Resistance exercise acutely enhances mesenteric artery insulin-induced relaxation in healthy rats

Aims

We evaluated the mechanisms involved in insulin-induced vasodilatation after acute resistance exercise in healthy rats.

Main methods

Wistar rats were divided into 3 groups: control (CT), electrically stimulated (ES) and resistance exercise (RE). Immediately after acute RE (15 sets with 10 repetitions at 70% of maximal intensity), the animals were sacrificed and rings of mesenteric artery were mounted in an isometric system. After this, concentration–response curves to insulin were performed in control condition and in the presence of LY294002 (PI3K inhibitor), L-NAME (NOS inhibitor), L-NAME + TEA (K⁺ channels inhibitor), LY294002 + BQ123 (ET-A antagonist) or ouabain (Na⁺/K⁺ ATPase inhibitor).

Key findings

Acute RE increased insulin-induced vasorelaxation as compared to control (CT: R_max = 7.3 ± 0.4% and RE: R_max = 15.8 ± 0.8%; p < 0.001). NOS inhibition reduced (p < 0.001) this vasorelaxation from both groups (CT: R_max = 2.0 ± 0.3%, and RE: R_max = − 1.2 ± 0.1%), while PI3K inhibition abolished the vasorelaxation in CT (R_max = − 0.1 ± 0.3%, p < 0.001), and caused vasoconstriction in RE (R_max = − 6.5 ± 0.6%). That insulin-induced vasoconstriction on PI3K inhibition was abolished (p < 0.001) by the ET-A antagonist (R_max = 2.9 ± 0.4%). Additionally, acute RE enhanced (p < 0.001) the functional activity of the ouabain-sensitive Na⁺/K⁺ ATPase activity (R_max = 10.7 ± 0.4%) and of the K⁺ channels (R_max = − 6.1 ± 0.5%; p < 0.001) in the insulin-induced vasorelaxation as compared to CT.

Significance

Such results suggest that acute RE promotes enhanced insulin-induced vasodilatation, which could act as a fine tuning to vascular tone.