through echocardiography, while oxidative stress markers, Heme Oxygenase-1 (HO-1) and Myeloperoxidase (MPO), were quantified using biochemical assays and enzyme-linked immunosorbent assay (ELISA). Statistical analyses were conducted by one-way analysis of variance (ANOVA), accompanied by Tukey’s post hoc test. Exercise performed post-MI and both pre- and post-MI significantly reduced ISO-induced infarct size and improved left ventricular function (stroke volume (SV), ejection fraction (EF), and Tei index). HO-1 protein concentration and HO enzyme activity were restored, while swim training reduced the activity of MPO compared to the ISO group. Moderate exercise training, when appropriately timed, provides cardioprotection against ISO-induced myocardial damage by reducing oxidative stress and cardiac dysfunction.

## Linked entities

- **Proteins:** TED4 (Plant heme oxygenase (decyclizing) family protein)
- **Chemicals:** isoproterenol (PubChem CID 3779)
- **Diseases:** myocardial infarction (MONDO:0005068)

## Full-text entities

- **Genes:** HMOX1 (heme oxygenase 1) [NCBI Gene 3162] {aka HMOX1D, HO-1, HSP32, bK286B10}, Akt1 (AKT serine/threonine kinase 1) [NCBI Gene 24185] {aka Akt}, Vegfa (vascular endothelial growth factor A) [NCBI Gene 83785] {aka VEGF-A, VEGF111, VEGF164, VPF, Vegf}, MPO (myeloperoxidase) [NCBI Gene 4353], G6pd (glucose-6-phosphate dehydrogenase) [NCBI Gene 24377] {aka G6pdx}, Sod2 (superoxide dismutase 2, mitochondrial) [NCBI Gene 20656] {aka MnSOD, Sod-2}, Il6 (interleukin 6) [NCBI Gene 24498] {aka ILg6, Ifnb2}, Hmox1 (heme oxygenase 1) [NCBI Gene 24451] {aka HEOXG, Heox, Hmox, Ho-1, Ho1, hsp32}, Pik3cb (phosphatidylinositol-4,5-bisphosphate 3-kinase, catalytic subunit beta) [NCBI Gene 85243], Tnf (tumor necrosis factor) [NCBI Gene 24835] {aka RATTNF, TNF-alpha, Tnfa}, Mpo (myeloperoxidase) [NCBI Gene 303413], Sod1 (superoxide dismutase 1, soluble) [NCBI Gene 20655] {aka B430204E11Rik, Cu/Zn-SOD, CuZnSOD, Ipo-1, Ipo1, SODC}
- **Diseases:** Infarct (MESH:D007238), cardiac remodeling (MESH:D020257), cardiac disfunction (MESH:D006331), CAD (MESH:D003324), myotoxic (MESH:D000081030), tissue injury (MESH:D017695), reperfusion injury (MESH:D015427), death (MESH:D003643), artery (MESH:D012078), CVDs (MESH:D002318), MI (MESH:D009203), I/R injury (MESH:C580424), Myocardial damage (MESH:D009202), Stroke (MESH:D020521), cardiotoxic (MESH:D066126), Ischemia (MESH:D007511), Inflammation (MESH:D007249), injury to (MESH:D014947), fibrosis (MESH:D005355), myocardial functional decline (MESH:D060825), myocardial disfunction (MESH:D057215), stunning (MESH:D017682), decline of ventricular function (MESH:D018754), edema (MESH:D004487)
- **Chemicals:** Evans blue (MESH:D005070), ISO (MESH:D007545), GSH (MESH:D005978), CO2 (MESH:D002245), sucrose (MESH:D013395), KCl (MESH:D011189), glucose (MESH:D005947), formalin (MESH:D005557), ROS (MESH:D017382), MgCl2_6H2O (-), NaHCO3 (MESH:D017693), HEPES (MESH:D006531), MgSO4 (MESH:D008278), heme (MESH:D006418), hexadecyltrimethylammonium bromide (MESH:D000077286), water (MESH:D014867), iron (MESH:D007501), DTT (MESH:D004229), CaCl2 (MESH:D002122), biotin (MESH:D001710), Krebs-Henseleit buffer (MESH:C074097), hemin (MESH:D006427), leupeptin (MESH:C032854), NaCl (MESH:D012965), phosphate (MESH:D010710), 2,3,5-triphenyltetrazolium chloride (MESH:C009591), bilirubin (MESH:D001663), CO (MESH:D002248), nitrogen (MESH:D009584), EDTA (MESH:D004492), glucose-6-phosphate (MESH:D019298), xylazine (MESH:D014991), Biliverdin (MESH:D001664)
- **Species:** Rattus norvegicus (brown rat, species) [taxon 10116], Homo sapiens (human, species) [taxon 9606], Mus musculus (house mouse, species) [taxon 10090]

## Full text

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## Figures

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## References

59 references — full list in the complete paper: https://tomesphere.com/paper/PMC12938271/full.md

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Source: https://tomesphere.com/paper/PMC12938271