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1 Center for Interdisciplinary Research in Cardiovascular Sciences, West Virginia University, Morgantown, West Virginia, United States
2 Exercise Physiology, West Virgnia University, Morgantown, West Virginia, United States
3 Exercise Physiology, West Virginia University, morgantown, Maine, United States
* To whom correspondence should be addressed. E-mail: jfrisbee{at}hsc.wvu.edu.
Reduced skeletal muscle microvessel density (MVD) in the obese Zucker rat (OZR) model of the metabolic syndrome is a function of a chronic reduction in vascular nitric oxide (NO) bioavailability. Previous studies suggest that exercise can improve NO bioavailability, reduce chronic inflammation, and that low vascular NO bioavailability may be associated with impaired angiogenic responses via increased matrix metalloproteinase (MMP)-2 and MMP-9 activity. As such, we hypothesized that chronic exercise (EX) would increase NO bioavailability in OZR and blunt microvascular rarefaction through reduced MMP activity, and potentially via altered plasma cytokine levels. 10 weeks of treadmill exercise (1 hr/d, 5 d/wk, 22 m/min) reduced body mass and fasting insulin and triglyceride levels in EX-OZR versus sedentary (SED) OZR. In EX-OZR, gastrocnemius muscle MVD was improved by 19±4%, while skeletal muscle arteriolar dilation and conduit arterial methacholine-induced NO release were increased. In EX-OZR, functional hyperemia was improved versus SED-OZR and minimum vascular resistance within perfused gastrocnemius muscle was reduced, although no change in arteriolar stiffness was identified. Western blotting and gelatin zymography demonstrated that neither expression nor activity of MMP-2 or MMP-9 were altered in skeletal muscle of EX versus SED animals. Plasma markers of inflammation associated with angiogenesis, MCP-1 and IL-1
were increased in SED-OZR, and were reduced with training, while IL-13 was reduced in SED-OZR and increased with exercise. These data suggest that exercise-induced improvements in skeletal muscle MVD in OZR are associated with increased NO bioavailability, and may stem from altered inflammatory profiles rather than MMP function.
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