0205 : Exercise training prevents microvascular dysfunction in a rat model of diet-induced metabolic syndrome

• Published in: Archives of Cardiovascular Diseases Supplements Vol. 7; no. 2; p. 137
• Main Authors: Nascimento, Alessandro Do, Meziat, Cindy, Battault, Sylvain, Meyer, Gregory, Gayrard, Sandrine, Reboul, Cyril, Walther, Guillaume
• Format: Journal Article
• Language: English
• Published: Elsevier France 01.04.2015
• ISSN: 1878-6480
• DOI: 10.1016/S1878-6480(15)30020-3

Metabolic syndrome (MetS) is associated with increased risk of cardiovascular disease (CVD). One important key feature underlying the pathophysiology of CVD is microvascular dysfunction. Although, exercise training is a well recognized strategy to reduce cardiovascular and metabolic disorders, the impact on MetS induced microvascular dysfunction is poorly described and the underlying mechanisms remain unknown. Thus, the aim of this work was to evaluate the effect of physical activity on microvascular reactivity in a rat model of MetS. Rats were fed with standard (Ctrl group) or high-fat and sucrose diet (HFS group) for 14 weeks. After 6 weeks, HFS rats were randomly assigned into 2 groups: sedentary (HFS) and trained group (HFS-Ex). In vivo endothelial function was evaluated by skin Laser Doppler technique associated to transcutaneous iontophoresis at 06 and 14 weeks. Body weight, metabolic parameters and blood pressure were also measured. High-fat and sucrose diet induced a significant body weight raise accompanied by the increase of serum level of glucose, triglycerides, HDL and LDL-cholesterol. All of these parameters were restored after 4 weeks of exercise training in HFS-Ex group. In addition, skin endothelium-dependent dilation, which was decreased in HFS compared to Ctrl, was prevented by exercise training. This result could be explained by increased level of eNOS expression and phosphorylation on its activation site (ser1177). These results mainly suggest that an exercise training strategy, which is able to partially correct metabolic disorders in a model of MetS in rats, also prevents in vivo microvascular dysfunction.