In order to examine muscle ischemia, muscle blood flow in the rat hindlimb was decreased by vessel ligation. Amino acid uptake, studied with [14C]alpha-aminoisobutyric acid, was decreased in ischemic Type I (soleus) muscle. Glucose uptake, studied with [14C]deoxyglucose, was increased in Type I muscle. These changes were temporally associated with histologic changes of ischemia in soleus muscle. Denervation, atrophy, and hypertrophy also produced uptake changes with these techniques, and although more prominent in soleus, the changes were also seen in Type II muscle.

Muscle blood flow, glucose uptake, and the ability of muscle to concentrate an inert amino acid have been studied in vivo using a variety of radiosotopes. The rate of blood flow is four times greater in the slow soleus muscle than in the fast gastrocnemius muscle of the rat, but the rate of deoxyglucose uptake is 14 times higher in the slow muscle relative to the fast muscle. Slow muscle is also able to accumulate the inert amino acid, α-aminoiso-butyric acid, more effectively than does fast muscle. A week after denervation, the rate of blood flow through denervated muscles was increased 30- to 40-fold over control values. However, deoxyglucose uptake was not significantly elevated in the gastrocnemius and was reduced to 20% of control levels in the soleus. The ability of the denervated muscles to concentrate α-aminoisobutyric acid was also impaired. These changes could not be accounted for in terms of an altered inulin space. There is no correlation between the rate of muscle blood flow and the ability of muscle to extract blood-borne nutrients. Impaired transport mechanisms precede and may initiate the major morphological changes that follow muscle denervation. © 1976.