Abstract

The direct effects of exercise on white adipose tissue morphology and metabolic function remain unclear, due in large part to confounding effects of the reduction in fat mass that often accompanies exercise training. The purpose of this study was to determine if a session of endurance exercise could impact the rate of adipogenesis. Eight lean, healthy human subjects performed a single session of exercise (1 hour of endurance exercise at 65% of their maximal aerobic capacity; VO2max). Blood samples were collected without prior exercise (No-EX) and immediately after exercise (EX). Serum was extracted, and human adipocyte precursor cells were incubated for 72 hours in vitro in either the No-EX or EX serum. This serum preincubation was immediately followed by a standard 14-day differentiation protocol. On both days 3 and 9 of differentiation, mRNA expression levels of differentiation markers, PPARG and FABP4, were significantly greater (P<0.01) in cells preincubated in the EX vs. No-EX serum (e.g., Day 3 PPARG expression: 11.4±0.6 vs. 8.3±0.4 2-∆Ct; P=0.005, and Day 9 FABP4 expression: 2185±82 vs. 1619±98 2-∆Ct; P<0.0001). In addition, after 14 days of differentiation, we also found significantly greater protein abundance of important lipolytic and esterification regulators, G0S2, ATGL, HSL and GPAT1 (all P<0.05). As expected, compared with No-EX, the EX sera had greater concentrations of IL-6, lactate, fatty acids, epinephrine, and growth hormone, some of which may contribute to the enhanced adipogenic signaling after exercise. In summary, factors released into the circulation during and/or immediately after a session of endurance exercise can accelerate the rate of differentiation in human adipocyte precursor cells. Enhanced adipogenic signaling in response to exercise may have metabolic health benefits by priming adipose tissue for a more effective energy storage during periods of weight gain. Disclosure P. Varshney: None. L.M. Guth: None. C.M. Anderson: None. A. Raajendiran: None. M.J. Watt: None. J.F. Horowitz: Research Support; Self; American Diabetes Association. Funding National Institutes of Health (R01DK077966, T32DK101357)

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