Arthrogenic Muscle Inhibition
Arthrogenic Muscle Inhibition (AMI) occurs when an otherwise healthy muscle becomes reflexively limited due to an injury or trauma to a surrounding joint. Muscle volume loss, activation failure, and muscle weakness are all clinical signs that an athlete is dealing with AMI following ACL reconstruction. (1)
Mechanisms for Arthrogenic Muscle Inhibition
Spinal reflexive deficits have been observed in various MSK injuries such as ACLR, patellar tendinopathy, ankle sprains creating reductions in spinal-reflexive excitability in the quadriceps, fibularis, and soleus musculature (2).
Effusion models have demonstrated that spinal reflexive inhibition was present without pain or injury to the joint or muscle. The combination of altered afferent input ( effusion, pain, trauma, inflammation) creates a more powerful inhibitory effect (2).
Following ACL reconstruction the joint has gone through significant trauma, creating effusion, tissue damage, pain, and inflammation which alters the neural signaling between the joint receptors and central nervous system(CNS) All of these factors lead to reflexive inhibition which occurs in multiple manners. (1)
1. Lesser motor neuron pool excitability: fewer motor neurons available to recruit
2. Central activation failure: decreased ability to actively recruit motor neurons
Following ACLR the quadriceps
muscle undergoes changes in fiber type and expression and becomes more fatty and fibrotic. Muscle atrophy in the presence of AMI does not respond the same as a muscle with disuse atrophy would to traditional strength training. Thus, rehab programs must address
the neurophysiological causes of muscle inhibition following ACL injury in order to maximize muscle strength and hypertrophy.
Muscle Atrophy After Joint Injury
Exercise is not the sole solution to regaining muscle mass after a traumatic joint injury due to the multiple factors and events that occur to the nervous system after a joint injury.
Neurophysiological Changes: Following ACL injury, the quadriceps goes through a significant decline in muscle volume and quality. There is a change in afferent signaling, inability to excite motor neurons, and loss of neuromuscular connections significantly limit the ability to contract the muscle during exercise/rehab. Interventions to combat neurophysiological changes include: TENS, NMES, Biofeedback, Motor Learning, and Eccentric Exercise
Fiber Type Transition: Post-traumatic fiber type transition from type 1 to type 2a/x that is unresponsive to loading and continues to occur during ACL rehab. This is most likely due to neurological alterations. Interventions to combat fiber type transition include: Endurance Type Stimuli and Eccentric Exercise
Muscle Fiber Changes: changes in muscle fiber architecture occurs following ACL injury and can be improved with eccentric exercise (3)
Evidence Based Interventions
During this phase the main goals are:
1. Decrease pain, effusion, and inflammation to the injured joint
2. Improve muscle activation
3. Minimize muscle atrophy
“Open and exploit” Theory: use strategies to disinhibit (open) an inhibited motor neuron pool prior to performing exercise in order to maximize (exploit) the amount of muscle that is recruited (1)
Focal Joint Cooling: 20-30 minutes of cryotherapy around the injured joint can increase motor unit excitability and voluntary activation of the muscle
TENS: 20 minutes at 120-150 hz prior to exercise can help reduce inhibition by masking inhibitory signals to increase voluntary quadriceps muscle contraction
Eccentric Cross Exercise: Improves muscle recruitment and strength in the injured limb through bilateral motor pathways.
NMES: Circumvents inhibited motor neurons through direct stimulation of the muscle to improve muscle strength and limit atrophy. Biphasic stimulation should be used multiple times per day during the first 2 weeks after surgery. NMES + exercise helps improve muscle strength by enhancing motor unit recruitment
Blood Flow Restriction Training: Promotes systemic anabolic growth factor, enhances fast twitch muscle fiber recruitment, and decreases myostatin expression. Increases metabolic stress to the muscle without overloading the healing joint. Low load BFR training does not directly target AMI or result in neural disinhibition
Biofeedback: Improves voluntary cortical driven muscle activation. A greater conscious control of descending motor pathways can override neural inhibition at the spinal cord level and restore voluntary quadriceps muscle contraction
Sub-Acute Recovery Treatment Strategies
Eccentric Exercise: Enhances morphological and neurological characteristics of muscle function by promoting hypertrophy and neural drive to the muscle
Vibration Therapy: A single session of vibration therapy (30-60s) can produce immediate, short term improvements in quad strength, rate of torque development, voluntary activation, and corticospinal excitability after ACL injury
1) Norte G, Rush J, Sherman D. Arthrogenic Muscle Inhibition: Best Evidence, Mechanisms, and Theory for Treating the Unseen in Clinical Rehabilitation. J Sport Rehabil. 2021 Dec 9;31(6):717-735. doi: 10.1123/jsr.2021-0139. PMID: 34883466.
2) Lepley AS, Lepley LK. Mechanisms of Arthrogenic Muscle Inhibition. Journal of Sport Rehabilitation. 2022;31(6):707-716. doi:10.1123/jsr.2020-0479
3)Lepley LK, Davi SM, Burland JP, Lepley AS. Muscle Atrophy After ACL Injury: Implications for Clinical Practice. Sports Health. 2020 Nov/Dec;12(6):579-586. doi: 10.1177/1941738120944256. Epub 2020 Aug 31. PMID: 32866081; PMCID: PMC7785904.