The aim of the present study was to determine whether oxygen supply to non-exercised muscle during recovery following fatiguing exercise is influenced by accumulated metabolites within exercised muscle. Twelve healthy male subjects performed 2-min isometric handgrip exercise at 40% maximal voluntary contraction with their right hand and the exercise was followed by a 3-min recovery period. Muscle oxygen saturation (SmO2) determined by near-infrared spatially resolved spectroscopy was used as an index of oxygen supply to non-exercised muscle and was measured in biceps brachii and tibialis anterior muscles on the left side. Compared to the pre-exercise baseline level, SmO2 in the biceps brachii muscle (SmO2BB) increased significantly from 30 sec to 1 min after the start of exercise, while SmO2 in the tibialis anterior muscle (SmO2TA) remained stable during the initial 1 min of exercise. Both SmO2BB and SmO2TA began to decrease at about 1 min and continued to decrease thereafter. Due to the initial increase in SmO2BB, only SmO2TA showed a significant decrease during exercise. During recovery, SmO2BB did not differ significantly from the pre-exercise baseline level, whereas SmO2TA remained significantly lower until about 1.5 min of recovery and then it did not differ significantly from the baseline level. In another bout, subjects performed handgrip exercise of the same intensity, but post-exercise arterial occlusion (PEAO) of the exercised muscle was imposed for 2 min immediately after the end of exercise. During PEAO, SmO2BB decreased significantly compared to the baseline level, whereas SmO2TA remained significantly lower until the end of PEAO. The significant decrease in SmO2BB and the prolongation of decrease in SmO2TA by PEAO suggests that the recovery of SmO2 in the non-exercised arm and leg is mediated by muscle metaboreceptors.