Animal experiments suggest that an increase in sympathetic outflow can depress muscle spindle sensitivity and thus modulate the stretch reflex response. The results are, however, controversial and human studies have failed to demonstrate a direct influence of the sympathetic nervous system on the sensitivity of muscle spindles. We studied the effect of increased sympathetic outflow on the short latency stretch reflex in the soleus muscle evoked by tapping the Achilles tendon. Nine subjects performed three maneuvers causing a sustained activation of sympathetic outflow to the leg: three min of static handgrip exercise at 30% of maximal voluntary contraction (MVC), followed by three min of post-handgrip ischemia and finally during a three min mental arithmetic task. Electromyography (EMG) was measured from the soleus muscle with bi-polar surface electrodes during the Achilles tendon tapping, while beat-to-beat changes in heart rate (HR) and mean arterial blood pressure (MAP) were monitored continuously. MAP was significantly elevated during all three maneuvers, while HR was significantly elevated during static handgrip exercise and mental arithmetic but not during post-handgrip ischemia. The peak-to-peak amplitude of the short latency stretch reflex was significantly increased during mental arithmetic (P<0.05), static handgrip exercise (P<0.001) and post-handgrip ischemia (P<0.005). When expressed in percent change from rest the mean peak-to-peak amplitude increased 111 (SD 100)% during mental arithmetic, 160 (SD 103)% during static handgrip exercise, and 90 (SD 67)% during post-handgrip ischemia. The study clearly indicates a facilitation of the short latency stretch reflex during increased sympathetic outflow. We note that the enhanced stretch reflex responses observed in relaxed muscles in the absence of skeletomotor activity support the idea that the sympathetic nervous system can exert a direct influence on the human muscle spindles.