# Intensity-dependent lipidomic dynamic regulation following acute swimming exercise

## TL;DR

This study shows that high-intensity swimming exercise causes more significant changes in blood lipids compared to moderate exercise, offering insights into how exercise intensity affects health at the molecular level.

## Contribution

The study identifies specific intensity-dependent lipid biomarkers and dynamic patterns in serum lipid responses to different swimming exercise intensities.

## Key findings

- HIIT swimming caused 1.49- to 2.87-fold more serum lipid downregulation than MICT despite similar energy expenditure.
- Five intensity-dependent lipid biomarkers were identified, including PC32:2, LPA18:2, and three TAGs containing 18:2.
- HIIT preferentially mobilized shorter-chain, saturated TAGs, and lipid recovery dynamics were intensity-dependent.

## Abstract

Exercise intensity critically determines health benefits, yet the underlying molecular mechanisms remain incompletely characterized. This study systematically compared the effects of high-intensity interval training (HIIT) versus moderate-intensity continuous training (MICT) swimming on serum lipidomics. In a randomized controlled trial (ChiCTR2400089036, registered on 30/08/2024, n = 42 healthy students), blood samples were collected at baseline, 0-, 15-, and 30-minutes post-exercise, followed by comprehensive lipidomics analysis. HIIT swimming induced 1.49- to 2.87-fold more extensive serum lipid downregulation than MICT, despite matched energy expenditure. We identified five robust intensity-dependent biomarkers: PC32:2, LPA18:2, and three 18:2-containing triacylglycerols (TAGs). Clustering analysis further revealed three distinct hierarchical patterns of lipid dynamic changes. Structurally, HIIT preferentially mobilized shorter-chain, saturated TAGs, and post-exercise lipid recovery dynamics were also intensity-dependent. The recurrent identification of linoleic acid (18:2)-enriched lipids, which negatively correlated with energy metabolites, suggests coordinated substrate channeling toward inflammatory eicosanoid pathways. These findings advance the mechanistic understanding of exercise intensity benefits and provide molecular evidence for intensity-stratified exercise prescription.