How many times have you racked your head wondering; why is this not getting better? How come they’re still in pain? How do we have all of this evidence and knowledge at our disposal, yet individuals do not respond as anticipated? The science says, for injury ‘Z’ treat with ‘X’ and rehabilitate with ‘Y’, yet when we apply those tools they don’t work? Why are they not getting better? What are you doing wrong? What are they doing wrong? Continue reading
Overview and etiology:
The term “tendinitis” or any [insert any body part] with “itis” is tossed around as if it is the only possible cause for musculoskeletal pain. However, the “itis” is not really true. A tendon, specifically the Achilles tendon, is not really inflamed, rather it is deranged (tendiopathic / tendinopathy). In January 2013 the Annals of Human Genetics published an article that demonstrated Achilles Tendinopathy is associated with gene polymorphism (Abrahams, et al., 2013). COL51A is a gene that encodes the development and organization of Type V collagen. This collagen can be found in ligaments, tendons, and connective tissue. COL51A plays an integral role in development and maintenance of connective tissue. Abrahams, et al. (2013) demonstrated that polymorphisms occur in the COL51A gene causing altered structure of collagen resulting in tendinopathy.
The tendon may become fusiform or thickened, but it is due to cellular derangement rather than inflammation. Kannus and Jozsa in a controlled study of 891 patients with Achilles tendon rupture found that 97% of patients had degenerative changes in the ruptured tendon. The study also found that 34% of asymptomatic tendons also had degenerative changes (2) Continue reading
Introduction and Anatomical Overview:
Muscle is made up of two types of fibers, intrafusal and extrafusal. Extrafusal fibers are the contractile fibers and intermixed within the extrafusal fibers are intrafusal fibers. Housed within intrafusal fibers is a specific type of mechanoreceptor. Mechanoreceptors, in general, are interspersed through the entire body – hair, skin, ligaments – and are responsible for sensing tissue pressure and distortion and give our body a sense of proprioception by detecting position of our muscles, bones, and joint. There are many types of mechanoreceptors, but one specifically – the muscle spindle – lives within the intrafusal muscle fibers. The muscle spindle transmits sensory data regarding changes in muscle length, and therefore movement, to the central nervous system (CNS) via the primary afferent (sensory) neurons. The intrafusal fibers receive neural stimulation from gamma efferent (motor) neurons. Think of the gamma motor neuron as a type of sensitivity adjuster. The efferent input adjusts the length of the spindle so that it remains at an optimal length to detect changes within the muscle.
In 2010, I left clinical rehabilitation and performance training. While I love my current job, I do miss the clinical aspect, which is why I seize opportunities to take on random clients with complex issues. I’ve never written about my clients, but this case is so common, yet complex, that I thought my readers might be challenged with similar clients/athletes, or might be experiencing similar issues themselves. Here is a runner’s story that went from marathon training, to painful walking and an inability to run. Her experiences with continued failed treatment and the road we have taken to get her back to training and setting personal records. Continue reading
In July I posted a blog discussing The Overuse of Cryotherapy. The controversy surrounding the topic made it one of the most popular blogs I’ve written. What is surprising to me is that a controversy exists at all. Why, where, and when did this notion of anti-inflammation start? Ice, compression, elevation and NSAIDs are so commonplace that suggesting otherwise is laughable to most. Enter an Athletic Training Room or Physical Therapy Clinic nearly all clients are receiving some type of anti-inflammatory treatment (ice, compression, massage, NSAIDs, biophysical modalities, etc). I evaluated a client the other day and asked what are you doing currently – “Well, I am taking anti-inflammatories and icing.” Why do you want to get rid of inflammation and swelling? I ask this question for both chronic and acute injury!
