Changes in tissue oxygenation of forearm muscles were measured by near infrared (NIR) spectrophotometry in 10 healthy adults during tourniquet ischemia and venous outflow restriction. Muscle O2 stores were depleted rapidly by forearm ischemia manifest by a progressive decrease in tissue oxyhemoglobin and oxymyoglobin over 4-5 min. Muscle ischemia significantly decreased the oxidation level of cytochrome aa3, to below resting base line after only 1.5 min, and the enzyme became fully reduced after 6.5 min. After 8 min of ischemia, tourniquet release was accompanied by a transient increase in muscle blood volume due to influx of oxyhemoglobin. The cytochrome aa3 oxidation level increased above resting base line within 1 min after tourniquet release. Transcutaneous PO2 measurements recorded simultaneously from the same forearm correlated poorly with the kinetics of O2 availability and cytochrome oxidation in the underlying muscle tissue; this was not unexpected because overlying skin did not contribute significantly to NIR muscle signals. Venous outflow restriction without inflow obstruction increased muscle deoxyhemoglobin and tissue blood volume but did not change muscle O2 stores or cytochrome aa3 oxidation level. The ability of the NIR technique to detect dynamic trends in tissue oxygenation reveals that muscle O2 is rapidly consumed during tourniquet ischemia and rapidly restored by hyperemic responses after brief ischemia.