Clinical Question: what is best practice when using NMES to facilitate quad strength after knee surgery
Quadriceps inhibition (arthrogenic muscle inhibition, activation failure) is the difficulty achieving full muscle activation/contraction after knee injury or surgery
NMES combats muscle inhibition by facilitating muscle by increasing motor unit recruitment and rate coding
High intensity NMES must be implemented early and frequently post-op
NMES needs to be dosed at >= 50% MVIC
Patient autonomy- allow the patient to turn up the stim to >50%MVIC
Clinicians should re-test knee extension MVIC every visit in order to properly dose NMES
Wave Form: Symmetrical Biphasic
400ms pulse width
50-75 pulses per second or 1000hz or 2000hz
Burst modulated 50-75 burst per second
2 second ramp up
10 second contraction (12s total )
50 second rest to mitigate fatigue
Strength of contraction increases with increased frequency, but motor units also fatigue faster
The patient does not produce a volitional contraction during this phase of NMES
Large 3”x5” electrodes to cover all 4 motor points of the quads, also more comfortable due to dispersing electric current through larger surface area
1. Arhos E, Ito N, Giordano A, Nolan TP, Snyder-Mackler L, Silbernagel KG. Who’s Afraid of Electrical Stimulation? Let’s Re-Visit the Application of NMES at the Knee. J Orthop Sport Phys Ther. October 2023:1-18. doi:10.2519/jospt.2023.12028
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.
This will be a brief blog to present a piece of material that we spoke about in our most recent podcast on ankle sprains. This is an exercise progression framework for the lower extremity that was developed while I was in residency at the University of Wisconsin.
During our ankle module our instructor had the resident cohort create a gradual progression of lower extremity exercise types from the very beginning to the very end of rehab. This assignment was called “Death to Dunking.”
Essentially, we had to begin with as low level of exercises as possible and then progress incrementally to very high-level movements.
The idea with this project was to use it as a framework to help formulate a plan of care for someone presenting with a lower extremity injury. Understanding control vs. chaos, planes of motion, and points of contact and how they apply to exercise progression/regression is a necessity when creating a comprehensive rehabilitation program. This framework should help you do that.
Again, understand that this is by no means comprehensive and could be further divided up and/or added to, however, we hope that this can be a helpful resource for your lower extremity programming.
Thanks for reading!
The purpose of this post is to provide an overview of the countermovement jump (CMJ) and how it relates to testing readiness to return to sport after ACLR.
Here are the things we will cover…
What is the CMJ?
The Countermovement Jump is depicted in the image above. Essentially, the athlete will start standing and then attempt to jump as high as they can. The movement requires the ability to control deceleration as your center of mass drops and then explode concentrically into the air and then control/absorb the landing forces. This can be done on both legs or on one leg. The movement gives an idea of limb to limb contributions to acceleration, deceleration, and landing velocity.
In an ideal environment, a force plate will be used to measure the performance of this movement. The force plate allows a deeper insight into the athlete’s strategy to absorb and produce force. Measuring conventional output variables (ie. jump height or distance) does not reveal anything about movement strategy and can lead to premature return to sport. See below for the output variables to look at with the DL- and SL-CMJ.
Double Leg CMJ (DL-CMJ) vs. Single Leg CMJ (SL-CMJ)
There are two types of CMJ’s: the DL-CMJ and the SL-CMJ. Each test can be valuable, but they do measure different things. The (DL-CMJ) is just as it sounds: jumping off two feet while the SL-CMJ requires jumping off one leg. There are pro’s and con’s to each of these movements. We will go over the DL-CMJ first.
How does the CMJ inform RTS?
The CMJ provides an assessment of the involved limb’s ability and strategy to accelerate, decelerate, and land at a high velocity. It is important to be aware of the different variables that you may monitor when deciding if an athlete’s training program can be progressed or concluded.
You have to look beyond common variables (ie. Jump Height) when utilizing the CMJ. Those variables give you an idea of output, but not the strategy in which the athlete is using. Paying attention to the eccentric and landing phase of the DL-CMJ will give you a better understanding of willingness to load the involved limb.
You can also assess the speed in which the eccentric/concentric phases are performed hoping to see faster movements as the patient improves. This is harder to measure without a force plate, however, it is important to look at if able to. There is a misleading outcome that is related to speed of descent. If someone is performing the CMJ well, but is unable to descend quickly, you will not have insight into their ability to stop at a high rate of velocity (An example analogy by the Sports Scientist Drew Cooper: testing the brakes on a car going 5 mph vs. 70 mph). Sports occur quickly, therefore, you need to get an idea of how the athlete performs at similar speeds.