Have you heard the old adage “if you don’t use it, you lose it”? Does this really happen? If so, to what degree does one “lose it”? I was riding dirt bikes since the age of three, began racing motocross at age six and ‘retired’ –moved from home and went to graduate school – around the age of 21. After 18 years of riding and racing, I know I can still swing my leg over a seat and take off and ride much better than most. But, I could not go as fast as I once could. I would not have the technique nor would I have the strength power or endurance to ride for long. What about my neural impulse and reaction – that would be nonexistent, wouldn’t it? Countless studies have demonstrated the positive correlation between practice and reaction. I haven’t practiced and with my luck, I’d hit a rock and run in to a tree. Continue reading
Vladamir Janda revolutionized human movement and rehabilitation when he described three compensatory movement patterns as a result of pattern overload and static posturing. Since Janda’s introduction we have continued to learn about hypertonic / hypotonic muscles and the delicate interplay they have on integrated functional movement. Static stretching helps correct dysfunctional movement by elongating shortened tissue. Unfortunately, the manner in which many stretches are performed does not target tissue appropriately. Continue reading
How does an ankle sprain lead to chronic knee pain, such as runner’s knee, jumper’s knee, Osteochondral defects, and/or general patellofemoral pain?
Three simple answers: Continue reading
This blog post is long overdue. I have had countless people – friends, family members, athletes, clients – all ask me about shin splints. OK, before the Athletic Trainers, Physicians, PTs and other health care providers jump down my throat. Yes, shin splints is a junk term. I am talking about MTSS. I understand this, but the people you treat know them as MTSS, so relax. What are they? How can I get rid of them? Can they be prevented? Despite being one of the most common athletic injuries, recreational or competitive, shin splints are easily treatable and very preventable. Too often sufferer’s deal with the pain and never fix the problem. My goal with this blog is to provide tips to fix the problem and resolve shin splint pain.
Shin splints, or Medial Tibial Stress Syndrome (MTSS), is a chronic injury typically described as dull-ache on the medial, mid-to-lower-third portion of the lower leg. Pain is common during or after activity. In severe cases pain may last for several hours after activity and occasionally the individual will experience nighttime throbbing in the lower leg.
The pain from MTSS is attributed to irritation of the periosteum – a saran wrap like covering around bone – or a stress reaction to the underlying bone. Repetitive pounding or muscle pulling from these structures precipitates the injury. Popular belief is that shin splints are due to poor shoes, training intensity, and training surfaces. However, a critical review article written by Moen, Tol, et al., published in 2009 Sports Medicine found this was not the case. MTSS is often caused by poor joint movement and muscle imbalance. These movement patterns and muscle imbalances are easily identifiable. The best part is that you can fix these problems at home by following a simple flexibility and strengthening program.
First, let’s see if you have these movement dysfunctions. Observe yourself (in a mirror) walking or doing repeated squats. Do you see one or more of these four things: hips in, knees in, feet flatten, or toes point out? You may have one or all of these patterns; some may be extremely pronounced or could be very subtle. The image here shows a moderate to severe movement. If you observe this, even to the slightest degree, you are at risk for developing shin splints. Overtime, these movement patterns create a muscle imbalance, where some muscles become overactive and some become underactive.
Using the above figure as an example, here are the typical overactive and underactive muscles we would see in a person with shin splints or with these movement patterns.
|Hip Flexors and Tensor Fascia Latae||Gluteal Group (Maximus, Medius)|
|Lateral calf (lateral gastrocnemius / soleus)||Medial Gastrocnemius|
|Groin muscles (anterior adductor complex)||Anterior and Posterior tibialis|
|Biceps Femoris||Medial Hamstrings|
Our goal is simple, turn-off the overactive and turn-on the underactive; simple as that. Below is a basic 3-step program that can help correct this issue, step 1 -Turn-off, step 2 – elongate, and step 3 – turn-on. This program can be done daily and would take no longer than 30 minutes from start to finish. Here is what a basic program would look like.
Step 1: Turn-off the overactive muscles using self-myofascial release
- Hip Flexors
Foam rolling is the best way to do this if you go at it alone. If you have a qualified therapist, manual release of these muscles will do the trick. When foam rolling, roll each muscle for 90 seconds and hold tender areas for 20-30 seconds. A YouTube playlist I created, provides good examples and tips on how to perform these techniques.
