Experimental validation of a novel spine model demonstrates the large contribution of passive muscle to the flexion relaxation phenomenon.

When an individual enters a maximally flexed spine position, their largest extensor muscles become electrically inactive despite a substantial extensor moment demand being placed on the low back; this is termed flexion relaxation. Stresses within intervertebral discs, ligaments, and passive muscles are thought to support this moment thereby allowing the extensor muscles to 'turn off'. While the mechanical behaviour of the intervertebral disc and ligaments have been studied extensively, less is known regarding the moment supported by passive muscle tissue during spine flexion. Here we estimated the L4/L5 moment supported by the passive musculature during spine flexion based on experimentally derived architectural and material properties. We then tested the validity of the passive muscle prediction by determining whether the cumulative passive tissue moment (including passive muscle, intervertebral discs, and ligaments) would support the extensor moment demand-calculated with inverse dynamics-near maximum spine flexion. The model predicted that the passive tissues were able to support the entire extensor moment demand, indicating that muscle activity was not required to support the weight of the upper body, consistent with the mechanism of flexion relaxation. The model further demonstrated that despite being inactive, spine muscles still greatly contribute to flexion relaxation by passively supporting ~47% of the extensor moment demand on the spine. Finally, there was strong agreement between the predicted active muscle moments and the recorded spine muscle activity (EMG); this strong agreement persisted when the external moment was manipulated using a pulley-system. These findings provide additional confidence that the estimated passive muscle moments are reasonably accurate throughout spine flexion.
Competing Interests: Declaration of Competing Interest The authors have no conflicts of interest associated with the work presented in this manuscript.
(Copyright © 2019 Elsevier Ltd. All rights reserved.)