Exercise-induced increases in tissue adenosine level vary in muscles having different oxidative capacities. These studies were designed to further evaluate the role of this potent vasodilator as a modulator of active hyperemia in muscles having different intrinsic metabolic profiles. Soleus (slow-twitch oxidative) and gracilis (fast-twitch glycolytic) muscles of anesthetized cats were stimulated to contract isometrically in the presence of adenosine deaminase (ADA) or ADA that had been deactivated by boiling (BADA). Stimulation parameters were chosen to provide similar high and low blood flow responses in the two muscle types. ADA did not affect resting blood flow or vascular resistance. In the soleus muscle, ADA attenuated both the increase in blood flow and oxygen consumption and the decrease in vascular resistance at the high level of muscle stimulation. In addition, muscle performance decreased to 60% of its initial level in the presence of ADA, although the same initial performance level was maintained over the stimulation period during BADA infusion. Temporal studies in the soleus muscle demonstrated an ADA-induced decrease in oxygen consumption, which was the product of an attenuated blood flow, followed by reductions in muscle performance. ADA had no effect on active hyperemia in either muscle at the low stimulation level. Additionally, ADA did not attenuate active hyperemia in the gracilis when stimulated at a level that normally produced muscle fatigue. Therefore these data support a role for adenosine in mediating vasodilation in skeletal muscle composed of high-oxidative fibers at high levels of muscle performance but do not support a role for adenosine in skeletal muscle having low-oxidative fibers, even at levels of exercise which produce fatigue.
- Copyright © 1990 the American Physiological Society