Step 2 – Elongate the overactive muscles with static stretching
- Gastrocnemius/Soleus Static Stretch
- TFL/IT Band Stretch
- Kneeling Hip Flexor Static Stretch
- Adductor Static Stretch
Perform 1-2 sets of the stretch per muscle group and hold the stretch for a maximum of 30 seconds. Brent Brookbush, has a good static stretching playlist that demonstrates these exercises.
Step 3 – Turn on the underactive with isolated strengthening
- Posterior Tibialis Strengthening
- Anterior Tibialis Strengthening
- Glute Medius Strengthening (Clams)
- Lateral tube walking
- Glute Maximus Strengthening (Ball Bridge)
The above exercises are just examples. There are many exercises to choose from. The important thing is to target the right muscles. Fix the core, attack the glute medius and glute maximus, and work the tibialis anterior and posterior.
In summary, too often I see individuals with shin pain ceasing activity, buying new shoes, investing hundreds of dollars in custom orthotics, or giving themselves an ice bath. Shin splints do not have to be the end of training. They are easily preventable and curable as long as you fix the problem. Following a simple and structured program to correct of common movement dysfunction patterns can eliminate shin splints and many other lower body injuries like Achilles pain, runner’s knee or hip pain.
Many years ago I got tired of watching my athletes roll in to the athletic training room and slap on ice. These athletes are in a drug-like induced state of ice addiction. Their athletic trainers keep feeding the disease, by recommending cold treatment and doing the easy – here’s ice, shut-up, leave. I felt I was doing a disservice to my athletes and asked myself, “Why are we icing this injury?” I never had an answer that was supported by evidence. So I began my own case study.
I took 9 Division I athletes (6 patellar tendinopathy, 2 bicipital tendinopathy and 1 subacromial impingement) and had the athletes cease all cryotherapy and electrical stimulation.
I have written about knee injuries so much. Every day we are bombarded with research that quite frankly, it gets boring. The problem is with approximately a quarter-million ACL injuries per year, it is safe to say the injury is rampant. The devastating nature and commonality of the injury has provided loads of information on prevention, rehabilitation and mechanisms of injury. I am not going to regurgitate them all, but do want to share some recently published articles that sports medicine experts should read.
Article 1: Negahban, Et al. A systematic review of postural control during single-leg stance in patients with untreated anterior cruciate ligament injury. Knee Surgery Sports Traumatology and Arthroscopy, May, 2013.
I love systematic lit reviews and this SLR aimed to determine postural control on those with ACL injuries. We have many internal systems and senses that help us balance. Beyond the use of our eyes and ears to sense balance, tiny mechanoreceptors and proprioceptors exist in our tissue that sense abnormal movement. This study found that when the eyes are closed individuals with ACL injuries had increased postural sway and loss of balance. This indicates that the injury and inflammation following injury inhibits our body’s internal mechanism to sense balance. When rehabilitating, be sure to emphasize proprioception exercises.
Article 2: Thomas, Abbey, et al. Lower Extremity Muscle Strength After Anterior Cruciate Ligament Injury and Reconstruction. Journal of Athletic Training published online first, 2013.
Despite advances in rehabilitation and the numerous studies published on ACL rehabilitation protocols, we appear to be failing. This study shows that at 6 months Status Post ACL reconstruction that global weakness still exists. When comparing strength output from injured vs. uninjured legs it appears the knee-extensors (quads) and knee flexors (hamstrings) are weaker at 6 months when compared to the contralateral side. Conversely hip and ankle strength was not significantly different at 6 months. The timeline to return a player back to competition and activity is 6 months following activity and/or 95% strength of the uninjured side. This study indicates 6 months might be too early. Also, we may need to adjust our strengthening protocols to further stress knee flexion / extension strength.
