# Role of Exercise in Visceral Adipose Tissue Inflammation and Macrophage Polarization in Hypertensive Mice

## TL;DR

Exercise reduces inflammation in fat tissue and improves health in hypertensive mice by changing immune cell behavior.

## Contribution

This study reveals how exercise modulates macrophage polarization in visceral adipose tissue during hypertension.

## Key findings

- Exercise reduced adipocyte size and collagen content in visceral adipose tissue of hypertensive mice.
- Exercise corrected the imbalance between pro-inflammatory and anti-inflammatory macrophages in visceral adipose tissue.
- Macrophage polarization changes were consistent with protein-level alterations in the tissue.

## Abstract

Macrophages accumulate in visceral adipose tissue (VAT) during hypertension and may contribute to hypertension-associated inflammation. Exercise has shown beneficial effects on hypertension; however, the exact mechanisms by which the activated immune cells lead to the protective effects remain unclear. Our study aimed to determine how exercise influences VAT inflammation by modulating the macrophage polarization in hypertensive mice. Renin transgenic (R+) mice were used as a hypertensive mouse model and subjected to exercise (8 weeks). The body weight and blood pressure were monitored, VAT morphology was assessed by H&E and Masson Trichrome staining, macrophage polarization was determined by immunostaining and flow cytometry, and macrophage phenotype-related proteins were analyzed within the VAT via Western Blots. Results showed that exercise reduced the adipocyte size and collagen content of VAT and increased cell infiltration in R+ mice. Immunostaining and flow cytometry data showed that the ratio of pro-inflammatory macrophages (M1) to anti-inflammatory macrophages (M2) was increased in the VAT of R+ mice, while exercise corrected the macrophage polarization, which was consistent with protein level changes in VAT. Together, our data suggest that exercise improves vascular remodeling and VAT function (reduced adipocyte size, loss of collagen) by modulating VAT inflammation (polarization of macrophages) in hypertensive mice.