Jeff Cubos on Shoulder packing and Kettle bells:

http://www.jeffcubos.com/2012/04/24/bad-day-good-day-and-kettlebells-from-the-ground-up-2/

Baseball strength & conditioning from Eric Cressey:

http://www.ericcressey.com/baseball-strength-and-conditioning-extra-day-between-pitching-starts

Vern Gambetta on the explosion of exercise videos on YouTube:

http://www.elitetrack.com/blogs/details/6977/#When:00:12:11Z

As important as cueing is, do we as clinicians over do it? Craig Liebenson discusses:

http://www.craigliebenson.com/?p=2323

Charlie Weingroff’s thoughts on pistol squats:

http://charlieweingroff.com/2012/03/to-pistol-or-not-to-pistol/

Quick Summary:

The interaction between temporal factors (the amount of exposure) and neuromuscular control will determine the load characteristics to the knee – this is the biggest determinant to the development of jumper’s knee. Main movement dysfunctions that occur with poor neuromuscular control include: 1) poor knee control (dynamic valgus), 2) poor trunk and pelvis control, and 3) poor ankle and foot control. Addressing motor control issues is our best strategy to prevent and manage patellar tendinopathies.

What Factors contribute to the development of Jumpers Knee?

The key factor that causes patellar tendinopathies are repetitive stress / load characteristics placed on the patellar or quadriceps tendon. Note there are other factors, namely hormonal contributions and neovascular contributions that are beyond the scope of this article that also contribute. As a result we’ll focus on the mechanical model to explain patellar tendinopathy.

The factors that effect patellar loads are primarily related to an athlete’s technique / control[8] of their body during jumping, hopping, landing, running and changing direction during sport and the amount of exposure (temporal factors) to those loads. Note the amount of exposure and the exact biomechanical loads applied to the tendon that cause a tendinopathy is not clear. Below is a diagram that illustrates the interaction between key factors that contribute to the development of jumpers knee, primarily focusing on the stress / load characteristics that are applied to the patellar tendon:

• temporal factors,
• biomechanical factors and neuromuscular control,
• Anthropometric combined with biochemical, nutrition and hydration factors
• intrinsic factors

It is important to understand the following points related to the diagram:

• Loads can be either good or bad. An appropriate overload load will lead to a positive adaptation, while an overloaded tissue will begin to breakdown causing the onset of patellar tendinopathy.
• Reversibility above degenerative tendinopathy. Based on modifying stress / load characteristics to the patellar tendon studies have shown that the process is reversible, but NOT once degenerative tendinopathy has occurred.
• It is the interaction between Neuromuscular Control combined with Temporal Factors that primarily determines the stress / load characteristics to the patellar tendon.

Understanding Temporal Factors

This concept refers to the amount of time exposure to patellar loads. Key considerations include the following major categories:

• Game Exposure
• Practice Exposure
• Tournament Exposure

   

For each type of exposure we’re interested in the amount of time per session / per week / per month and the density of the exposure compared to rest for a given period of time.

“Exposure to Rest Ratio”

High density exposure can exceed tissue adaptation or recovery leading to the beginnings of patellar tendinopathy. A delicate balance between adaptation and breakdown exists which is determined primarily by neuromuscular control. To illustrate this important concept lets’ compare two athletes. Athlete A and B play on the same rep team and they are exposed to identical game exposure, practice exposure, and tournament exposure. Athlete B develops a tendinopathy while Athlete B does not? Why is this the case?

The most common explanation relates to neuromuscular control or movement quality. To illustrate this point let’s take a look at the following video, assuming that athlete B represents a movement pattern seen in the video.

Athlete B: Demonstrates significant dynamic valgus with poor trunk and pelvis control. This leads to increased patellar load.

In comparison here is an idea pattern

Athlete B (first video) is at a much greater risk per unit time of exposure due to their poor knee control – this is termed dynamic valgus. I’m sure you can observe the difference between athlete A and B. Therefore during all sport exposure Athlete A is more likely adapting, while Athlete B is breaking down. Athlete B will begin a viscous cycle that can only be stopped by addressing the causative factor … which is ….can you guess??

You guess it! MOVEMENT. The relationship between patellar loads and temporal and neuromuscular control is how patellar tendinopathies occur and how they are effectively treated. Understanding this relationship is absolutely critical in preventing and treating patellar tendinopathy. Whether an athlete moves forward or backwards in the tendonopathy continuum is directly related to the interaction between temporal factors and biomechanical factors which are based on motor control

Understanding Biomechanical Factors and Neuromuscular Control

As we discussed in the previous section, patellar loads are heavily influenced by the interaction between temporal factors and neuromuscular control. In this section we’ll explore neuromuscular control in more depth.