Article 3 – Bell, DR, Clark, MA, Padua, DA, et al., Two- and 3-Dimensional Knee Valgus Are Reduced After an Exercise Intervention in Young Adults With Demonstrable Valgus During Squatting. Journal of Athletic Training published online first, 2013.
Darin Padua and the UNC Department of Exercise and Sport Science has done a lot of work on knee displacement and correlating the findings with ankle hypomobility and hip underactivity. This particular model used the NASM Corrective Exercise Model as the intervention procedure. This method systematically turns off hyperactive tissue and activates hypotonic tissues. The data revealed that following intervention of the ankle and hip medial knee displacement was significantly reduced. This information is important as several studies have shown medial knee displacement to be a primary cause of ACL injuries and chronic knee pain.
Article 4: Ericksen, et, al. Different Modes of Feedback and Peak Vertical Ground Reaction Force During Jump Landing: A Systematic Review. Journal of Athletic Training published online first, 2013.
The inability of the body to absorb and control joint movement during high levels of ground reaction forces has been shown to increase risk of ACL injury as well as other chronic knee conditions. This study evaluated the effect of expert provided and self-analysis feedback reduced peak ground reaction forces. This is not a paramount study but does shows the effectiveness of verbal queuing and observation to correct suboptimal neuromuscular control, specifically during landing and absorption of ground reaction forces through the kinetic chain. Rehab practitioners should incorporate feedback to teach clients appropriate muscle control during ACL rehabilitation.
I would like to say thank you to Darin Padua, PhD, ATC for keeping me abreast with current data. Darin is a leader in sports medicine research and specifically has many published papers on ACL injuries. Darin manages his blog site and also shares info on his twitter account. If you are a health and wellness professional seeking important information rehabilitation and prevention of injury, I recommend you give Darin a follow.
I have been looking for something to blog. No idea surfaced that said, “Yes, that is a great blog idea.” That was until yesterday’s tragic Boston Marathon bombing. Runners are a rare breed. You cannot keep them down. A runner’s passion for sport, resilience to challenge, and unique characteristic to rise above is unparalleled by any other athlete. I am not a runner. In fact I am the antithesis of a runner. I go in to anaphylactic shock just hearing the word aerobic exercise, but have many friends who are passionate runners. I dedicate this blog to my running friends, competitors of the Boston Marathon, the friends and family of those impacted by yesterday’s events, and runners everywhere from the competitive to non-competitive. I will keep it true to my blog site and remain sports medicine focused. I hope you find the information useful.
Running is one of the most popular recreational sports in the US. Race events can be found in almost every town. My town – Champaign, IL – has 2 events in the next 4 weeks. Some estimates say 20% of the population is runners and 10% of these people participate in race events. The benefits of exercise are well documented. Running has shown to build confidence and character, reduce stress and improve mood. However, the due to their very nature – the unwillingness stop – running does bring about an increased incidence of musculoskeletal injury.
You don’t need to be an astrophysicist to know running injury is secondary to cumulative overload. Running injuries are multifactorial; neuromuscular imbalance, poor arthrokinematics and other things such as age, nutritional status and environment are to blame. From a biomechanical point of view frontal plane knee adduction moments play a significant role in lower extremity injury. Q-angle – a measure of knee alignment – can indicate risk for running injury. An increased Q-angle can be a result of many neuromusculoskeletal inefficiencies from poor muscular hip control to limited ankle dorsiflexion and excessive forefoot pronation.
Running brings about many injuries, but the most common are Patellofemoral Syndrome, Iliotibial Band Syndrome, Medial Tibial Stress Syndrome / Tibial Stress Fracture, Achilles Tendinitis, Plantar Fasciitis, and Sacroiliac Joint Pain. What is interesting is that all of these injuries can be caused by biomechanical breakdown and neuromusculoskeletal inefficiency. The good is the dysfunctional patterns are identifiable, preventable and correctable. Below is a sample 15 minute injury prevention program from a blog I wrote in Sept 2012. Yes, 15 minutes is all you need to prevent many running injuries.
