Fatigue-Induced Adaptations in Central Control Increases the Risk of Non-Contact ACL Injury

Abstract

Dynamic sports landing execution in a combined fatigued and unanticipated state is proposed as a worst case scenario for non-contact ACL injury risk. To date, however, the extent to which this phenomenon stems from a compromise in central control remains unclear. Elucidating the link between central fatigue and ACL injury is crucial to prevention strategies that can successfully cater to the random and physically taxing nature of sports. PURPOSE: To determine the impact of fatigue on the central control of dynamic lower limb landing mechanics. METHODS: Eighteen female athletes (19.8 ± 1.2 yrs) performed anticipated (AT) and unanticipated (UT) single leg landing tasks both before and during a fatigue protocol. Jump direction was determined by random light stimuli activated prior to or during the pre landing phase of AT and UT respectively. For fatigue trials, subjects performed three single leg squats immediately followed by a randomly ordered landing, with this sequence repeated until squats were no longer possible. Subject-based initial contact (IC) and peak stance (0%-50%) lower limb joint mechanics were calculated across pre-fatigue trials, and for trials denoting 25%, 50%, 75% and 100% maximal fatigue. Data were submitted to a 3-way ANOVA to test for the main effects of and interactions between decision (AT and UT), limb (fatigued and non-fatigued) and fatigue level. RESULTS: UT promoted significant (p<0.05) increases in IC hip extension and internal rotation and knee flexion angles, maximum knee abduction and internal rotation angles and moments and maximum knee flexion moment. IC knee extension, peak knee abduction angle, and peak knee flexion and abduction moments all significantly (p<0.05) increased as fatigue progressed. Further, fatigue induced increases in peak knee abduction motions and loads were more pronounced (p<0.05) during UT compared to AT. Changes in joint mechanics due to decision and/or fatigue level conditions were similarly evident in both the fatigued and non-fatigued limb. CONCLUSIONS: Mechanical adaptations in the non-fatigued limb strongly suggest high risk movement strategies stem from fatigue induced central pathway degradation. Prevention strategies should thus target the interaction between fatigue and central (spinal and supraspinal) control within the training paradigm.