Role of Chronic Stress and Exercise on Microvascular Function in Metabolic Syndrome

AbstractPurposeThe present study examined the effect of unpredictable chronic mild stress (UCMS) on peripheral microvessel function in healthy and metabolic syndrome (MetS) rodents, and whether exercise training could prevent the vascular dysfunction associated with UCMS.MethodsLean and obese (model of MetS) Zucker rats (LZR; OZR) were exposed to 8 weeks of UCMS, exercise (Ex), UCMS+Ex, or control conditions. At the end of the intervention, gracilis arterioles (GAs) were isolated and hung in a pressurized myobath to assess endothelium-dependent (EDD) and -independent (EID) dilation. Levels of nitric oxide (NO) and reactive oxygen species (ROS) were measured through DAF-FM and DHE staining, respectively.ResultsCompared to LZR controls, EDD and EID was lower (p=0.0001) in LZR-UCMS. The OZR-Ex group had a higher EDD (p=0.0001) and EID (p=0.003), compared to OZR-Controls; whereas only a difference in EDD (p=0.01) was noted between LZR-Control and LZR-Ex groups. Importantly, EDD and EID were higher in the LZR (p=0.0001; p=0.02) and OZR (p=0.0001; p=0.02) UCMS+Ex groups compared to UCMS alone. Lower NO bioavailability and higher ROS were noted in the LZR-UCMS group (p=0.0001), but not OZR-UCMS, compared to controls. Ex and UCMS-Ex groups had higher NO bioavailability (p=0.0001) compared to control and UCMS groups, but ROS levels remained high.ConclusionsThe comorbidity between UCMS and MetS does not exacerbate the effects of one another on GA EDD responses, but does lead to the development of other vasculopathy adaptations, which can be partially explained by alterations in NO and ROS production. Importantly, exercise training alleviates most of the negative effects of UCMS on GA function. Purpose The present study examined the effect of unpredictable chronic mild stress (UCMS) on peripheral microvessel function in healthy and metabolic syndrome (MetS) rodents, and whether exercise training could prevent the vascular dysfunction associated with UCMS. Methods Lean and obese (model of MetS) Zucker rats (LZR; OZR) were exposed to 8 weeks of UCMS, exercise (Ex), UCMS+Ex, or control conditions. At the end of the intervention, gracilis arterioles (GAs) were isolated and hung in a pressurized myobath to assess endothelium-dependent (EDD) and -independent (EID) dilation. Levels of nitric oxide (NO) and reactive oxygen species (ROS) were measured through DAF-FM and DHE staining, respectively. Results Compared to LZR controls, EDD and EID was lower (p=0.0001) in LZR-UCMS. The OZR-Ex group had a higher EDD (p=0.0001) and EID (p=0.003), compared to OZR-Controls; whereas only a difference in EDD (p=0.01) was noted between LZR-Control and LZR-Ex groups. Importantly, EDD and EID were higher in the LZR (p=0.0001; p=0.02) and OZR (p=0.0001; p=0.02) UCMS+Ex groups compared to UCMS alone. Lower NO bioavailability and higher ROS were noted in the LZR-UCMS group (p=0.0001), but not OZR-UCMS, compared to controls. Ex and UCMS-Ex groups had higher NO bioavailability (p=0.0001) compared to control and UCMS groups, but ROS levels remained high. Conclusions The comorbidity between UCMS and MetS does not exacerbate the effects of one another on GA EDD responses, but does lead to the development of other vasculopathy adaptations, which can be partially explained by alterations in NO and ROS production. Importantly, exercise training alleviates most of the negative effects of UCMS on GA function. Corresponding Author: Paul D. Chantler, 1 Medical Center Drive, P.O. Box 9227, Morgantown, WV 26506, pchantler@hsc.wvu.edu This work was supported by the American Heart Association grants IRG 14330015 and pre-doctoral fellowship AHA 14PRE 20380386, and the National Institute of General Medical Sciences of the National Institutes of Health under award numbers U54GM104942 and 5P20GM109098. The authors declare no conflicts of interest. The results of the present study do not constitute endorsement by the American College of Sports Medicine and are presented clearly, honestly, and without fabrication, falsification, or inappropriate data manipulation. Accepted for Publication: 15 December 2017 © 2017 American College of Sports Medicine

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