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Received December 22, 2003
Revised January 22, 2004
Accepted after revision March 2, 2004
1 Texas A&M University
* To whom correspondence should be addressed. E-mail: mdd{at}hlkn.tamu.edu.
Aging reduces endothelium-dependent vasodilation in humans and animals, and in humans, exercise training reverses the aging-associated reduction in endothelium- dependent vasodilation. The purpose of this study was to determine the mechanism(s) by which 10-12 wks of treadmill exercise enhances endothelium-dependent vasodilation in muscles of differing fiber composition from young and old rats. Three- and 22-month old male Fischer 344 rats were assigned to young sedentary (young SED), young exercise-trained (young ET), old sedentary (old SED), or old exercise-trained (old ET) group. Arterioles were isolated from the soleus and gastrocnemius muscles; luminal diameter changes were determined in response to the endothelium-dependent vasodilator acetylcholine (ACh, 10-9 - 10-4 mol/L) alone and in the presence of the nitric oxide synthase (NOS) inhibitor L-NAME (10-5 mol/L) or the combination of L- NAME and the cyclooxygenase inhibitor indomethacin (10-5 mol/L). Training ameliorated the aging-induced reduction in endothelium-dependent vasodilation in soleus muscle arterioles. Treatment with L-NAME alone and in combination with indomethacin abolished differences in ACh vasodilation occurring with aging and training. Expression of endothelial NOS (eNOS) mRNA in soleus arterioles was unaltered by aging, whereas eNOS protein was increased with age; training elevated both eNOS mRNA and protein. In gastrocnemius muscle arterioles, aging did not alter maximal vasodilation, but aging and training increased maximal arteriolar diameter. These results demonstrate that aging-induced reductions and training-induced enhancement of endothelial vasodilation both occur through the nitric oxide signaling mechanism in highly oxidative skeletal muscle, but aging and training do not appear to act on the same portion of the signaling cascade.
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