Step 1: Decrease neurological drive to hypertonic tissue – 3 minutes
- Self-Myofascial Release (foam roll) or Manual Trigger Point Therapy
- Gastrocnemius/Soleus – 60 seconds
- Adductors – 60 sec
- TFL/IT-band – 60 sec
Step 2: Lengthen hypertonic muscle or joint tissue – 3 minutes
- Static stretch or joint mobilization
- Gastrocnemius/Soleus Stretch – 1 set @ 30 sec
- Kneeling Hip Flexor Stretch – 1 set @ 30 sec
- Adductor stretch – 1 set @ 30 sec
- Posterior joint mobilizations at the ankle – 90 seconds
Step 3: Increase neurological drive to hypotonic tissue – ~ 6 minutes:
- Exercise: Isolated Strengthening or positional isometrics
- Resisted Ankle Dorsiflexion – 2 sets x 15 reps (slow) (2 minutes)
- Resisted Hip Abduction and External Rotation- 2 sets x 15 reps (slow) (2 minutes)
- Resisted Hip Extension – 2 sets x 15 reps (slow) (2 minutes)
Step 4: Integrated Dynamic Functional Movement – ~ 3 minutes
- Box step-up with overhead dumbbell press – 2 sets x 15 reps (slow)
Beyond the correction of movement dysfunction there are alternatives to treat running injuries which are effective and gaining popularity. This table highlights a few.
|Prolotherapy||This has been around since the late 1800’s, but has since become popular. The basis of prolotherapy is that it expedites healing by increasing fibroblastic activity and collagen repair.|
|Autologous Blood||Blood is the medium that carries tissue repairing materials to injury sites. However, sometimes, blood cannot deliver adequate amounts of material to the injured area. Thus, injections directed right at the injury site deliver tissue repairing material.|
|PRP||Like autologous blood, Platelet Rich Plasma (PRP) is injection of a concentrated mix of tissue repairing blood components, specifically platelets, which facilitate tissue repair healing.|
|Bone Marrow Aspirate Concentrate||Despite the negative press and belief that stem cells are only derived from an unborn fetus, stem cells do come from other sources – such as bone marrow. By taking stem cells from bone marrow and injecting in to damaged areas will facilitate tissue repair.|
|ESWT||Extracorporeal Shock Wave Therapy might best be known as lithotripsy. Lithotripsy is a procedure in which sound waves blast and destroy kidney stones. ESWT is the use of sound waves to destroy calcific tendons and ligaments.|
I prefer preventing and rehabilitating injury through correcting neuromuscular inefficiencies and dysfunctional movement. The problem with the above treatments is that they are treatments. If an injury is caused by dysfunctional movement patterns and those patterns are not corrected it is likely the above treatments will simply serve as a Band-Aid because the true problem was not fixed.
If the person(s) responsible for the Boston Marathon bombing were looking to put fear in people, they chose the wrong population to target. Runners are the most stubborn and prideful athletes. No means yes, and yes means do more. If you took a graphical representation of marathon registration numbers from last night through the end of this week I would bet you’d find a spike, rather than a decline. Social media is exploding with a rise of the runner. A quote from a friends Facebook page: “If you’re trying to defeat the human spirit, marathoners are the wrong group to target” –unknown. Other movements like, wear a race shirt tomorrow, donations, and wear yellow and blue (Boston Marathon colors) have already begun. So, thank you runners for inspiring this blog post!
You have an athlete with a stress fracture. The physician prescribes active rest and places the athlete in a non-weight bearing boot. Sound familiar? Suppose I told you the better option is to place some load on that bone and non-weight bearing is not recommended. Would you think I am nuts? Maybe I can convince you otherwise. Let me explain but, before you read the next paragraph and decide to leave the page, bear with me. What follows this introductory piece may provide insight to further understanding of injury pathophysiology and could revolutionize the future of rehabilitation science.
