beta-Endorphin (BEP) has been implicated in the analgesic response to transcutaneous electrical nerve stimulation (TENS). The anterior pituitary gland is a source of beta-endorphin which shares the prohormone proopiomelanocortin (POMC) with adrenocorticotropin (ACTH). Current theory proposes that the stimulation-induced breakdown of POMC results in ACTH release with a subsequent elevation in blood cortisol levels. The purpose of this study was to determine the potential application and mechanism of TENS as an anti-inflammatory agent. Eight female subjects received low frequency, 300 musec pulse width TENS at four sites associated with relief of upper arm pain once when pain free and again while experiencing delayed onset muscle soreness (DOMS) of the elbow flexor muscle group. Blood samples were withdrawn 15 and 1 minute before and 1, 20, and 40 minutes after treatment. Serum was analyzed for cortisol by radioimmunoassay. TENS treatment failed to elevate serum cortisol concentration, but there was a significant reduction in perception of pain (p < 0.05) and an improvement in range of elbow extension (p < 0.05) when subjects were treated for DOMS. These results suggest that the anterior pituitary is not a source of BEP in TENS-induced analgesia. J Orthop Sports Phys Ther 1989;11(3):100-103.