Quadriceps & Hamstrings Activation Failure

Arthrogenic Muscle Inhibition & Central Activation Deficit

Quadriceps & Hamstrings Activation FailureArthrogenic Muscle Inhibition (AMI) refers to an impairment caused by an ongoing reflex inhibition of the musculature surrounding a joint. Joint injury causes AMI to the surrounding musculature as a protective mechanism to the injured joint. Unfortunately, AMI may impede recovery after injury by preventing complete activation of a muscle. Quadriceps Activation Failure after knee joint reconstruction may persist for years after major joint trauma and reconstruction. A related phenomenon called central activation deficits (CAD) also occurs after total knee arthroplasties (TKA), performed to alleviate knee osteoarthritis (OA)-related pain and disability. Hamstrings dysfunction also is present and should be addressed.

The exact mechanisms causing and regulating quadriceps and hamstrings AMI after knee joint injury and CAD after surgery remain unclear. The decreasing volitional force output associated with AMI and CAD may be caused by altered afferent input originating from mechanoreceptors within the diseased joint reflexively which reduce efferent output from quadriceps alpha motor neurons. Although poorly understood, cortical pathways may also contribute to reduced alpha motoneuron excitability.

Other factors such as joint effusion, pain, and disuse may also contribute to quadriceps and hamstrings inhibition after joint injury. The effused joint may reduce the excitatory input of the surrounding muscles by activate several gating mechanisms within the central nervous system (including both pre- and post-synaptic inhibition). Joint effusion may also activate Ruffini endings, which influence muscle tone and movement, by their influence on Golgi Tendon Organ to regulate joint stiffness and stability. Interestingly, pain-free, experimental knee joint effusions with as little as 20–30 ml of saline have been shown to produce quadriceps activation failure.

Strength Training may help attenuate quadriceps and hamstrings CAD. Rehabilitation progressing to high intensity can produce greater quadriceps strength and attenuate CAD compared to lower intensity rehabilitation. Training programs require intensities of at least 30–50% of maximal voluntary effort to overload the muscle sufficiently to induce strength gains. This intensity may not be possible in muscles effected with CAD and AMI. For this reason, strength training alone does not seem to be an effective modality for Quadriceps Activation Failure particularly for those whose weakness is centrally mediated. Hurley et al reported that a 4 week strength training therapy did not improve Quadriceps Activation Failure in ACLd patients.

Other therapies aimed at removing posttraumatic AMI include:

  • Manual therapy
  • Transcutaneous electric nerve stimulation (TENS)
  • Neuromuscular electric stimulation (NMES)
  • Focal knee joint cryotherapy

Neuromuscular Electrical Stimulation

Electrical Musle Stimulation (EMS), also known as Neuromuscular electrical stimulation (NMES), may override AMI and CAD assisting in the restoration of quadriceps muscle function and restore muscle mass more effectively than voluntary exercise alone.

Early NMES treatment after TKA (before one month) may result in better quadriceps function. Rehab can begin within 48 hours after surgery and continue for several weeks. Protocols have included:

  • twice per day sessions
  • 15 repetitions per session
  • biphasic waveforms at 50 pps
  • 250 s pulse duration
  • duty cycle 15 seconds on and 45 seconds off

Less frequent NMES application after surgery or injury (2 times/week) has not been effective even with a minimum 30% treatment dose. High intensities result in greater gains in strength and hypertrophy if used for a sufficient length of time, however these higher intensities are often uncomfortable for patients. Larger electrodes have a lower current density and, thus, may decrease patient discomfort compared to smaller electrodes. Current density is also influenced by the distance between electrodes, with further distances resulting in lower densities and discomfort. .


Knee joint cryotherapy has been shown to improve quadriceps function temporarily in those with AMI, thereby providing an window of time to improve quadriceps muscle activation and strength. Applying ice to the knee joint for 20 minutes before therapeutic exercises results in greater strength gains compared either intervention alone. In this particular application, cryotherapy does not undo the damage to a joint, it only serves as a disinhibitory modality to enhance motoneuron-pool availability during controlled rehabilitation exercises. The goal of using cryotherapy is to provide a transient period after application during which the resulting enhanced quadriceps muscle function can be exploited.


Initiating therapy for Quadriceps and Hamstrings Activation Failure early after injury or surgury is safe and achieves better long term improvements in patient outcomes, rather than waiting the deficit to resolve naturally


Hart JM, Pietrosimon B, Hertel J, Ingersoll CD (2010). Quadriceps Activation Following Knee Injuries: A Systematic Review. J Athl Train. 45(1): 87–97.

Hart JM, Kuenze CM, Diduch DR, Ingersoll CD (2014). Quadriceps muscle function after rehabilitation with cryotherapy in patients with anterior cruciate ligament reconstruction. J Athl Train. 49(6):733-9.

Stevens-Lapsley JE, Balter JE, Kohrt WM, Eckhoff DG (2010). Quadriceps and Hamstrings Muscle Dysfunction after Total Knee Arthroplasty. Clin Orthop Relat Res. 468(9): 2460–2468.

Thomas AC, Stevens-Lapsley JE (2013). Importance of Attenuating Quadriceps Activation Deficits after Total Knee Arthroplasty. Exerc Sport Sci Rev. 40(2): 95–101.

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