In January 2013 the Annals of Human Genetics published an article that demonstrated Achilles Tendinopathy is associated with gene polymorphism (Abrahams, et al., 2013). I am not a geneticist by any stretch of the imagination, so pardon my basic explanation. COL51A is a gene that encodes the development and organization of Type V collagen. Type V collagen is a collagen that is distributed in tissues as a component of extracellular matrix and composed of one pro alpha 2 (V) and two pro alpha 1 (V) chains. This collagen can be found in ligaments, tendons, and connective tissue. COL51A plays an integral role in development and maintenance of connective tissue. Abrahams, et al. (2013) demonstrated that polymorphisms occur in the COL51A gene causing altered structure of collagen resulting in tendionpathy. Continue reading
I have posted on this topic many, many times. Unfortunately, many still revert to antiquated rehabiltiation protocols. Thus, I feel compelled to keep talking about it. If you or a client has knee pain focus on the hip, not the knee. There is so much data out there on linking decreased glute strength to knee pain. A weak or inhibited glute medius is unable to control femoral internal rotation and obligatory knee frontal plane motion. These motions are a primary cause in knee pain – traumatic and acute. Today I discovered two, recently-published, systematic reviews to prove my point.
The first review examined 47 studies which looked at factors causing Patellofemoral Pain Syndrome (PFPS) (1). This review identified decreased muscle strength for hip abduction and hip external rotation as an important factor associated with the cause of PFPS. The pooled data also found increased Q-angle and sulcus angle to be factors – both of which have been linked to muscle imbalance.
The second systematic review was more specific by evaluating gluteal muscle activity – via EMG – and PFPS (2). The authors identified ten studies to be included in their review, with six of these studies considered to be high-quality and eight studies having a score of 8 or higher on the Downs and Black scale. The authors conclude there is moderate to strong evidence linking delayed or short Glute medius muscle activity to PFPS. The authors also state, “If gluteal muscle activation is delayed, frontal and transverse plane hip motion control may be impaired, leading to increased stress on the PFJ and subsequent symptoms associated with PFPS.”
Rehabilitation practitioners should note this when developing rehabilitation programs. Specifically targeting glute weakness and inhibition will limit hip internal rotation and obligatory knee frontal plane motion. Correcting faulty movement patterns will allow for optimal neuromuscular recruitment and joint kinematics, ultimately relieving or preventing pain.
If you are wondering which exercises will target the glute medius look at the study published in the recent JOSPT (3) and my recent blog titled “The Glute vs TFL Muscle Battle: Proper Exercise Selection to Correct Muscle Imbalance”. The data represented in the JOSPT article demonstrate the bilateral bridge, unilateral bridge, side step, clam, squat and two quadruped exercises are best for activating the glute medius.
Are you ready to change your rehabilitation program?
- Lankhorst NE, Bierma-Zeinstra, SMA, and van Middelkoop, M. Factors associated with patellofemoral pain syndrome: a systematic review. Br J Sports Med. 2013;47:193–206.
- Barton CJ, Lack, S, Malliaras, P, and Morrissey, D. Gluteal muscle activity and patellofemoral pain syndrome: a systematic review. Br J Sports Med. 2013; 47:207–214.
- Selkowitz, DM, Beneck, GJ, and Powers CM. Which Exercises Target the Gluteal Muscles While Minimizing Activation of the Tensor Fascia Lata? Electromyographic Assessment Using Fine-Wire Electrodes. J Orthop Sports Phys Ther. 2013; 43(2):54-64.
Selkowitz, DM, Beneck, GJ, and Powers CM. Which Exercises Target the Gluteal Muscles While Minimizing Activation of the Tensor Fascia Lata? Electromyographic Assessment Using Fine-Wire Electrodes. J Orthop Sports Phys Ther. 2013; 43(2):54-64.
