A15 Failure of Neuromuscular Control

Topic

In general, the nervous system experiences a neuromuscular control failure whenever an error occurs during the planning, execution, or correction of a sports movement. Consequently, the nervous system may fail to generate the correct sequence of muscle activations required for the movement, fail to synchronize the agonist and antagonist muscles, or fail to timely correct the movement's final trajectory via proprioceptive feedback.

The neuromuscular system's electromechanical reaction time limits the speed of the corrective response; when an unexpected impact occurs within a timeframe shorter than this reaction time, the system fails to activate stabilizing muscles in time to prevent the distractive force on the anterior cruciate ligament—the very ligament modeled elsewhere in this framework—from exceeding its ultimate strength, even in the absence of direct external contact with the joint. If the unexpected impact occurs within an even shorter timeframe, the activation of stabilizing muscles is further delayed, thereby increasing the risk of a non-contact ligament injury.

Following such a ligament injury, the joint loses some of its proprioception because the afferent signal previously transmitted by the now-injured ligament is reduced; this impairs the joint-position feedback the nervous system requires to timely correct the trajectory of future movements. A further reduction in the afferent signal from the injured joint results in even poorer feedback regarding joint position to the nervous system; this compounds the joint laxity already established by another model in this series concerning the unstable joint.

Conversely, the control response of the injured joint follows a proportional-derivative control model with an inherent time delay; this model accounts for the oscillation and instability exhibited by the injured limb during movement. An increase in this control response time delay leads to more pronounced oscillation in the injured joint, thereby compounding the mechanical instability—already modeled in the context of a torn ligament that fails to limit abnormal joint displacement.

Consequently, this model—characterized by the initial errors in planning, execution, and correction—causes the injured organism to adopt a compensatory movement strategy to avoid using the damaged joint. This generates a suboptimal biomechanical pattern that overloads another structure within the organism. This overload on the other structure creates a risk of secondary injury—similar to the risks identified in the previous models—affecting a tendon, bone, or another joint. As the compensatory biomechanical pattern becomes increasingly suboptimal, the resulting overload on the other structure intensifies, ultimately leading to a new secondary injury within the organism, thereby concluding the model.

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