Neuromuscular control represent how we sense where we are in space and how we control our body. Based on the word itself, it is based on our nervous system (“neuro”) and muscular (“muscles”) system. Key components in this model are:

• Sensory receptors and organs:
• Muscles:
• Connective Tissue:
• Skeleton:
• Nervous System:
• Processing Centres in our brains:

   

With respect to injury prevention and injury management we’re concerned with the following key components of neuromuscular control 1) awareness, 2) mobility, 3) control, and 4) expression which if dysfunctional in any way will be displayed as a movement dysfunction[9]. The typical movement dysfunctions associated with patellar tendinopathies are listed below. Note these same movement dysfunctions can be responsible for other injuries in other parts of the body that occur because of different sport exposure. This concept is gaining a lot of interest in the research world and has been well observed in the applied world of coaching, strength and conditioning, and health care professionals. To say this more simply, many sport injuries are caused by movement dysfunctions. Which injury occurs will be based on the sport, but the same underlying movement dysfunction exists. How we move is the biggest determinant of our injury risk. I would refer interested readers to refer to our evolving Principles of Neuromuscular Control.

Motor Control, Strength and conditioning factors:

• Dynamic Valgus (inward movement of the knee)
• Overpronation (collapse of the arch of the foot)
• Poor trunk control[10, 11]
• Poor force absorption from the musculoskeletal system (ankle, knee, hip, and lumbo-pelvis complex)
• Poor concentric and elastic coupling
• Decreased Strength[4]
• fatigue

Mobility Factors

• Poor Dorsi-flexion of the ankle[2][12] (inability to bring the foot to your head)
• Decreased Quadriceps flexibility [3, 4]

Implication of Anthropometric Factors

Body Mass Index[13] and high waist-to-hip ratio has been identified as risk factors for patellar tendinopathy. High BMI is theorized to increase mechanical loads to the patellar tendon by virtual of additional weight. Fat distribution around the abdomen has additional implications to the already mentioned mechanical contribution. It has been suggested that the hormones profile which contributes to abdominal fat distribution also plays a factor in tendon health[14]. In addition elevated abdominal adipose tissue has been shown to increase free fatty acids and pro-inflammatory cytokines explaining in part the relationship of higher waist-to-hip ratios to patellar tendinopathy[14].

The factors that create an unhealthy body mass index or high waist-to-hip ratio, namely nutrition and hydration status contribute to an unhealthy patellar tendon environment. It is beyond the scope of this article to review nutrition and hydration habits for ideal body composition.

Intrinsic Factors that contribute to Patellar Tendinopathy

Intrinsic factors can’t be changed. They contribute to the development of patellar tendinopathies but to a much less degree that temporal and neuromuscular control factors. In this article we’ll make mention of them, but because they are inherent and non-modifiable we won’t provide further explanation – it’s kinda boring and technicalJ. Just remember the meat and potatoes of this condition is related to temporal and neuromuscular control factors.

Intrinsic Factors include:

• Gender
• Genes

Summary of the factors that contribute to Patellar Tendinopathy

The relationship between patellar loads and temporal and neuromuscular control is how patellar tendinopathies occur and how they are effectively treated. Understanding this relationship is absolutely critical in preventing and treating patellar tendinopathy. Whether an athlete moves forward or backwards in the tendonopathy continuum is directly related to the interaction between temporal factors and biomechanical factors which are based on motor control.

The Pathology of Jumper’s Knee?

Purdam and Cook[5] have suggested that jumper’s knee represents a continuum – meaning there are stages of jumper’s knee. They have classified three stages which are Reactive Tendinopathy, Dysrepair Tendinopathy, and Degenerative Tendinopathy – each stage has been explained in depth below and represent a pathological process that maybe irreversible
when it reaches Degenerative Tendinopathy. Note the three stages are descriptive out of convenience, rather a continuum exists between the three stages.

Patellar stress / load is the primary factor that determines whether the tendon moves forwards or backwards within the continuum – especially in the early stages[5]. Matching the appropriate strategies with the appropriate pathological stage will greatly improve treatment outcomes. We’ll explain more about the factors in the next article: Factors that contribute to the development of patellar tendinopathies.

