Fatigue in complete spinal cord injury and implications on total delay

The use of neuromuscular electrical stimulation (NMES) to artificially restore movement in people with complete spinal cord injury (SCI) induces an accelerated process of muscle fatigue. Fatigue increases the time between the beginning of NMES and the onset of muscle force (DelayTOT ). Understanding how much muscle fatigue affects the DelayTOT in people with SCI could help in the design of closed-loop neuroprostheses that compensate for this delay, thus making the control system more stable. The aim of this study was to evaluate the impact of the extent of fatigue on DelayTOT and peak force of the lower limbs in people with complete SCI. Fifteen men-young adults with complete SCI (paraplegia and tetraplegia) and stable health-participated in the experiment. DelayTOT was defined as the time interval between the beginning of NMES application until the onset of muscle force. The electrical intensity of NMES applied was adjusted individually and consisted of the amplitude required to obtain a full extension of the knee (0°), considering the maximum electrically stimulated extension (MESE). Subsequently, 70% of the MESE was applied during the fatigue induction protocol. Significant differences were identified between the moments before and after the fatigue protocol, both for peak force (P ≤ .026) and DelayTOT (P ≤ .001). The medians and interquartile range of the DelayTOT were higher in postfatigue (199.0 ms) when compared to the moment before fatigue (146.5 ms). The medians and interquartile range of the peak force were higher in unfatigued lower limbs (0.43 kgf) when compared to the moment postfatigue (0.27 kgf). The results support the hypothesis that muscle fatigue influences the increase in DelayTOT and decrease in force production in people with SCI. For future applications, the combined evaluation of the delay and force in SCI patients provides valuable feedback for NMES paradigms. The study will provide potentially critical muscle mechanical evidence for the investigation of the evolution of atrophy.