We were interested in whether stretching the muscle via elastic tissue recoil during partial muscle deactivation could trigger stretch-induced mechanisms that subsequently enhance the muscle's steady-state neuromechanical output. Two torque-controlled experiments were conducted to test this aim. In Experiment 1, fifteen participants performed fixed-end dorsiflexion contractions to a moderate or high-then-moderate level with torque-drop rates of 0, 10, 20, 40, or 80% MVC.s-1 from 60-40% MVC, while net ankle joint torque, tibialis anterior (TA) muscle activity level, and TA ultrasound images were recorded. The same measurements were performed in Experiment 2, which tested twelve different participants who performed fixed-end contractions to three reference levels or to a higher-then-lower level (with torque-drop amplitudes of 85-45, 85-30, and 85-15% MVC at 20% MVC.s-1). Increased fascicle shortening amplitudes (Experiment 1: 1-2 mm, p less than or equal to .049; Experiment 2: 5-10 mm, p less than .001) to initially higher joint torques and different fascicle stretch rates (0.6 to 4.3 mm.s-1, p less than or equal to .041) and amplitudes (4-9 mm; p less than or equal to .001) did not significantly affect TA's subsequent muscle activity level relative to the reference contractions at similar joint torques (0-1% MVC, p greater than or equal to .659 and p greater than or equal to .626). However, the torque steadiness relative to the reference conditions was significantly reduced after the 85-15% MVC (p = .036) and 85-30% MVC (p = .036) torque drops. Consequently, the history of force production affected the control of muscle force more than TA's steady-state neuromuscular output. These findings indicate that assessing fascicle kinematics concurrently with motor unit behavior during fixed-end contractions with large torque drops might provide unique insights into the neuromechanical contributors to impaired torque control.