Positive adaptation to training would be a greater CMJ height and shorter eccentric/concentric phases. Essentially, you want the movements to be faster and you want the athlete to be able to control deceleration in both the eccentric and landing phases. If these are improving, you can be confident that the athlete is positively adapting to their program.
[Don’t completely rule out jump height measurement with the SL-CMJ as that will provide insight into the involved limb’s capacity to produce force, but you do have to be aware of intralimb compensations.]
How do we measure this without a force plate?
Having a force plate in the clinic is a luxury. If you don’t have one, there is a cheaper option in the form of the My Jump 2 app, which only costs $13.99.
The My Jump 2 app allows you to perform various vertical and horizontal jump tests, force-velocity profile, asymmetries between limbs, and repeated jumps. It is a valid and reliable tool for assessing countermovement jump height and provides detailed metrics such as Flight Time (ms), Velocity (m/s), Force (N), and Power (W) to give insight to the athlete’s physical profile. These metrics can be tracked over the course of rehab in order to determine how well the athlete is adapting to their reconditioning program. Their performance can be compared to age, sport, and position normative standards to help determine whether the athlete is prepared to return to training or competition.
The DL- and SL-CMJ can be used to inform progression and return to sport when understood properly. Both of these provide insight into different performance indicators regarding the involved and uninvolved LE.
If you read this whole way, I hope you picked up something useful for your clinical practice and athletes looking to return to sport safely.
Shoulder special tests are currently a hot topic of debate in the PT world. They are a staple in PT school, residency, and even fellowship education, but over the past several years there have been more and more people questioning how special they actually are.
We understand that there are many causes of shoulder pain and we are becoming aware that special tests are not specific enough to determine the painful tissue. There have been studies now that even refute MRI as the “Gold Standard”. 123 people with unilateral shoulder pain underwent bilateral shoulder MRI and found there were as many abnormalities in the symptomatic shoulder as there were in the pain-free shoulder(1). This makes it difficult to show that abnormalities on imaging can explain the true source of pain.
I have put a much greater emphasis on the subjective portion of my evaluation as I have gained more experience and have gotten better at pattern recognition. Listening to the patient's symptoms and history results in gaining a lot of great information, which should lead you to several hypothesis prior to even starting the objective exam. One thing that I have learned through residency and fellowship education is that your job is to either rule in or rule out your hypothesis during the objective exam so that you are not performing every test under the sun and have more questions than answers when you are done.
Understanding the patient's symptoms in regards to severity and irritability plays a big factor in how aggressive I am with my exam and what special tests/provocation tests that I actually perform. If an athlete comes in with a hot/painful shoulder, anything that I have them do will most likely re-create their pain. I view special testing as more of a test-retest/asterisk sign over the course of treatment. For example, if an athlete comes in with the MD diagnosis of “shoulder impingement” and they have pain with overhead and across-body motions, I will use a Hawkins-Kennedy or Neers impingement sign as their asterisk to help determine the effectiveness of my treatment. Once they have a negative exam on the table, it helps give me a better understanding of how hard we can push the athlete with their training, as well as take off any restrictions they might have had in the weight room or practice.
1. Salamh P, Lewis J. It Is Time to Put Special Tests for Rotator Cuff–Related Shoulder Pain out to Pasture. J Orthop Sports Phys Ther. 2020;50(5):222-225. doi:10.2519/jospt.2020.0606
The purpose of this post is to provide an overview of the evidence in regards to Achilles Tendinopathy (AT). This is by no means an all encompassing post about every minute detail that is AT, however, it is an attempt to provide an accompanying summary to our previous podcast on the topic (Found Here)
Here are the things we will cover…
The Anatomy and Physiology of the Achilles Tendon
The Healthy Tendon
The Achilles’ tendon is the thickest and strongest tendon in the body. It is able to withstand repetitive loads up to 12x body weight with activities such as running and jumping.1
It spans 3 different joints and produces knee flexion, tibiotalar flexion, and subtalar inversion.
The tendon is unique in that it doesn’t have a synovial sheath as other tendons do. It is instead surrounded by a paratenon sheath (a flexible connective tendon that allows tendon gliding).1 It is innervated by nearby nerves that stem from the Sural N.1
As far as vascularity goes, there isn’t much within the tendon. However, the paratenon is highly vascular. Interestingly, one of the more hypovascular portions of the tendon is at the mid-portion, which makes sense based on the location of mid-portion AT.1
The Injured Tendon
Initially, when a tendon is injured, it will begin a healing process in which various inflammatory mediators will influx into the area and Type III Collagen will be laid down quickly as a “patch.” This leads to a weaker tendon initially due to the unorganized orientation of the Type III Collagen. An effective healing process will eventually lead to the Type III collagen being replaced by Type I collagen restoring the tendon’s original function.
