723-P: A Single Session of Exercise Increases Resident Macrophages in Subcutaneous Adipose Tissue from Healthy Human Subjects

Abstract

Infiltration of pro-inflammatory adipose tissue macrophages (ATMs) is implicated in systemic low-grade inflammation that underlies metabolic health complications in obesity. Exercise training has been linked to reduced adipose tissue and systemic inflammation, but these observations are often confounded by concomitant weight loss. Many metabolic benefits of exercise are a cumulative effect of each bout of exercise, thus the aim of this study was to determine changes in ATMs (using flow cytometry) in response to a single exercise session. We collected subcutaneous abdominal adipose tissue samples from 10 obese (BMI: 33±3kg/m2; fat mass: 41±20kg) and 14 lean (BMI: 23±13kg/m2; fat mass: 16±5kg) adults, 12 hours after exercising for 60 minutes at 70% VO2max (EX); and again 3 days after their most recent exercise session (No-EX). To characterize the cellular response to exercise without the confounding influence of exercise novelty, all subjects were habitual exercisers. The exercise session did not alter total immune cell number (OBESE: 30±7 vs. 31±7; LEAN: 27±9 vs. 28±8% live cells) or total ATM number (OBESE: 3.9±1.7 vs. 4.0±1.6; LEAN: 3.5±1.5 vs. 4.3±1.9% live cells; for No-EX and EX, respectively). However, there was a main effect for exercise to increase the number of CD11c- ATMs (OBESE: 1.3±1.4 vs. 1.5±1.5; LEAN: 1.0±0.6 vs. 2.0±1.6% live cells; P=0.03), indicating the abundance of resident ATMs increased after exercise. Surprisingly, the response to exercise was not different in lean vs. obese subjects. Although the change in resident ATM content after exercise was rather subtle in this cohort of healthy regular exercisers, these are the first single cell data to suggest each session of exercise may induce a phenotypic shift in subcutaneous ATMs. This could be a mechanism contributing to the anti-inflammatory health benefits of exercise. Disclosure A. Ludzki: None. E.M. Krueger: None. T.C. Baldwin: None. N.M. Taylor: None. L.A. Muir: None. C. Lumeng: None. J.F. Horowitz: Research Support; Self; American Diabetes Association. Funding National Institutes of Health (R01DK077966) Canadian Institutes of Health Research (DFS146190)