TIME-COURSE OF ENHANCED ENDOTHELIUM-MEDIATED DILATION IN AORTA OF TRAINED RATS

Citation
Md. Delp et Mh. Laughlin, TIME-COURSE OF ENHANCED ENDOTHELIUM-MEDIATED DILATION IN AORTA OF TRAINED RATS, Medicine and science in sports and exercise, 29(11), 1997, pp. 1454-1461
Citations number
34
Categorie Soggetti
Sport Sciences
ISSN journal
01959131
Volume
29
Issue
11
Year of publication
1997
Pages
1454 - 1461
Database
ISI
SICI code
0195-9131(1997)29:11<1454:TOEEDI>2.0.ZU;2-4
Abstract
Previous work has demonstrated that 10 wk of exercise training enhance s the responsiveness of rat abdominal aortas to acetylcholine (ACh), a n endothelium-dependent vasodilator. The purpose of this study was to determine the time course for this training-induced adaptation of vasc ular endothelium. Additionally, the contribution of the cyclooxygenase and nitric oxide synthase mechanisms to the enhanced endothelium-medi ated relaxation were examined. Male rats were divided into sedentary ( SED) and exercise groups. Exercised animals were further subdivided in to postexercise (POST-EX), 1 DAY, 1 WK, 2 WK, 4 WK and 10 WK groups. E xercise consisted of treadmill running at 30 m.min(-1) (15 degrees inc line) for 1 h.d(-1) (5 d.wk(-1) for the 1 WK, 2 WK, 4 WK, and 10 WK gr oups). Maximal vasodilator responses induced by 10(-4) M ACh (10(-7) M norepinephrine preconstriction) were determined on abdominal aortic r ings in vitro immediately after a single exercise bout in POST-EX rats and 24 h after a single bout of exercise in 1 DAY animals. Maximal 10 (-4) M ACh-induced dilation of aortas from 1 WK, 2 WK, 4 WK, and 10 WK animals was determined 24 h after the last exercise bout. Soleus musc le citrate synthase activity was greater in 2 WK (31 +/- 1 mu mol.min( -1).g wet wt(-1)), 4 WK (34 +/- 2), and 10 WK (36 +/- 1 mu mol.min(-1) .g wet wt(-1)) rats than in SED (27 +/- 1 mu mol.min(-1).g wet wt.(-1) ) animals. Maximal ACh-induced relaxation was greater in aorta from 4 WK (72 +/- 2%) and 10 WK (79 +/- 1%) rats than SED (61 +/- 2%) rats. A Ch-mediated dilatory responses remained enhanced in the presence of th e cyclooxygenase blocker indomethacin (10(-5) M), but were abolished b y the nitric oxide synthase inhibitor N-G-nitro-L-arginine methyl este r (300 mu M) In addition, the expression of endothelial nitric oxide s ynthase (ecNOS) protein in aortas from 4 WK (P = 0.057) and 10 WK (P < 0.05) rats was greater than in aortas from SED animals. These data in dicate that the enhanced endothelium-dependent, ACh-mediated dilation of the rat aorta is present by 4 wk of endurance exercise training. Th is adaptation appears to be mediated primarily through the nitric oxid e synthase pathway and is associated with an increased expression of e cNOS.