• temporal factors,
• biomechanical factors and neuromuscular control,
• Anthropometric combined with biochemical, nutrition and hydration factors
• intrinsic factors

It all begins with Reactive Tendinopathy ….

All athletes that experience tendinopathy symptoms will begin with reactive tendinopathy. Progression to other stages is dependent primarily on the stress / load characteristics to the patellar tendon. Stress or load is a biomechanical term used to describe how much force is applied to the tendon. We’ll explain more about the stress / load characteristics when we explore factors that contribute to the development of jumper’s knee.

Happy to very aggravated Tendon

I consider reactive tendinopathy to be much like a baby? A baby because when they are happy they are the best to be around, but when they get upset – WATCH OUT. The good thing is they typically cry and become upset for a reason. Once you figure out what they need and provide them with it they quickly become happy again. But if you don’t address their needs and this goes on for months…years…

(I think you get the picture). To me this describes how our tendons respond. They are very happy to do everything we ask, but if they become aggravated WATCH-OUT. You better address the problem or big problems will result. Tendons can change from being happy to very, very upset.

So how do you know if something is going wrong?

Early symptoms include:

• Swelling
• Pain after activity in the knee

Early Detection and monitoring

It is imperative that once the condition has started careful monitoring is necessary. This is best done by a health care professional that is experienced dealing with tendinopathies – we’ll explain how to look for an ideal healthcare professional when we explain treatment options. This is case because the link between pathological changes and pain are not clearly linked. Studies have shown there are cases where there are pathological changes in the tendon that are painless. Likewise, just because there is pain it doesn’t mean there are pathological changes. Understanding which condition an athlete is experiencing is imperative to know if they can continue to play or therapy (including load modification) is necessary. Failure to properly monitor early signs can lead to unnecessary progression of the condition.

Interestingly, it appears that once the process has started tendocytes (cells that make up tendons) become sensitized. When they are sensitized they produce several substances that are responsible for the symptoms, including swelling. However, while the area looks inflamed there are typically no inflammatory cells. The swelling is caused by large proteoglycans that draw water into the cell matrix. How long these cells become sensitized is very contextual or it depends. We’ve seen cases where tendinopathies have started because of knee impact that has taken months to return to normal levels. We’ve also seen cases where the tendon has resolved in a couple of days after being sensitized during a hard weekend tournament. The most important part of this is to get checked out. Better yet begin a program to prevent the injury – we’ll explain more about prevention when we explain our injury prevention game plan.

Progression of symptoms

Sometimes an athlete ignores the early symptoms and continues to play, hoping the pain will go away. I’ve seen this happen many times. Not paying attention to tendon pain is not a good idea. Careers’ have ended because of jumper’s knee. Remember research has shown that the stress / load characteristics will determine if the condition will progress into an irreversible condition. You get to decide how you want to proceed.

The condition is already difficult enough to treat with long term residual effects, particular if left unattended.

During upcoming Posts we’ll explore:

• The Pathology of Jumper’s Knee
• What factors contribute to the development of Jumper’s Knee
• Treatment options for Jumper’s Knee
• A Game Plan to prevent Patellar Tendinopathies
• Addressing “Classic” Movement Dysfunctions
• System Stability (“THE CORE”) and Jumper’s Knee
• How does Strength relate to Tendinopathies?
• Your ankles and your feet are very important in preventing Jumper’s Knee
• System Alignment and Injury Prevention
• Dynamic Stiffness and the prevention of Sport Injuries
• Your coach can be your best ally or your worse enemy regarding sport injuries
• Does a patellar Strap work?

References

1. Cook, J., Tendinopathy: no longer a ‘one size fi ts all’ diagnosis. Br J Sports Med, 2011. 45(5): p. 385.
2. Maffulli, N., et al., Similar histopathological picture in males with Achilles and patellar tendinopathy. Med Sci Sports Exerc, 2004. 36(9): p. 1470-5.
3. Cook, J.L., et al., Prospective imaging study of asymptomatic patellar tendinopathy in elite junior basketball players. J Ultrasound Med, 2000. 19(7): p. 473-9.
4. Fredberg, U. and L. Bolvig, Significance of ultrasonographically detected asymptomatic tendinosis in the patellar and achilles tendons of elite soccer players: a longitudinal study. Am J Sports Med, 2002. 30(4): p. 488-91.
5. Cook, J.L. and C.R. Purdam, Is tendon pathology a continuum? A pathology model to explain the clinical presentation of load-induced tendinopathy. Br J Sports Med, 2009. 43(6): p. 409-16.
6. Lian, O., et al., Performance characteristics of volleyball players with patellar tendinopathy. Am J Sports Med, 2003. 31(3): p. 408-13.
7. van der Worp, H., et al., Risk factors for patellar tendinopathy in basketball and volleyball players: a cross-sectional study. Scand J Med Sci Sports, 2011.

