Effects of Exercise Training on PPARβ/δ Expression in Skeletal Muscle of Rats with Spontaneous Hypertension.

Abstract

ABSTRACTPurposeThis study aimed to identify the relationship and mechanism between skeletal muscle peroxisome proliferator–activated receptor β/δ (PPARβ/δ) and spontaneous hypertension.MethodsRats were divided into four groups (n = 10): spontaneous hypertensive rats exercise group (SHR-E), spontaneous hypertensive rats sedentary group (SHR-S), Wistar-Kyoto control rats exercise group (WKY-E), and Wistar-Kyoto control rats sedentary group (WKY-S). Although the sedentary groups were placed on the treadmill without moving during the training sessions, the exercise groups were forced to run on a treadmill for 8 wk, 1 h·d−1, 5 d·wk−1. After training, the density and area of gastrocnemius microvessels were observed. PPARβ/δ, vascular endothelial growth factor A (VEGFA), superoxide dismutase 2 (SOD-2), and nitric oxide synthase in gastrocnemius were measured by real-time quantitative polymerase chain reaction (RT-qPCR) and Western blot.ResultsExcept the sixth week of age, the systolic blood pressure of SHR-S was significantly higher than that of WKY-S at all time periods. Exercise significantly reduced systolic blood pressure in SHR rats. Compared with the SHR-S group, the WKY-S group had significantly higher PPARβ/δ protein level and density of skeletal muscle microvessels. Eight weeks of exercise increased the PPARβ/δ, SOD-2, VEGFA, and microvessel density and area in the skeletal muscle of SHR.ConclusionsExercise training promoted PPARβ/δ mRNA and protein-level expression of PPARβ/δ, SOD-2 and VEGFA in skeletal muscle, thus increasing the density and area of skeletal muscle blood vessels. These regulations contribute to the reduction of peripheral vascular resistance. This may be a potential mechanism of exercise to reduce blood pressure.