# Minutes that matter: time-efficient high-intensity interval training improves cardiac function with transcriptomic evidence in post–myocardial infarction mice

## TL;DR

Short bursts of intense exercise improve heart function in mice after heart attacks, with changes in heart cell activity and gene expression.

## Contribution

This study shows that HIIT improves cardiac function and gene expression in post-MI mice, with transcriptomic evidence of pro-contractile and anti-inflammatory changes.

## Key findings

- HIIT improved left-ventricular ejection fraction and reduced fibrosis in post-MI mice.
- RNA sequencing revealed upregulated contractile and metabolic pathways and downregulated apoptosis and inflammation.
- HIIT increased DNA synthesis and running capacity in mice.

## Abstract

High-intensity interval training (HIIT) improves cardiovascular performance, but the mechanisms remain incompletely delineated. We investigated whether HIIT improves left-ventricular (LV) remodeling after myocardial infarction (MI) in adult mice. Animals underwent permanent coronary ligation or sham surgery and were randomized to Control, HIIT-only, Sham, MI-only, and MI + HIIT. HIIT comprised 15 treadmill bouts (60 s at 90%–110% maximal running speed followed by 30 s rest), 3 days/week for 6 weeks. Baseline echocardiography 1 week after MI confirmed comparable LV dysfunction in MI-only and MI + HIIT groups. After intervention, the MI + HIIT group showed higher running capacity, improved LV ejection fraction (26.18% vs. 16.19%; p < 0.01) and fractional shortening (12.24% vs. 7.41%; p < 0.01), and less LV dilation versus MI-only. Myocardial fibrosis was reduced in MI + HIIT (8.85% vs. 13.17%; p < 0.01), consistent with physiological remodeling. 5-ethynyl-2′-deoxyuridine (EdU) incorporation identified more DNA synthesis in MI + HIIT (1.71%) and HIIT-only (1.24%) hearts. Bulk RNA sequencing showed coordinated upregulation of contractile and metabolic pathways and downregulation of apoptosis and inflammatory signaling, aligning with improved cell-cycle activity and oxidative–metabolic efficiency. Collectively, HIIT enhanced exercise capacity and cardiac function, attenuated fibrosis, and reprogrammed cardiac gene expression toward pro-contractile and anti-inflammatory programs consistent with a cell-cycle-permissive state in a post-MI mouse model.

Illustration summarizing a study on myocardial infarction (MI) and high-intensity interval training (HIIT) in mice. The background highlights improved cardiovascular fitness. Methods include a timeline with HIIT and MI procedures. Results show enhancements in running capacity, cardiac function, and cell proliferation, with changes in cardiac contraction, glycolysis, cell cycle, and inflammation. The conclusion notes that six weeks of HIIT improved exercise capacity, cardiac function, cardiomyocyte proliferation, and transcriptome change.