Once again the whole weekend was fantastic and at times a little overwhelming with the amount of information presented. This ranged from dissection displays of the shoulder and elbow by fellows at the Andrews Institute to a live biomechanics analysis of the pitching motion of a young boy.

Below is a brief synopsis of my highlights, some of which will provide me with lots of blog info for the next few months, so stay tuned.

My first highlight came very early, and this was the chance to see Dr. James Andrews and Dr. Steven O’Brien perform and talk about their clinical evaluation of the shoulder.

For any therapists reading this, you will appreciate that this was like seeing Babe Ruth and Ted Williams talk about hitting a baseball. It was so helpful to me seeing how they handle the joint and perform the different tests that we use everyday when assessing a patient.

The most interesting thing to come out of this was seeing Dr O’Brien demonstrate his tests (the ones he invented) for diagnosing labral tears. This followed perfectly into his talk later in the day about the biceps-labral complex. He discussed how there are 3 factors that influence this complex and the traditional O’Brien’s test that we do isn’t specific enough to differentiate between all 3. This was completely novel for me, and thus very interesting.

I will provide more detail on this in coming weeks.

Highlight number 2 was Mike Reinold’s demonstration of manual therapy techniques for the throwers shoulder.

When I go to seminars like this, or get the chance to spend time with more experienced therapists and trainers, the thing I really want to learn is how they apply things practically. I feel comfortable enough reading literature and understanding concepts, but to see and feel manual techniques or receive coaching on exercise and movements better allows me to implement it into my practice, or better teach it to my athletes.

Mike talked about his manual therapy being structured in the same way you would structure and exercise program. He started with a trigger point release, followed that with an instrument assisted technique and finished with an ART style pin and move technique. His logic was that a structure prepares the tissue better for what you are trying to do, but is also less painful for the patient, and after all the patient is the most important person.

Mike was assisted by Nate Shaw, ATC for the Arizona Diamondbacks and someone I have had the chance to learn from personally last summer in the D-Backs clubhouse. Nate talked about being a “mutt” for therapy. He felt it was very important to not be locked into one style of manual therapy because it won’t work for every person, you need to gather as many tools as possible and implement them as you see fit. He also discussed making them your own, and modifying things as you see fit and find the best result.

I really enjoyed this demonstration because it helped me think about my Manual therapy more, and like my exercise prescription, have a plan, ALWAYS.

My third highlight was more of a pat on the back than anything else.

Bob Mangine from the University of Cinncinati talked about the use of eccentric training for both the shoulder, and other injuries.

This gave me particular satisfaction because eccentric training for the shoulder is something I have been thinking about since before last years conference. In fact I wrote a blog on it here

The talk was also helpful because it showed some different ways of training eccentrics and some suggestions on their use that I have already begun to implement. For example, we recently regressed an elite wrestler to an eccentric leg extension and hamstring curl protocol because he was having some much trouble controlling his knee even in a single leg press. 2 weeks later and he is jumping and landing with no problems.

Highlight 4 was a talk by Marcus Elliot of Peak Performance Project.

Dr Elliot has taken over the athletic development of the Seattle Mariners in the past year and he made some very interesting comments about how he goes about his role. He described how in his experience baseball players aren’t particularly strong or athletic, especially when compared to elite athletes of other sports. He also talked extensively about how he feels the current methods employed by many teams and trainers aren’t sufficient to develop performance in this population, especially when we consider the demands they place on their bodies.

I really enjoyed hearing someone else have similar thoughts to what I have been thinking, and will go into more detail on Dr Elliot’s talk and my own thoughts on athletic development of the overhead athlete in the coming weeks.

Highlight 5 was the implementation of DNS in elite baseball players.

This is a topic that is gaining more and more traction within the rehab community via the likes of Craig Liebenson, and during last years conference I found it very interesting to hear Ken Crenshaw and Nate Shaw of the diamondbacks talk about their use of the system in a performance AND rehab setting. This year Nate was back providing more insight on this technique, but we also got to learn from Adam Olsen from the St Louis Cardinals and his interpretations of DNS. Adam showed some really interesting variations of DNS such as incorporating rhythmic stabilistions into some one the positions. Once again I’ll discuss this in more detail in coming weeks.

