Resistance training increases insulin-induced vasodilation in the mesenteric artery of healthy rats.

João E.S Araujo,Marcio R.V Santos,Fabrício N Macedo,Jullyana S.S Quintans,Rosana S.S Barreto,André S Barreto,Davi P.M Oliveira,Lucindo J.Q Junior,Rodrigo M Dos Santos,Sandra L Santos

doi:10.1590/0001-3765202120210222

João E.S Araujo, Marcio R.V Santos + Show 8 more

Open Access

https://doi.org/10.1590/0001-3765202120210222

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Abstract

This study evaluated the ability of resistance training (RT) of moderate intensity to promote vascular changes in insulin-induced vasodilation in healthy animals. Wistar rats were divided into two groups: control (CON) and trained (eight weeks of training, performing 3 sets with 10 repetitions at 60% of maximum intensity). Forty-eight hours after the last session of the RT, the animals were sacrificed and vascular reactivity to insulin in the absence and presence of LY294002 (phosphatidylinositol 3-kinase inhibitors (PI3K), L-NAME (nitric oxide synthase (NOS) inhibitors) and BQ123 (endothelin A antagonist (ET-A) receptor). In addition, phenylephrine (Phe)-induced vasoconstriction in the absence and presence of L-NAME was also evaluated. The RT group showed greater vasodilation in maximal response compared to the CON group. After PI3K inhibition, vasodilation was reduced in both groups. However, when the NOS participation was evaluated, the RT group showed contraction in relation to the CON group, which was abolished by BQ123. In addition, the RT group had an increase in nitrite levels compared to the CON group. When the Phe response was evaluated, there was a reduction in tension in the RT group compared to the CON group. The results suggest that RT improves vascular reactivity.

Highlights

The vascular endothelium (EV) is involved in several functions, including maintenance of vascular tone, prevention of vascular smooth muscle proliferation, reduction in leukocyte adhesion and activation, inhibition of platelet aggregation, formation of thrombi and flow regulation of blood (Rajendran et al 2013, Cahill & Redmond 2016)
The body weight of the animals was similar between the groups at the beginning of the study, and with no difference at the end of the eight weeks, even the resistance training (RT) group presenting lower values compared to the CON group
Insulin-mediated vasodilation was increased in the RT group compared to CON, which may be associated with increased nitric oxide (NO) production

Summary

Introduction

The vascular endothelium (EV) is involved in several functions, including maintenance of vascular tone, prevention of vascular smooth muscle proliferation, reduction in leukocyte adhesion and activation, inhibition of platelet aggregation, formation of thrombi and flow regulation of blood (Rajendran et al 2013, Cahill & Redmond 2016). One of the main mechanisms responsible for maintaining endothelial function is nitric oxide (NO), which induces endothelium-dependent vasodilation by increasing intracellular calcium concentrations ([Ca2+]i). Insulin, in addition to playing an important role in regulating glucose homeostasis, acts in maintaining vascular health (Muniyappa et al 2008, Arce-Esquivel et al 2013). Some studies have shown that this hormone acts in vascular modulation, playing an important role in controlling blood flow, directly participating in the maintenance of homeostasis and vascular tone, which can represent up to 25% of maximum vasodilation (Arce-Esquivel et al 2013, Fontes et al 2014, Mota et al 2015). Akt activates endothelial nitric oxide synthase (eNOS) through the phosphorylation of its specific site, the serine1177 residue, promoting an increase in eNOS activity and, the production of NO (Muniyappa et al 2008, Muniyappa & Sowers 2013)

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