Reductions in active joint range of motion (ROM) are responsible for decreased work-generating capacity during fatiguing repetitive isotonic shortening contractions. Factors responsible for impairing the joint-angle-specific net torque developed during muscle shortening could include fatigue-induced torque loss, shortening-induced torque depression in the agonist muscle, and opposing passive tension of the antagonists, but these have not been systematically explored. Nine men (aged 25.8 ± 2.0 years) performed a maximal-effort fatiguing task that consisted of repetitive loaded shortening dorsiflexions through a 40° ankle joint ROM until active ROM decreased by 50%. Torque developed during contractile shortening, as well as passive opposing tension, was quantified before and after the reduction in active ROM. Before fatigue, and compared with maximum voluntary isometric contraction torque at the terminal ROM, shortening-induced torque depression in the agonist muscle and passive tension from the antagonists reduced net torque developed at the end of contractile shortening by ∼42% and ∼19%, respectively. After fatigue, a steepened ascending joint torque–angle relationship remained during contractile shortening, but neither muscle coactivation nor contractile slowing contributed to the fatigue-induced torque loss. Fatigue-induced torque loss, shortening-induced torque depression in the agonist, and passive tension in the antagonist greatly depressed net torque developed at the end of contractile shortening. These contributed to the fatigue-induced reduction in active ROM by impairing the ability of the dorsiflexors to generate sufficient torque to overcome the imposed load at the end of contractile shortening.