EFFECT OF COMBINED PHYSICAL TRAINING ON VASCULAR REACTIVITY OF HEART FAILURE RATS
Authors: Fontes Milene Tavares , Couto Gisle Kruger , Rossoni Luciana Venturini 
Published: June 2021

AIMTo evaluate the effect of combined (aerobic and resistance) training on vascular reactivity of heart failure (HF) rats, focusing on the role of the endothelium and perivascular adipose tissue (PVAT).METHODSEthics Committee 053/2014. Male, Wistar rats were submitted to occlusion of the coronary artery (HF) or fictitious surgery (SO). After 4 weeks, the maximal running (MR) and load (ML) tests were performed and the rats were divided into groups: untrained (uSO: n = 12 and uHF: n = 7) and resistance (ladder) and aerobic (treadmill) exercise training, on alternate days (5x/week/8 weeks, tHF: n = 5). At the end of the training protocol, left ventricular (LV) catheterization was performed, the rats were killed and the abdominal aorta was removed. The aortic rings with (+) and without (−) endothelium (E) or PVAT were mounted on a wire myograph. The E and PVAT were mechanically removed. To evaluate the vascular reactivity, concentration‐response curves to phenylephrine (PHE, 10−9–10−5M) were performed in the presence or absence of the non‐selective nitric oxide (NO) synthase inhibitor (L‐NAME, 100 μM). The results were expressed as mean ± SEM, ANOVA (p <0.05, *vs. uSO; #vs. uHF).RESULTSHF reduced and training increased MR (uSO: 8±10 vs. uHF: 2±9* vs. tHF: 163±21m*#) and ML capability (uSO: 119±14 vs. uHF: 92±17* vs. HFt: 247±17g*#). LV systolic pressure (uSO: 140±2 vs. uHF: 125±2* vs. tHF: 122±3mmHg*), contractility index (dP/dt+; uSO: 7294±254 vs. uHF: 5397±267* vs. tHF: 5480±301mmHg/s*) and relaxation index (dP/dt‐; uSO: −4645±148 vs. uHF: −3803±183* vs. tHF: −3994±201mmHg/s*) were reduced in HF and training did not modify these parameters. Moreover, LV end diastolic pressure was enhanced in uHF and training partially reduced it (uSO: 6.1 ± 0.3 vs. uHF: 18.2 ± 2.3* vs. tHF: 11.9±1.1mmHg*#). In uSO abdominal aortic rings, the PHE‐induced contraction was increased in E− and unchanged in E+/PVAT+ as compared to E+ rings; while, it was reduced in E−/PVAT+ as compared to E− rings. In uHF, PHE contraction was increased in E− rings as compared to E+; however, PVAT did not change this response in E+ or E− rings. HF increased PHE contraction in E+ and E+/PVAT+ rings as compared to uSO and training partially reduced this response. However, HF and training did not change the PHE‐induced contraction in E− rings as compared to E− uSO rings. Training partially restores the anti‐contractile PVAT effect in E−/PVAT+ rings of HF. In all groups, L‐NAME enhanced PHE contraction in E+ or E+/PVAT+ rings, but not in E− or E−/PVAT rings. However, the L‐NAME effect was higher in E+ in comparison to E+/PVAT+ rings. In the presence of L‐NAME no difference in PHE contraction was observed among groups.CONCLUSIONHF induced endothelial dysfunction in the abdominal aorta and reduced the anti‐contractile action of PVAT on E− rings. The training restores the PHE hypercontractility observed in uHF rings in an endothelium‐dependent and NO‐dependent way, with a smaller effect on PVAT.Support or Funding InformationCAPES, FAPESP and CNPq.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.