Overview and Introduction:
Vladamir Janda revolutionized human movement dysfunction and rehabilitation when he described three compensatory movement patterns as a result of pattern overload and static posturing. Most musculoskeletal injuries are multifactorial, but more often than Janda’s described three compensation patterns – upper crossed syndrome, lower crossed syndrome and pronation distortion syndrome – are the key contributor to our pain complaints.
Since Janda introduced this topic research has continued to answer what and why questions surrounding these compensatory patterns. We have learned hypertonic / hypotonic muscles and the delicate interplay they have on integrated functional movement. Studies continue to show how these dysfunctional patterns lead to our most common injuries – PFPS, ITBS, Achilles tendinopathy, plantar fasciitis, epicondylopathy, biceps tendinosis, impingement syndromes, MTSS, etc.
As research evolves we continue to fine-tune our clinical decision making. For several years now rehabilitation journals have published articles linking a myriad of injuries to lower-crossed syndrome, gluteal inhibition, and over-activation of the tensor fasciae latae (TFL). We have learned that these should be a focal point in our rehabilitation techniques to resolve lower extremity overuse injuries. The article by Selkowitz, et al., in the Feb 2103 edition of JOSPT is unique and what I believe to be one of the most clinically relevant studies to be published in the last few months. I liked it so much I had to blog it.
Statement of the Problem:
A common descriptor associated with lower-crossed syndrome is femoral internal rotation and hip adduction. From a rehabilitation perspective we must enhance neuromuscular firing of hip abduction and external rotation. In addition we must inhibit over activity of hip adductors and hip internal rotators.
As a health care practitioner we understand the delicate interplay of functional anatomy. The problem is how do we inhibit a chronically hypertonic TFL while activating the hypotonic gluteal group if they both produce similar movements? It is a fine balance we must be cognizant of when designing rehabilitation programs.
This study examined which exercises elicit the greatest gluteal (medius / maximus) activation while minimizing activation of the TFL. This is exactly what we need to know when designing a rehabilitation program to target lower crossed compensatory patterns.
Electromyographic data of the gluteus medius and superior gluteus maximus was collected utilizing fine-wire electrodes on 20 healthy participants during the execution of 11 exercises.
Seven of the 11 exercises -bilateral bridge, unilateral bridge, side step, clam, squat and two quadruped variations – demonstrated statistically significant greater muscle activation in the gluteus medius and gluteus maximus when compared to the TFL. Side-lying hip abduction, hip hike, the lunge, and the step-up were either not significant or demonstrated higher TFL values compared to the gluteal group.
The authors ranked the exercises in order of highest gluteal to TFL ratios. Clam, side step, and unilateral bridge had the highest ratios, while lunge, hip hike, and squat had the lowest ratios.
Clinical Application of Data:
Altered arthrokinematics and muscle imbalances are a common cause of overuse injuries. Lower-crossed syndrome is a common compensatory pattern that is associated with hypertonicity of the hip flexors complex, which elicits altered reciprocal inhibition of the gluteal group. Targeting this dysfunctional pattern using proper exercise selection indicated here can prevent injuries, improve patient outcomes, and restore optimal function. When designing your program be sure to reference the material here to determine a proper rehabilitation program.
Studies are equivocal on reliability of surface EMG vs intramuscular. However, the authors cite using the method by Delagi and Perotto, which appears reliable. Still one has to question specificity and sensitivity to a minimal degree.
The participants were instructed on proper exercise technique. However, substitutions patterns are common in patients exhibiting muscle imbalance. Any slight deviation from proper technique can skew the data. I am curious how closely exercise technique was monitored and what occurred when deviation did occur.
Like I said from the top, rarely do we have a published data with such clinical relevance. Studies that show how deep ultrasound penetrates a rats muscle are great, but clinically have little clinical utility. Data revealed here will guide decision making on proper exercise selection and ensure they are applying the proper strengthening exercise to specifically target the underactive glutes while avoiding the over active TFL. Kudos to the authors.