When the tendon is in a “state of disrepair” due to various factors (one being lack of adequate recovery) you won’t see a gradual transition from type III to type I collagen. Instead, there will be an accumulation of type III collagen along with neovascularization and neoinnervation resulting in a weaker and more painful tendon.2 It is now understood that chronic tendinopathy is a result of failed healing as opposed to an inflammatory condition. This process results in degeneration of the tendon and the aforementioned neural ingrowth and neovascularization. This “failed healing process” creates a vicious cycle in regards to tendon strength, pain, and tolerance to activity.3
What Type Of Achilles Tendinopathy Are We Dealing With?
There are generally two types of AT. One being Mid-portion AT and one being Insertional AT.
Mid-portion : Occurring 2-6 cm proximal to the insertion at the calcaneus.4,5
Insertional: Occurring within 2 cm of the Calcaneus-Achilles junction. 4,5
Mid-portion AT is going to be seen in the more active population while Insertional AT is seen more in the less active, overweight population.
Mid-portion AT is a result of repetitive loading with inadequate healing or recovery. Insertional AT is more of a compression issue at the tendon insertion in which the the posterior edge of the calcaneus impinges against the AT and surrounding structures including the bursa and paratenon. (This difference in physiology of the injury leads to one of the big differences in the management of these two forms of AT.)4
How Common Is Achilles Tendinopathy and Who Is At Risk?
You will typically see AT with athletes in sports that require repetitive loading of the gastroc/soleus/achilles complex. Those whose sports require repetitive running and jumping are more at risk. In general, it has been shown that LE Tendinopathy (includes all tendinopathies) has an occurs at a rate of 10.52 per 1000 persons per year, which exceeds OA.6
There are many risk factors (RF) that may predispose someone to experiencing AT. Below are a list of extrinsic and intrinsic factors. This is by no means an exhaustive list and you will find varying lists depending on what you are reading in the literature.8
Extrinsic (factors that are external to the body that may increase load on the tendon)8
Intrinsic (internal factors that may increase loading or impair healing of the tendon)8
Evaluation (History and Exam)
I won’t get into our standard process of taking a history, but instead will focus on aspects specifically related to AT.
The main goal is to get an insight into activity level changes particularly in an athletic population. Due to training errors being a very common and modifiable risk factor, it is important to understand the patient’s activity history. Keep in mind that a change in activity/training can be a result of one factor such as increasing mileage abruptly in the case of a long distance runner OR it can be due to a combination of factors that may present in a biopsychosocial perspective (ie. Lack of sleep + stress + change in training).
Beyond that, we need to know what the patient is attempting to return to, how fast, and at what intensity. Your management may change if you are working with an in-season athlete vs. someone in their offseason vs. someone without a particular time frame for return (ie. The weekend warrior).
The earlier you can see these patients the better (as is typical with most injuries). Initial symptoms might appear as soreness/stiffness at the beginning of an activity that then undergoes a “warm-up” phenomenon in which the pain resides as the activity progresses. Eventually, you may start to see pain in the morning that worsens as the day goes on, stiffness, swelling, crepitus, pain with palpation, and possibly hypertrophy of the tendon.1
“On the table testing” includes special tests, palpation, and ROM/strength testing.
As with most pathologies, there are a ton of special tests out there. Unfortunately, these tests haven’t been proven to be very helpful. However, according to the Revision of the Clinical Practice Guidelines for Achilles Pain, Stiffness, and Muscle Deficits for Mid-portion AT, the Royal London Hospital Test and the Arc Sign can be useful.6
Having said that, we mainly rely on symptom report and location of pain. Assessing strength and ROM will help in regards to treatment strategy.
“Off the table testing” consists of functional testing including single leg calf raises, hopping (both double leg and single leg), and visualization of the painful activity if able including walking, stair descent, jumping, or running.
Because it is important to rule out, before ruling in keeping in mind possible differential diagnoses can be helpful.
