# Different types of exercise and myocardial angiogenesis regulation: A scoping review of cardiac‐specific evidence in animal models

## TL;DR

This review explores how different types of exercise affect heart blood vessel growth in healthy animals, highlighting varied molecular responses.

## Contribution

The study maps cardiac-specific angiogenesis regulators across exercise types in healthy animal models.

## Key findings

- Aerobic exercise consistently upregulates the VEGF-VEGFR axis and related signaling pathways.
- Interval/HIIT exercise activates endothelial markers and increases vascular indices.
- Resistance/combined training involves AMPK-PGC-1α and VEGFR2 pathways but has limited mechanistic data.

## Abstract

Exercise promotes myocardial angiogenesis, yet molecular responses vary by modality, and cardiac‐specific evidence in healthy models remains fragmented. This study aimed to map biomolecular regulators of myocardial/coronary angiogenesis across exercise types in healthy animal models. PRISMA‐ScR scoping review. Literature searches were conducted in PubMed, Scopus, and SpringerLink. Eligible studies were structured exercise interventions in physiologically healthy animals reporting myocardial/coronary tissue angiogenesis biomarkers and/or structural microvascular indices; disease models and studies reporting only circulating markers were excluded. FITT parameters and outcomes were charted and synthesized by exercise type. From 4674 records, 23 studies were included across swimming, continuous treadmill/running, interval/HIIT, resistance, and combined training. Aerobic protocols most consistently upregulated the VEGF‐VEGFR axis with downstream PI3K/Akt‐eNOS/NO and context‐dependent HIF‐1α signaling. Interval/HIIT showed prominent endothelial activation (e.g., miR‐126 and CD34/KDR) alongside increased vascular indices. Resistance/combined training was less represented, but implicated AMPK‐PGC‐1α/FNDC5‐irisin signaling, VEGFR2/FLK‐1 upregulation, and eNOS/NO support in combined protocols. Exercise modality appears to recruit distinct upstream regulators that converge on myocardial angiogenic remodeling; evidence is dominated by male‐only models, and mechanistic data for resistance/combined training remain limited.