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Effective storage of excess energy in abdominal subcutaneous adipose tissue during periods of overeating may help attenuate weight-gain-related insulin resistance. The objective of this study was to assess changes in the expression of factors regulating abdominal subcutaneous adipose tissue storage capacity in response to a brief exposure to overeating in nonobese adults. Because exercise can alter the expression of genes involved in regulating adipose tissue storage capacity, we compared the responses to overeating in regular exercisers (EX, n = 11) and nonexercisers (nonEX, n = 11). Abdominal subcutaneous adipose tissue samples and oral glucose tolerance tests were performed before and after participants ate 30% above their estimated daily energy requirements for 1 week. Both EX and nonEX gained ∼1 kg ( P

Although the health benefits of exercise in adults with obesity are well described, the direct effects of exercise on adipose tissue that may lead to improved metabolic health are poorly understood. The primary aims of this study were to perform an unbiased analysis of the subcutaneous abdominal adipose tissue transcriptomic response to acute exercise in adults with obesity, and to compare the effects of moderate-intensity continuous exercise versus high-intensity interval exercise on this response. Twenty-nine adults with obesity performed a session of either high-intensity interval exercise (HI; 10 × 1 min at 90%HRpeak, 1 min recovery between intervals; n = 14) or moderate-intensity continuous exercise (MI; 45 min at 70%HRpeak; n = 15). Groups were well matched for BMI (HI 33 ± 3 vs. MI 33 ± 4 kg/m(2)), sex (HI: 9 women vs. MI: 10 women), and age (HI: 32 ± 6 vs. MI: 29 ± 5). Subcutaneous adipose tissue was collected before and 1 h after the session of HI or MI, and samples were processed for RNA sequencing. Gene set enrichment analysis revealed 7 of 21 gene sets enriched postexercise overlapped between HI and MI. Interestingly, both HI and MI upregulated gene sets involved in inflammation (IL6-JAK-STAT3 signaling, allograft rejection, TNFα signaling via NFκB, and inflammatory response; FDR q value < 0.25). Exercise also downregulated adipogenic and oxidative metabolism gene sets in both groups. Overall, these data suggest genes involved in subcutaneous adipose tissue metabolism and inflammation may be an important part of the initial response after a session of exercise. NEW & NOTEWORTHY This study compared the effects of a single session of high-intensity interval exercise versus moderate-intensity continuous exercise on transcriptional changes in subcutaneous abdominal adipose tissue collected from adults with obesity. Our novel findings indicate exercise upregulated inflammation-related gene sets, while it downregulated metabolism-related gene sets – after both high-intensity and moderate-intensity exercise. These data suggest exercise can alter the adipose tissue transcriptome 1 h after exercise in ways that may impact inflammation and metabolism.

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)