Purpose: Fatigue contributes directly to anterior cruciate ligament (ACL) injury via promotion of high risk biomechanics. The potential for central fatigue to dominate this process, however, remains unclear. With centrally mediated movement behaviors being trainable, establishing this link seems critical for improved injury prevention. We thus determined whether fatigue-induced landing biomechanics were governed by a centrally fatiguing mechanism.
Methods: Twenty female NCAA athletes had initial contact (IC) and peak stance (PS) three-dimensional hip and knee biomechanics quantified during anticipated and unanticipated single-leg landings, before and during unilateral fatigue accumulation. To induce fatigue, subjects performed repetitive (n = 3) single-leg squats and randomly ordered landings, until squats were no longer possible. Subject-based dependent factors were calculated across prefatigue trials and for those denoting 100%, 75%, 50%, and 25% fatigue and were submitted to three-way mixed-design analyses of covariance to test for decision, fatigue time, and limb effects.
Results: Fatigue produced significant (P < 0.01) decreases in IC knee flexion angle and PS knee flexion moment and increases in PS hip internal rotation and knee abduction angles and moments, with differences maintained from 50% fatigue through to maximum. Fatigue-induced increases in PS hip internal rotation angles and PS knee abduction angles and loads were also significantly (P < 0.01) greater during unanticipated landings. Apart from PS hip moments, significant limb differences in fatigued landing biomechanics were not observed.
Conclusions: Unilateral fatigue induces a fatigue crossover to the contralateral limb during single-leg landings. Central fatigue thus seems to be a critical component of fatigue-induced sports landing strategies. Hence, targeted training of central control processes may be necessary to counter successfully the debilitative impact of fatigue on ACL injury risk.
1Division of Kinesiology, University of Michigan, Ann Arbor, MI; and 2Department of Biomedical Engineering, University of Michigan, Ann Arbor, MI
Address for correspondence: Scott G. McLean, Ph.D., Division of Kinesiology, University of Michigan, 401 Washtenaw Ave, Ann Arbor, MI, 48109; E-mail: firstname.lastname@example.org.
Submitted for publication December 2008.
Accepted for publication January 2009.