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Abstract

PURPOSE: A recent novel adipocytokine, C1q/TNF-related protein-9 (CTRP9), has been shown to increase activation of endothelial nitric oxide synthase and reduce vasoconstrictors (e.g., endothelin-1). In addition, CTRP9 may play a compensatory role in obesity-related endothelial dysfunction. Although there is limited information regarding exercise-mediated CTRP9, high-intensity interval exercise (HIIE) has been shown to be as or more effective than continuous moderate-intensity exercise (CME) in improving indicators of endothelial function (e.g., brachial artery flow-mediated dilation [BAFMD]). Therefore, the purpose of this study was to investigate the effect of acute HIIE vs. CME on serum CTRP9 and BAFMD responses in obese individuals. METHODS: Sixteen young male subjects (9 obese and 7 normal-weight) participated in a counterbalanced and caloric equated experiment: HIIE (30 minutes, 4 intervals of 4 minutes at 80-90% of VO2max with 3 minutes rest between intervals) and CME (38 minutes at 50-60% VO2max). Serum CTRP9 and BAFMD, were measured prior to, immediately following exercise, and 1 hour and 2 hours into recovery. RESULTS: The concentration of serum CTRP9 was significantly increased immediately following acute HIIE and CME in both obese and normal-weight groups (p = 0.003). Furthermore, both significant treatment by time and group by time interactions for BAFMD were observed following both exercise protocols (p = 0.018; p = 0.009; respectively), with a greater CME-induced BAFMD response at 2 hours into recovery in obese compared to normal-weight subjects. Additionally, a positive correlation in percent change (baseline to peak value) between CTRP9 and BAFMD was found following acute CME (r = 0.589, p = 0.016). CONCLUSIONS: Acute HIIE is as effective as CME to upregulate CTRP9 expression in both obese and normal-weight individuals, although CTRP9 may potentially improve CME-mediated BAFMD. The novel results from this study provide a foundation for additional examination of the mechanisms of exercise-mediated CTRP9 on endothelial function.

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