Key points are not available for this paper at this time.
The purpose of this study was to determine whether exercise training induces changes in the contractile behavior of proximal coronary arteries. Female Yucatan miniature swine were either exercise trained (ET) on a motor-driven treadmill or allowed to remain sedentary (SED) for 16-22 wk. Responses to vasoactive compounds were evaluated in vitro using coronary arterial rings (approximately 2 mm diam) isolated from ET and SED pigs. Each ring was stretched to the apex of the length-active tension relationship. Concentration-response relationships for isometric contractions evoked with KCl (5-100 mM), prostaglandin F2 alpha (PGF2 alpha; 10(-8)-3 x 10(-5) M), acetylcholine (ACh; 10(-9)-10(-4) M), and endothelin (10(-10)-10(-7) M) were similar in arteries from SED and ET pigs. In contrast, arteries from the ET group developed 50-60% less maximal tension in response to norepinephrine (NE; 10(-6)-10(-4) M) than did controls. Vasodilator responses of rings precontracted with either KCl or PGF2 alpha were evaluated with adenosine (ADO; 10(-9)-10(-4) M), isoproterenol (10(-9)-10(-4) M), forskolin (10(-9)-10(-4) M), and sodium nitroprusside (NP; 10(-10)-10(-4) M). Vasodilator responses were similar in SED and ET groups for all agents except ADO and NP; arteries from ET pigs were more sensitive to ADO and less sensitive to NP. The ET-induced alterations in vasomotor responses to NE and ADO appear to be due to changes in vascular smooth muscle because they were still present after removal of endothelium. We conclude that chronic exercise training in pigs induces selective alterations in NE and ADO receptor-second messenger coupling and/or postreceptor-related events in epicardial coronary vascular smooth muscle.
Oltman et al. (1992) studied this question.