Changes in muscle blood flow, PO2 and pH during and after contraction were studied on the quadriceps muscle of the anesthetized rabbits. Muscle blood flow was measured with a heated thermocouple technique, PO2 with an oxygen electrode and pH with a micro glass electrode. The muscle contraction was produced by supramaximal stimuli (7-9 V, 0.1 msec) of the femoral nerve. During weak contraction by lower frequent stimuli (1-17 Hz), muscle blood flow and muscle PO2 increased linearly in response to various frequencies of the stimulation. During strong contraction by higher frequent stimuli (more than 25 Hz), however, muscle blood flow and PO2 decreased gradually. These findings suggest the occurrence of anoxia in the muscle tissue during strong contraction. On the other hand, changes in muscle blood flow after contraction were different from those in muscle PO2. In the ischemic muscle caused by the femoral artery occlusion, increased muscle PO2 remained low level during contraction in various frequencies of the stimulation and durations of the contraction. During strong contraction of the normal and ischemic muscles, increased muscle PO2 remained low in various durations of the contraction; this seems to imply an anoxia in the muscle tissue. Muscle pH began to decrease during contraction and continued decreasing after contraction. These changes in muscle pH were correlated to the intensity and duration of the contraction, but were not similar to the changes in muscle blood flow. Changes in muscle pH after the femoral artery occlusion were different from those of muscle blood flow and from the pattern of reactive hyperemia. These findings suggest that postcontraction hyperemia and reactive hyperemia are not only due to anoxia nor acidosis in the muscle tissue, but also due to some other factors associated with the changes in muscle PO2 and pH.