1. The effects of the Ca2+ antagonist gallopamil (D600) upon force development in short skeletal muscle fibres (m. lumbricalis digiti IV) of the frog were investigated under voltage-clamp control, using two flexible internal micro-electrodes (temperature = 6-7 degrees C). 2. In the presence of 5-100 microM-gallopamil muscle fibres developed one normal phasic contracture when they were depolarized from a holding potential of -90 to 0 mV. Subsequent depolarizations caused no mechanical response (paralysis). However, the ability to contract could be restored by hyperpolarizing the membrane to potentials between -120 and -150 mV. 3. In the absence of gallopamil, mechanical refractoriness could be fully reversed within 5-7 s by repolarizing the fibre from 0 to -120 mV. In the presence of 100 microM-gallopamil, no detectable restoration occurred within the first minute at -120 mV, and 45 to 100% of maximum force was eventually reached after 6 min of restoration. 4. The potential V at which the 'steady state' 50% of maximum force of a refractory fibre was restored shifted from -51 mV under normal conditions to -83 and -90 mV in the presence of 5 and 100 microM-gallopamil, respectively. 5. Paralysis in the presence of gallopamil and recovery from paralysis during hyperpolarization could also be observed when 2 mM-Cd2+ was applied to the external solution, i.e. when most Ca2+ channels in the T-tubular system were blocked. 6. Gallopamil shifted the threshold for activation of force to more negative potentials. Fibres developed force when they were depolarized to membrane potentials between -60 and -80 mV, whereby a fast phase of activation was followed by a slower one. Upon repolarization relaxation likewise occurred in a fast and a slow phase. 7. High concentrations of gallopamil (greater than 500 microM) caused a slowly developing contracture, independent of membrane potential (-90 or 0 mV). 8. It is proposed that gallopamil binds to a receptor at the force-controlling system in the T-tubular membrane (potential sensor) with a high affinity in the depolarized state and a lower affinity at negative potentials. Therefore association of gallopamil mainly leads to stabilization of the inactive state (paralysis) but can also stabilize the active state.