Should the knees migrate past the toes when performing a squat? I posted this question on social media, and the immediate response by most was “No!”. I expected this answer from most everyone, from novice to advanced lifters. To you, I happily say, you’re wrong! The debate on proper squat mechanics will never die, but I am going to steal a line from Randy B., an athletic training, and performance enhancement peer, who answered my question: “Absolutely, [the knees] should [go past the toes]. Don’t believe urban legends or follow sports med sacred cows!” I couldn’t have said this any better! Randy is spot on. This urban legend could lead to injury. The purpose of this blog is to shed some light on the debate and provide the rationale for proper squat technique.
I’ve written several articles on the use of ice on injuries, the need for inflammation, and the intricate physiological process of tissue healing. Despite the mounds of evidence that ice is not all it is cracked up to be, there still exists a dogmatic polarization that it has magical tissue-healing properties. I often get told “Prove to me that ice does not work.” No; that is not how evidence-based practice works. You need to prove that ice does work for the reasons you use it.
Read the comments I receive, and you will recognize our ice dependency. “If I don’t ice, then what do I replace it with?” That statement screams dependency. When we take away ice, we feel that a void must be filled. It doesn’t! The treatment decision is multifactorial; the injury type, severity, tissues involved, the person, etc., all play a role in how you treat that specific injury.
A 2013 position statement made by the National Athletic Trainers’ Association on the management of ankle sprains found ice therapies had a C-level of evidence 1. Meaning little or poor evidence exists. In an interview, the author of that article said: “I wish I could say that what we found is what is really being done in a clinical setting…. Maybe our European colleagues know something we don’t…there is very little icing over there.”
The blog shows how I treated an acute ankle sprain without ice by using all of the fun little tools learned through school and further honed with clinical experiences, trial, and error. I did what I thought was best. This protocol should not be used for every ankle injury. My treatment and rehabilitation plan changed daily. Everything I did was based on my ankle needs. I did NOT use any biophysical or electromagnetic modalities. Everything I did was manual. This is not to say that I would not use other modalities, I just chose not to. My only rule? No ice. 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
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
If you read my blog before you are well aware that I am a big proponent of identifying human movement dysfunction and correcting functional imbalances to reduce chronic pain, such as knee osteoarthritis (OA), patellofemoral pain syndrome (PFPS), and low back disorders such as sacroiliac dysfunction, facet arthropathy, or generalized lumbago.
A few years ago I read about a new neuromuscular technique called AposTherapy. For those unfamiliar, AposTherapy corrects gait abnormalities by retraining muscles to adopt an optimal gait mechanics. The primary goal of AposTherapy is to correct the foot center of pressure (COP) during gait. This is done by wearing a unique, foot-worn biomechanical device. At the time, I heard good results about the use of AposTherapy, but data was too young to consider valid just yet or share-able, just yet.
Recently, when looking at functional rehabilitation techniques for chronic knee pain I came across an interesting study in the Journal of Biomechanics the evaluates the benefits of AposTherapy, to correct kinetic chain dysfunction responsible for the development of knee OA (1). The results of the study were significant. Following the intervention patients demonstrated significant reduction in knee adduction (valgus) moment (KAM). Several authors have demonstrated KAM to be a primary cause of knee OA, including Miyazaki, who noted KAM correlates with the progression of knee OA (2). In addition, patients who participated in AposTherapy demonstrated increased walking velocity, reduced pain, and improvement of functional living (1).
The foot-worn biomechanical device alters foot COP, allowing for proper kinetic chain alignment neuromuscular efficiency. Clark and Lucett, noted that dysfunction at one joint precipitates altered movement patterns, at adjacent joints, both proximally and distally (3). This is the foundation of AposTherapy. By correcting foot COP during gait, altered joint mechanics up the kinetic chain are nullified and neuromuscular efficiency is enhanced. Overtime, strength gains occur allowing for optimal gait patterns. Sharma, stressed the role of neuromuscular ineffciency, suggesting that secondary to elevated joint stress with higher impact loads and altered joint mechanics facilitate the pathogenesis of the chronic joint disease (4).
Biomechanical interventions focusing on foot COP, neuromuscular development and agility, enhance functional ability, reduce pain and increase spatiotemporal patterns of gait (1). Working knowledge of human movement dysfunction and human movement compensation patterns are prudent to health practitioners. Health practitioners should emphasize and correct human movement dysfunction when treating clients with chronic joint pain such as and certainly not limited to knee OA, PFPS, SI pain, and other low back disorders like facet arthropathy. Training to enhance neuromuscular recruitment, force-coupling, as well as the correction of altered length-tension relationships and poor joint arthrokinematics will go far in reduction of pain, prevention of chronic pain, and improved functional outcomes.
What techniques do you implement to train for optimal neuromuscular efficiency?
1. Haim, A, et al. Reduction in knee adduction moment via non-invasive biomechanical training: A longitudinal gait analysis study. J of Biomechanics. 45 (2012) 41–45.
2. Miyazaki, T., Wada, M., Kawahara, H., et al. Dynamic load at baseline can predict radiographic disease progression in medial compartment knee osteoarthritis. Annals of the Rheumatic Diseases. 2002. 61, 617–622.
3. Clark, MA, and Lucett, SC. NASM Essentrials of Corrective Exercise Training. Lippincott, WIlliams and Wilkins. 2010.
4. Sharma, L., Dunlop, D.D., Cahue, S., et al. Quadriceps strength and osteoarthritis progression in malaligned and lax knees. Annals of Internal Medicine. 2003. 138, 613–619.