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Anna L Boudoures Division of Basic Science Research, Department of Obstetrics and Gynecology, Washington University in St. Louis School of Medicine, 425 South Euclid Avenue, Campus Box 8064, St Louis, Missouri 63110, USA

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Maggie Chi Division of Basic Science Research, Department of Obstetrics and Gynecology, Washington University in St. Louis School of Medicine, 425 South Euclid Avenue, Campus Box 8064, St Louis, Missouri 63110, USA

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Alysha Thompson Division of Basic Science Research, Department of Obstetrics and Gynecology, Washington University in St. Louis School of Medicine, 425 South Euclid Avenue, Campus Box 8064, St Louis, Missouri 63110, USA

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Wendy Zhang Division of Basic Science Research, Department of Obstetrics and Gynecology, Washington University in St. Louis School of Medicine, 425 South Euclid Avenue, Campus Box 8064, St Louis, Missouri 63110, USA

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Kelle H Moley Division of Basic Science Research, Department of Obstetrics and Gynecology, Washington University in St. Louis School of Medicine, 425 South Euclid Avenue, Campus Box 8064, St Louis, Missouri 63110, USA

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Obesity negatively affects many aspects of the human body including reproductive function. In females, the root of the decline in fertility is linked to problems in the oocyte. Problems seen in oocytes that positively correlate with increasing BMI include changes to the metabolism, lipid accumulation, meiosis, and metaphase II (MII) spindle structure. Studies in mice indicate that dietary interventions fail to reverse these problems. How exercise affects the oocytes has not been addressed. Therefore, we hypothesized an exercise intervention would improve oocyte quality. Here we show that in a mouse model of an exercise, intervention can improve lipid metabolism in germinal vesicle (GV) stage oocytes. Oocytes significantly increased activity and transcription of the β-oxidation enzyme hydroxyacyl-coenzyme A dehydrogenase in response to exercise training only if the mice had been fed a high-fat diet (HFD). An exercise intervention also reversed the lipid accumulation seen in GV stage oocytes of HFD females. However, delays in meiosis and disorganized MII spindles remained present. Therefore, exercise is able to improve, but not reverse, damage imparted on oocytes as a result of an HFD and obesity. By utilizing an exercise intervention on an HFD, we determined only lipid content, and lipid metabolism is changed in GV oocytes. Moving forward, interventions to improve oocyte quality may need to be more targeted to the oocyte specifically. Because of the HFD-induced deficiency in β-oxidation, dietary supplementation with substrates to improve lipid utilization may be more beneficial.

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