Arthrogenic Muscle Inhibition

Our nervous system continuously integrates sensory information from multiple modalities (vision, orientation, sensory, sound, etc.) to perceive the environment. Subsequent motor actions change sensory input, and the cycle continues. When injury occurs, changes in sensory input serve to generate a negative feedback loop.

This schematic illustrates the healthy sensorimotor system and how this negative feedback loop gets generated after ACL injury.

What we manage.

We are great at managing symptoms we can measure. Swelling, pain, loss of mobility, loss of strength, atrophy, and changes in biomechanics. However, I believe we can all do better to anchor these impairments within the sensorimotor system.

What we miss.

We miss what we can't measure. And even when we stop to consider it, these impairments are not possible to manage because we can't assess them, measure impairment, or track improvements. But know they are there. Laboratory techniques have detailed deafferentation, alterations in sensory input, motor inhibition, impaired proprioception, and psychological interference with optimal motor control. Not everyone after ACL injury will have all these impairments, but most will have some.

Muscle function is dependent on sensory input.

Relieving the source of muscle inhibition is the only way to recover natural muscle function. As discussed in the previous post, the timeline of impairments through ACL rehabilitation features a large magnitude impairment in spinal-reflexive excitability.

Spinal-reflexive excitability is the percentage of muscle capacity a person can access. More specifically, the proportion of motor units that are able to be recruited. A healthy percent can access around 95% of their quadriceps muscle capacity. Just the presence of swelling in the knee lowers this to 65%.

In theory, training a muscle with fewer available motor units contributes to learned non-use of inhibited units and less variable contractility of the quadriceps. We believe this contributes to structural changes (e.g., atrophy, fiber-type changes) and functional impairments (e.g., weakness, asymmetry, slower rate of torque development) seen in the long term after ACL injury.

In the presence of inhibition, muscle contraction is weak because motor neurons are inhibited. Patient’s can’t access their full muscle capacity. What we “see” is lower force output and assume we need to strengthen the muscle. However, in the subacute stages capacity is not reduced. The muscle is not weak, it is powered down.

Say a healthy individual can access 95% of their muscle's maximum force generating capacity. This is true regardless of the raw force output (i.e., strength). As an individual losses access to that capacity, the capacity itself does not necessarily decrease. Instead, what we measure as a factor of force output does. Through this lens, inhibited muscles look no different than weak muscles. But that's a terrible assumption to make.

Weak muscles and inhibited muscles present similarly, but need different treatments.

When we ask someone less than 3 months post ACL reconstruction to do quadriceps strengthening, its like putting gas in a car with a dead battery: Fuel and horsepower are meaningless if the engine won't start.

Clinical Bottom Line

Training inhibited muscles, trains only the active motor units. Treatment needs to increase access to existing capacity, not build new capacity.