The temporal structure, or complexity, of torque output is thought to reflect the adaptability of motor control and has important implications for system function, with high values endowing greater adaptability in response to alterations in task demand. Neuromuscular fatigue has been demonstrated to reduce torque complexity during repeated isometric knee extension contractions (Pethick et al., 2015); however, the mechanism(s) behind this fatigue-induced loss of complexity is not known. We hypothesised that caffeine, an ergogenic aid thought to act primarily through central mechanisms, would attenuate the fatigue-induced loss of torque complexity previously observed. Ten healthy participants performed, on separate days, intermittent isometric submaximal contractions at a target torque of 50% MVC, with a 60% duty factor (6 s contraction, 4 s rest), after having ingested either 6 mg.kg-1 caffeine or the same amount of placebo one hour prior to the commencement of the contractions. Torque and surface EMG signals were sampled continuously. Complexity and fractal scaling of torque were quantified by calculating approximate entropy (ApEn) and the detrended fluctuation analysis (DFA) scaling exponent, α. Global, central and peripheral fatigue were quantified using maximal voluntary contractions (MVCs) with femoral nerve stimulation. Values are means ± SEM, compared by ANOVA and t-test. Caffeine ingestion significantly increased time to task failure by 2.4 ± 0.9 mins (P = 0.019). Complexity decreased in both trials (decreased ApEn and increased DFA α, both P < 0.01), as global, central and peripheral fatigue increased (all P < 0.01). However, the rate at which complexity decreased was significantly lower following caffeine ingestion (ApEn, -0.06 ± 0.01 vs. -0.04 ± 0.01, P = 0.014), as were the rates of global (-22.1 ± 5.7 vs. -17.8 ± 4.7 N.m.min-1, P = 0.011), central (-5.7 ± 1.3 vs. -3.7 ± 1.1 %.min-1, P = 0.046) and peripheral (-8.2 ± 2.1 vs. -6.5 ± 1.6 N.m.min-1, P = 0.043) fatigue development. This slower loss of complexity and slower rate of fatigue development, in all its forms, following caffeine ingestion suggests that the mechanisms responsible for the loss of torque complexity and caffeine’s ergogenesis are intrinsically linked. However, the slowing of fatigue in all its forms does not allow the identification of a single mechanism responsible for the loss of torque complexity. Instead, the loss of torque complexity could be the expression of an integrated response to neuromuscular fatigue, including both central and peripheral components.