CONTRIBUTION OF ENDOTHELIUM-DERIVED NITRIC-OXIDE (EDNO) TO THE SKELETAL-MUSCLE BLOOD-FLOW RESPONSE TO EXERCISE

Blood flow (BF) to active muscle increases dramatically during exercis e. This increase in BF is permitted by relaxation of smooth muscle (an d ensuing vasodilation) in the vasculature of muscle tissue. Recently, attention has focused on the possible role of the endothelium-derived relaxing factor nitric oxide (EDNO) in the vasodilation of muscle vas culature during exercise. A variety of experimental approaches have be en used in elucidating the role of EDNO. These include isolated vessel , isolated muscle or muscle group, and conscious exercising animal pre parations. Studies utilizing isolated vessels have shown that arteriol es from muscle dilate, in an endothelium-dependent manner, to stimuli present during exercise (e.g., increased flow rates). A limitation of such studies, however, is that only the potential for EDNO-induced vas odilation is indicated. The isolated muscle/muscle group approach has consistently demonstrated a role for EDNO in determining resting BF. F indings for muscle BF during contractions are equivocal. A limitation of this approach is that exercise is simulated by stimulating the moto r neuron of the muscle of interest. Since this type of muscle activity elicits a relatively small active hyperemia, it may be that a role fo r EDNO in exercise-induced hyperemia is masked. Findings from exercisi ng animals are equivocal. Some studies demonstrate a role for EDNO in permitting increased muscle blood flow during exercise, while others s how no impact of inhibition of EDNO synthesis. Some studies suggest th at the importance of EDNO may vary with the muscle (and its fiber type composition) studied. Additional research is needed to clarify the ro le of EDNO in mediating increased BF to skeletal muscle during exercis e.