1. Transcranial magnetic stimulation over the motor cortex of one hemisphere is known to decrease the excitability of the motor cortex of the other hemisphere. We investigated the effect of this interhemispheric or transcallosal inhibition of the motor cortex on the reflex response to stretch in the long flexors of the fingers in human subjects. 2. Stretch of the long finger flexors, through extension of the proximal interphalangeal joints with a torque pulse, resulted in a reflex EMG response with short- and long-latency components. Magnetic stimulation was applied over the motor cortex ipsilateral to the muscles being stretched. When a magnetic shock but not stretch was given, a decrease in background EMG in the ipsilateral finger flexors occurred at a latency of 33 +/- 6.2 ms after the stimulus and with a duration of 25 +/- 8.5 ms. 3. If the magnetic shock and the stretch were given at appropriate interstimulus intervals, the long-latency stretch reflex (LLSR) showed inhibition in all subjects. LLSR was reduced to 49.2 +/- 19% (S.D.; n = 9) of the area of the control response. 4. The LLSR did not act as a single event in response to the magnetic shock. That is, part of the LLSR could be reduced in amplitude while the remainder was unaffected. The reduction in LLSR had an onset latency of 27 +/- 3.8 ms after the magnetic stimulus and a duration of 29-55 ms. Inhibition was only obvious when this interval after the magnetic stimulus coincided with the LLSR. 5. In most subjects the short-latency stretch reflex (SLSR) also showed some inhibition (83.4 +/- 11.2% of the control). However, this was less than the effect on the LLSR in all subjects. 6. The site of stimulation, over the ipsilateral motor cortex, was specific for inhibition of the LLSR. When the coil was moved anteriorly or to the midline, inhibition was significantly decreased. 7. We suggest that the inhibition of the LLSR of the long flexors of the fingers resulted from a reduction in excitability of the motor cortex produced by an inhibitory transcallosal pathway and conclude that the LLSR in this muscle has a transcortical component.