SHORT-TERM DAILY EXERCISE ACTIVITY ENHANCES ENDOTHELIAL NO SYNTHESIS IN SKELETAL-MUSCLE ARTERIOLES OF RATS

We aimed to test the hypothesis that as a consequence of short-term daily bouts of exercise the control of arteriolar smooth muscle by endothelium is altered. Rats ran on a treadmill once a day, 5 days/wk, for 2-4 wk (with gradually increasing intensity, up to 26 min at 22 m/min at a 1% grade by the beginning of the 3rd wk and up to 38 min at 28 m/min at a 2% grade by the beginning of the 4th wk) while a control group remained sedentary (SED). Cannulated and pressurized arterioles of rat gracilis muscle developed spontaneous myogenic tone, which was slightly enhanced in exercised (EX) compared with SED rat arterioles. At 80 mmHg pressure, the passive (Ca2+-free solution) and active diameters of SED and EX rat arterioles were 105.4 +/- 3.8 and 55.1 +/- 2.3 mu m and 107.1 +/- 3.4 and 50.2 +/- 2.2 mu m, respectively. Dose-dependent dilations to sodium nitroprusside (10(-8)-10(-6) M) and constrictions to norepinephrine (10-(8)-10-(6) M) were not affected in EX arterioles, whereas dilations to adenosine (10(-6)-10(-4) M) were significantly reduced. In contrast, dose-dependent dilations to acetylcholine (ACh; 5 x 10(-9)-10(-7) M) and L-arginine [precursor of nitric oxide (NO); 10(-4)-10(-3) M] were significantly enhanced (by 33-78 and 57-75%, respectively) in arterioles of EX compared with those of SED rats. Responses of arterioles to sodium nitrite were not different in SED and EX groups. In both groups of arterioles, endothelium removal abolished dilation to ACh (10(-8) M) and L-arginine (10(-4) hi) but did not affect responses to sodium nitroprusside (10(-7) M). Administration of 10(-4) M N-omega-nitro-L-arginine (an NO synthase inhibitor) significantly inhibited responses to ACh and elicited a similar decrease (similar to 15%) in the basal diameter of arterioles of SED and EX rats. These findings suggest that, in skeletal muscle arterioles of rats, short-term daily exercise enhances endothelial synthesis of NO induced by ACh or L-arginine. We suggest that these adaptations are most likely due to the increases in blood flow to skeletal muscle during the periods of daily exercise activity.