Prolonged skeletal muscle ischemia is disruptive to cellular respiration. Upon reperfusion, the metabolic rate of the affected tissue is altered in a fashion dependent on the duration and totality of ischemia. This can be used as an indicator of the changes undergone in cellular metabolism. We have employed Phosphorescence Quenching Microscopy in conjunction with a flow‐arrest technique to assess the influences of external, pressure‐induced 1‐ to 30‐min focal ischemic durations on interstitial oxygenation (PO2) and the consumption of oxygen (VO2) in spinotrapezius muscles of SD rats. VO2 was assessed by the rate of PO2 decline during brief flow‐arrest compressions during reperfusion. Our tests of this intermittent compression technique have indicated that 5 s of flow‐arrest followed by 15 s of flow restoration allow for measurement of VO2 without compromising baseline or reperfusion recovery of interstitial PO2. Our preliminary studies show a ~5‐fold increase in VO2 following 30 min of ischemia, which then follows an exponential decay over several minutes back to baseline levels. Chemical modification of mitochondrial function, [NO], and [ROS] are expected to reveal the sources of this VO2 spike and how they influence the return to baseline. As hypoxia is central to I/R injury, a description of mitochondrial function during this insult will be helpful.