Treatment: Comparing Heavy Slow Resistance vs. Eccentrics vs. Isometrics
Eccentrics have been the mainstream treatment for AT. The most widely used protocol initially described by Alfredson et al. is listed below.7 The mechanism behind improvements noted with eccentric training is not quite clear. It has been proposed that eccentrics can create structural adaptations at the tendon, improve tendon length, reduce neuro-vascular ingrowth, create neuro-chemical and neuro-muscular alterations, and alter fluid dynamics.11
Now, not all of these proposed changes have been clearly supported in the literature. For example, tendon changes related to a reversal of the degenerative process is not needed for and does not guarantee success or failure of treatment. However, knowing and learning about the possible results of eccentric exercises may help your understanding as well as your patient’s understanding of the purpose of this treatment protocol.11
Alfredson’s Potocol for Eccentric Exercises with AT3,7
Exercises: Unilateral heel raise off a step with a straight knee and a bent knee.
Frequency: 2x/day; 7 days/week
Volume: 3x15 each exercises
Tempo: 3 second eccentric
Rest: 2 min b/w sets; 5 min b/w exercises
Tendon Load Time: 63 min/week
Total Time Commitment: 308 min/week
Note: Load is increased gradually using a backpack as the patient tolerates.
Heavy Slow Resistance (HSR)3
HSR is another treatment option for AT. Essentially, you are loading up exercises that address the gastroc/soleus complex. These exercises are performed at a tempo of 3030 (3 seconds down, 3 seconds up) for a total of 6 seconds per repetition. The protocol used by Beyer et al in their article comparing HSR vs Eccentrics is listed below.
In this study, it was determined that both HSR and eccentric cohorts achieved positive results in both the short- and long-term.3 They also noted a reduction in A-P thickness and neovascularization that was associated with clinical improvements. So, HSR is not more effective than eccentrics, however, it does provide another treatment option that is of similar efficacy.
Exercises: seated heel raise, standing heel raise deficit, straight leg calf raise on leg press.
Volume: 3-4 sets; 3x15 —> 3x12 —> 4x10 —> 4x8 —> 4x6 (progressed over a period of 12 weeks)
Rest: 2-3 min b/w sets; 5 min b/w exercises
Tendon Load Time: 41 min/week
Total Time Commitment: 107 min/week
Note: The repetitions noted above are intended to be maximal. For example, 3x15 refers to 3x15 RM. Load was increased and repetitions were decreased as tolerated over a 12 week period.
Isometrics are another possible treatment for AT. Previous studies have shown isometrics to be beneficial in those with patellar tendinopathy.9 That protocol included 5 sets of 45s isometrics at 70% MVC. However, in AT, isometrics did not change pain or increase motor output of the plantarflexors. There isn’t clear indication of why it is beneficial in patellar tendinopathy and not AT, however, the difference may lie in the fact that they are two distinctly different tendons in that the patellar tendon essentially has a sesamoid bone in the middle of it.9
Despite isometrics not being the most effective treatment for AT, we believe that it could still be useful in a graded exposure sense. If a patient is unable to tolerate isotonics, isometrics could be used to initiate loading in non-painful ranges. The intent would be to improve the tolerance of the tendon to loading and then eventually progress to HSR or eccentrics.
We now know that there are multiple ways to attack achilles tendinopathy. It is clear, at this point, that eccentrics or HSR are the gold-standard and should be utilized during treatment. It is really up to the patient and therapist as to which strategy you use. They both promote similar results. However, there a couple things that you may want to think about when adding these to a patient’s program.
(Other treatment strategies include dry needling and BFR. These won’t be covered here, but you can hear our thoughts about them in Ep. 1 of the podcast.)
(The interventions above focus on mid-portion AT. To apply them to Insertional AT you would decrease the ROM in that you won’t go into a deficit with heel raises to prevent impingement of the tendon on the calcaneus.)
Return To Sport After Achilles Tendinopathy
The final stage of rehab and likely the most important when it comes to active individuals and athletes is Return to Sport.
In order to properly progress a patient back to their goal activity, it is imperative to understand the demands of the sport including cumulative loads, peak loads, and rate of loading. This will vary based on the activity, but, in general, running and jumping activities will demand the highest load tolerance.
For example, in the sense of a runner, you can control loads based off distance, steps taken recorded via a smart watch, or based off time on feet. Beginning with a tolerable activity such as level ground walking or a walk/run program. Then progressing to higher load activities including hill running and speed work.
There are multiple papers out there that provide return to sport methodology. One that we really like is a clinical commentary by Silbernagel and Crossley.10 They provide a very structured approach detailing progression based on pain, RPE, and level of activity (light, medium, hard). It also provides sample programs for inspiration.
Hopefully you were able to pick up something from this write-up, that is, if you got this far. We do not pretend to be experts in any topic, but we enjoy putting our ideas on paper for our own sanity and, possibly, for your benefit.
References are below. Feel free to reach out with any questions or comments and if you aren’t sick of achilles tendinopathy at this point check out Episode 1 of the Athletes First Performance podcast.