The aim of this study was to determine whether a 4-wk handgrip training program would elicit changes in endothelium-dependent and endothelium-independent vasodilatation in resistance vessels of the human forearm. Minimum vascular resistance after a 10-min ischemic stimulus, an index of peak vasodilator capacity, was also determined. Forearm blood flow response to the endothelium-dependent vasodilator methacholine chloride did not change over the 4-wk-intervention period either in the group undertaking training (n = 11) or in control subjects (n = 6). Similarly, the response to sodium nitroprusside was not influenced by the handgrip training program. Peak vasodilator capacity of the trained forearms significantly increased, whereas no change was evident in the untrained limbs. These results suggest that 4 wk of forearm exercise training enhances peak vasodilator capacity of the vasculature without influencing stimulated activity of the nitric oxide dilator system.

The aim of this study was to determine whether physical conditioning induced by a repetitive exercise stimulus would elicit changes in the response of forearm resistance vessels to an infusion of substances that modulate nitric oxide synthesis. Forearm blood flow responses to a 5-min ischemic stimulus and intrabrachial infusion of acetylcholine, sodium nitroprusside, and NG-monomethyl-L-arginine were examined in the preferred and nonpreferred limbs of eight habitual tennis players. Forearm volume, girth, and grip strength were significantly greater in the preferred limb, indicating a bilateral difference in physical condition. This was associated with an enhanced reactive hyperemic response in the preferred limb (53.5 +/- 9.4 vs. 38.8 +/- 4.7 ml.100 ml-1.min-1; P < 0.05). No differences between the limbs were evident in response to acetylcholine, sodium nitroprusside, or NG-monomethyl-L-arginine. These results suggest that exercise training enhances the peak vasodilator capacity of the vasculature without influencing basal or stimulated activity of the nitric oxide dilator system in vivo.