The relation between muscle pain, muscle activity, and muscle co-ordination is still controversial. The present human study investigates the influence of experimental muscle pain on resting, static, and dynamic muscle activity. In the resting and static experiments, the electromyography (EMG) activity and the contraction force of m. tibialis anterior were assessed before and after injection of 0.5 ml hypertonic saline (5%) into the same muscle. In the dynamic experiment, injections of 0.5 ml hypertonic saline (5%) were performed into either m. tibialis anterior (TA) or m. gastrocnemius (GA) and the muscle activity and co-ordination were investigated during gait on a treadmill by EMG recordings from m. TA and m. GA. At rest no evidence of EMG hyperactivity was found during muscle pain. The maximal voluntary contraction (MVC) during muscle pain was significantly lower than the control condition (P < 0.05). During a static contraction at 80% of the pre-pain MVC muscle pain caused a significant reduction in endurance time (P < 0.043). During dynamic contractions, muscle pain resulted in a significant decrease of the EMG activity in the muscle, agonistic to the painful muscle (P < 0.05), and a significant increase of the EMG activity of the muscle, antagonistic to the painful muscle (P < 0.05). Muscle pain seems to cause a general protection of painful muscles during both static and dynamic contractions. The increased EMG activity of the muscle antagonistic to the painful muscle is probably a functional adaptation of muscle co-ordination in order to limit movements. Modulation of muscle activity by muscle pain could be controlled via inhibition of muscles agonistic to the movement and/or excitation of muscles antagonistic to the movement. The present results are in accordance with the pain-adaptation model (Lund, J.P., Stohler, C.S. and Widmer, C.G. In: H. Vaerøy and H. Merskey (Eds.), Progress in Fibromyalgia and Myofascial Pain. Elsevier, Amsterdam, 1993, pp. 311-327.) which predicts increased activity of antagonistic muscle and decreased activity of agonistic muscle during experimental and clinical muscle pain.