Key result
Low intensity resistance training for 8 weeks increased ACh-induced relaxation of mesenteric arterial rings (pD2 7.1 vs 6.2) and increased NO bioavailability and NOS expression in animals.
Why the study?
Does low intensity resistance training improve vascular reactivity and NO bioavailability in animal models?
Does low intensity resistance training improve vascular reactivity and NO bioavailability in animal models?
Absolute Event Rate: 7.1% vs 6.2%
Low intensity resistance training promotes endothelial adjustments and improves vascular reactivity, likely mediated by increased NO synthases.
Low-intensity resistance training may enhance NO-mediated vascular reactivity in animals; hypothesis-generating for humans and should not yet change practice.
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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Macedo et al. (2015) studied this question. Resistance training vs. Fictitious trained (no exercise) was evaluated on ACh-induced relaxation of mesenteric arterial rings (pD2). Low intensity resistance training for 8 weeks increased ACh-induced relaxation of mesenteric arterial rings (pD2 7.1 vs 6.2) and increased NO bioavailability and NOS expression in animals.
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