721-P: Exercise Training Alters Subcutaneous Adipose Tissue Morphology in Obese Adults Even without Weight Loss

Many metabolic health complications in obese adults are linked to abnormalities within their enlarged adipose tissue mass, which include hypertrophic adipocytes, a fibrotic extracellular matrix (ECM), and suppressed capillary density. Exercise training is a first-line treatment for obesity-related diseases, but the direct effects of exercise on adipose tissue structure and metabolic function remain unclear. The purpose of this study was to determine the effects of moderate-intensity continuous training (MICT) and high-intensity interval training (HIIT) on subcutaneous adipose tissue morphology. 17 obese adults were randomly assigned to 12 weeks (4 days/week) of MICT (45 minutes at 70% HRmax, n=9) or HIIT (10 X 1 minutes at 90% HRmax, 1 minute recovery, n=8) and were required to maintain their body weight throughout. Abdominal subcutaneous adipose tissue biopsy samples were collected before and after training for histological and immunoblot measures to assess adipocyte cell size, markers of ECM remodeling and capillarization. Aerobic fitness (VO2peak) improved ∼10% in both MICT and HIIT (P<0.001), while body weight and fat mass remained unchanged, as designed. However, even in the absence of weight loss, adipocyte size decreased slightly (∼10%), yet significantly after training (P=0.04). The reduction in adipocyte cell size in HIIT was accompanied by a significant increase in the protein abundance of a key adipogenic regulator, CEBPα (P=0.03). Exercise training also induced a strong trend for a reduction in the abundance of collagen 6a (P=0.07). We also found a strong trend for HIIT to increase the protein abundance of the angiogenic regulator VEGFα (P=0.06), although this did not translate to a measurable increase in capillarization. In summary, exercise training, perhaps especially HIIT, may increase adipogenic and angiogenic capacity in adipose tissue, as well as trigger adipose ECM remodeling. Disclosure C. Ahn: None. B.J. Ryan: None. J.B. Gillen: None. A. Ludzki: None. M.W. Schleh: None. B.A. Reinheimer: None. J.F. Horowitz: Research Support; Self; American Diabetes Association. Funding National Institutes of Health (R01DK077966, P30DK089503, T32DK007245); Canadian Institutes of Health Research (DFS146190)