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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Exercise training causes skeletal muscle venular growth and alters hemodynamic responses in spontaneously hypertensive rats

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Author(s):
Amaral, Sandra L. [1] ; Silveira, Neide P. ; Zorn, Telma M. T. ; MIchelini, Lisete C.
Total Authors: 4
Affiliation:
[1] Universidade de São Paulo (USP). Instituto de Ciências Biomédicas. Departamento de Biologia Celular e do Desenvolvimento - Brasil
Total Affiliations: 4
Document type: Journal article
Source: Journal of Hypertension; v. 19, n. 5, p. 931-940, May 2001.
Field of knowledge: Biological Sciences - Physiology
Abstract

o investigate whether training changes skeletal muscle venular profile and hemodynamic responses to exercise we studied spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats submitted to training programme (T = 50-60% of VO(2)max). Training (T) was performed on a treadmill over a period of 13 weeks. Age-matched control groups were kept sedentary (S), T and S rats were chronically instrumented for hindlimb flow (HLF) and arterial pressure (AP) measurements at rest, during dynamic exercise and recovery in two different situations: control and after extensive intravenous blockade (hexamethonium + losartan + N-omega-nitro-L-arginine methyl ester + hydralazine), For morphometric analysis, skeletal muscle samples (gracilis) were obtained after transcardiac perfusion with fixative. T caused a significant reduction of resting mean arterial pressure (MAP) (-11%) only in the SHR group without changing basal HLF. In the sedentary SHR (SHRS), basal relative hindlimb resistance was increased by 45%, but was significantly reduced after T (P < 0.05), During dynamic exercise, MAP increased similarly (10-20 mm Hg) in all groups. HLF increases were similar for the four groups up to 0.8 km/h; at higher workloads, HLF was higher in trained SHR (SHRT) versus trained WKY (WKYT) (3.9- versus 2.9-fold increase over basal HLF, respectively). After blockade (and pressure correction with IV phenylephrine infusion), steady-state exercise was performed with similar hindlimb vasodilation in all groups and was accompanied by MAP reduction (-17 <plus/minus> 8 mmHg) only in SHRT group. Skeletal muscle venular profile (density, diameter and lumen cross-sectional area) was similar in WKYT, WKYS and SHRS, but significantly increased in SHRT. In this group the two-fold increase in venule density was correlated with both the reduction in baseline MAP and the increase in HLF during dynamic exercise. The results suggest that increased venule density is a specific adaptation of SHR skeletal muscle to training. Venular growth may contribute to both the pressure-lowering effect and the large HLF at high exercise intensities observed in the trained SHR. (AU)