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Perivascular adipose tissue (PVAT) is a metabolically active endocrine organ surrounding most arterial beds, and one of its key functions in healthy individuals is exerting an ‘anticontractile effect’ on small resistance arteries through the release of vasoactive adipokines and paracrine signalling. In individuals with obesity, excess caloric intake promotes a pro-inflammatory phenotype within these adipose depots, leading to PVAT dysfunction and contributing to hypertension and diabetes. We have previously demonstrated using a swimming model that exercise alleviates inflammation of PVAT and restores function; however, the mechanism by which this occurs remains elusive. Some studies have reported that the beneficial effects of exercise on adipocyte phenotype and inflammation varies between exercise modalities. Given that running is the most popular method of exercise in the UK, we aimed to develop a treadmill-training model of exercise to investigate the effects of running on PVAT function in obesity. Male C57BL6/j mice were randomly assigned to four groups: sedentary control (SC, n=15), sedentary obese (SO, n=15), exercised control (EC, n=5), and exercised (EO, n=5). Obese groups were fed a 60% kcal from fat diet from 8 weeks old. At 14 weeks old, treadmill training of EC and EO groups began. Mice were run on the treadmill at a speed of 12cm/s starting at 10 minutes and increasing by intervals of 5 minutes per day for 5 days a week at an incline of 10°. Once mice reached 1 hour at 12cm/s, mice continued at this speed for 1 week and speed was increased by 1cm/s each week for 4 weeks, reaching a max speed of 16cm/s for the final week of training. Body weight was recorded weekly for all groups. At 20 weeks old, blood pressure was measured in conscious restrained animals using the non-invasive tail-cuff method. Mice were then culled and blood glucose was measured. Mice fed a high-fat diet had significantly increased body weights compared to controls, and exercise had no effect on weight. Furthermore, SO animals exhibited hypertension and hyperglycaemia, and blood pressure and blood glucose levels were reduced in EO animals. The mesenteric bed was isolated and mesenteric resistance arteries (<250µm diameter) were mounted into a wire myograph system ±PVAT to measure the contractile response to noradrenaline (NA; 1x10-9 – 3x10-5). In vessels from SC and EC mice, PVAT intact arteries exhibited an attenuated response to NA which is consistent with the previously reported PVAT anticontractile effect, and this effect was absent in vessels from SO mice. However, in vessels from EO mice, treadmill-training restored PVAT function. Now that we have established a model of treadmill-training which restores PVAT function, next we aim to determine the mechanism. These results may aid in the future development of therapies that can restore PVAT function in obesity to reduce cardiovascular mortality.