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Vascular Adjusts Induced by Low Intensity Resistance Training

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The aim of this study was to evaluate the vascular effects and participation of nitric oxide (NO) after a period of resistance training (RT). One group was submitted to RT (Ex). Control animals (SED) were fictitious trained (no exercise). After 8 weeks, mesenteric artery was removed and divided, one part was sliced in rings for vascular reactivity analysis (Acetilcholine (ACh): 10 ‐9 ‐ 10 ‐4 M; Nω‐nitro‐L‐arginine methyl ester hydrochloride (L‐NAME): 100µM; Phenylephrine (Phe): 10 ‐6 M) and the other half was probed with DAF‐FM dye to evaluation of NO bioavailability. Other animals were used to verify the nitric oxide synthases (NOS) expression using western blot technique. RT was able to increase percentage of ACh‐induced relaxation of mesenteric arterial rings (pD2: SED 6.2 ± 0.1 vs Ex 7.1 ± 0.1) and addition of L‐NAME abolished this effect (SED 52.0 ± 3.2% vs Ex 35.8 ± 3.7%). Moreover, RT reduced the level of tension in mesenteric rings with Phe‐induced contraction (SED 0.39 ± 0.06 vs Ex 0.20 ± 0.05) and addition of L‐NAME abolished this effect (SED 0.65 ± 0.05 vs Ex 0.88 ± 0.07). RT also increased the bioavailability of NO in both, basal (SED 0.99 ± 0.1 vs Ex 2.22 ± 0.16) and stimulated with ACh 10 ‐7 (SED 2.32 ± 0.16 vs 2.95 ± 0.2). In addition, RT increased eNOS (SED 0.21 ± 0.03 vs Ex 0.71 ± 0.07) and nNOS expression (SED 0.28 ± 0.06 vs Ex 0.76 vs 0.21). In conclusion, RT were able to promote endothelial adjustments, probably mediated by increased NO synthases.
Title: Vascular Adjusts Induced by Low Intensity Resistance Training
Description:
The aim of this study was to evaluate the vascular effects and participation of nitric oxide (NO) after a period of resistance training (RT).
One group was submitted to RT (Ex).
Control animals (SED) were fictitious trained (no exercise).
After 8 weeks, mesenteric artery was removed and divided, one part was sliced in rings for vascular reactivity analysis (Acetilcholine (ACh): 10 ‐9 ‐ 10 ‐4 M; Nω‐nitro‐L‐arginine methyl ester hydrochloride (L‐NAME): 100µM; Phenylephrine (Phe): 10 ‐6 M) and the other half was probed with DAF‐FM dye to evaluation of NO bioavailability.
Other animals were used to verify the nitric oxide synthases (NOS) expression using western blot technique.
RT was able to increase percentage of ACh‐induced relaxation of mesenteric arterial rings (pD2: SED 6.
2 ± 0.
1 vs Ex 7.
1 ± 0.
1) and addition of L‐NAME abolished this effect (SED 52.
0 ± 3.
2% vs Ex 35.
8 ± 3.
7%).
Moreover, RT reduced the level of tension in mesenteric rings with Phe‐induced contraction (SED 0.
39 ± 0.
06 vs Ex 0.
20 ± 0.
05) and addition of L‐NAME abolished this effect (SED 0.
65 ± 0.
05 vs Ex 0.
88 ± 0.
07).
RT also increased the bioavailability of NO in both, basal (SED 0.
99 ± 0.
1 vs Ex 2.
22 ± 0.
16) and stimulated with ACh 10 ‐7 (SED 2.
32 ± 0.
16 vs 2.
95 ± 0.
2).
In addition, RT increased eNOS (SED 0.
21 ± 0.
03 vs Ex 0.
71 ± 0.
07) and nNOS expression (SED 0.
28 ± 0.
06 vs Ex 0.
76 vs 0.
21).
In conclusion, RT were able to promote endothelial adjustments, probably mediated by increased NO synthases.

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