So the above was just 5 of the things that caught my attention during the conference, it was definitely worth going again and I hope I get to attend next year.

Stay tuned in the coming weeks for more detailed synopsis of the topics mentioned above as well as others.

For more information contact: FITS Toronto 300 Campbell Ave Suite 208 Toronto, M6P3V6

Jumper’s knee or patellar tendinopathy is a common injury to the anterior portion of the knee effecting either:

• the attachment of the patellar tendon to the inferior patellar pole;
• the attachment of the quadriceps tendon to the superior patellar pole; or
• the attachment of the patellar tendon to the anterior tuberosity of the tibia

The exact area of injury has implications on symptoms, prognosis, and determining the best therapeutic modality (both short term and long term effects)[1] – i.e. cortisone shot, eccentric exercise, plasma-rich platelet injection, heavy resistance training, load modification etc.) to treat jumpers knee.

It is caused primarily due to repeated stress / load characteristics to the patellar tendon that damages the structure of the tendon. Tendinopathies occur during physical activity, primarily during running, hopping, jumping, and changes in direction.

Pain in the tendon is called a tendinopathy and represents a group of injuries that effect tendons at different anatomical locations. Tendons connect muscle to bone and are a special type of connective tissue that has various amounts of elastin for storage and utilization of elastic energy.

Common site of Tendinopathies

Tendinopathies may occur in the Achilles tendon, patellar tendon, supraspinatus Tendon, Forearm extensors (extensor carpi radialis brevis and longus), and adductor tendon. While the site of injury differs between tendinopathies the mechanism and pathology of all tendinopathies is thought to be similar[2]. This finding has huge implications for prognosis and rehab. We’ll explore the factors that contribute to the development of patellar tendinopathy in a future article, followed by rehabilitation options.

Symptoms of Jumper’s Knee

Symptoms that are common with Jumper’s Knee include the following:

• Pain when you touch the patella
• Swelling
• Pain going up and down stairs
• Pain when landing or taking off during jumping and or hopping
• Pain and difficulty when trying to perform a squat
• Pain and difficulty when trying to perform a lunge
• Feeling bumps or nodules at the site of pain
• Decreased sport performance

Symptom severity depends on the stage of the injury (we’ll discuss this in the next article) but without question jumper’s knee is very tricky to treat, treatments once they begin typically take at least 3 months, where many athletes never completely resolve jumper’s knee once started. This has to do with many factors that we’ll discuss in this series such as:

• Temporal factors – exposure to aggravating factors (jumping, hopping, running and changing directions)
• Biomechanical and poor neuromuscular control (we’ll explain this in part three)
• Poor relationship between pain and tissue sensitization
• Athletes desire to play vs. addressing the problem – hoping it will go away

Pain and Jumper’s Knee

The relationship between pain and pathology (damage to the tendon) is not exact. Research has shown there are cases where an athlete has “pathological” changes in their tendon without pain[3]. Likewise, there are athletes with pain who do not have pathological changes. The best example of this is the number of Achilles tendon ruptures nearly two thirds that have occurred seemingly without warming[4]. In these cases the tendon was degenerating without pain, until it finally ruptured. The significance of asymptomatic damage is critical. We’ll explore this concept in more depth when we explore how the condition progresses based on the work of Purdam and Cook[5] (two great Australian researchers) and our game plan to prevent patellar tendinopathies.

One common approach to evaluate the stage of patellar tendinopahy is related to when pain occurs relative activity and the impact it has on performance – see Figure 1: Stages of Tendinopathy in relation to pain and activity.

Figure 1: Stages of Tendinopathy in relation to pain and activity

Scoring the Severity of Jumper’s Knee

A great validated tool / survey used in research to evaluate the severity of jumper’s knee is called the VISA – Victorian Institute of Sport Assessment Scale. Note this tool / survey does not replace the qualified advise of a health care professional. The tool is intended to demonstrate the functional impact Jumpers Knee can have on an athlete evaluating the following qualities on a 10 point scale:

1. How many minutes can you sit pain free?
2. Do you have pain walking down stairs with a normal gait cycle?
3. Do you have pain at the knee with full active non-weight bearing
   knee extension?
4. Do you have pain when doing a full weight bearing lunge?
5. Do you have problems squatting?
6. Do you have pain during or immediately after doing 10 single leg hops?
7. Are you currently undertaking sport or other physical activity? This is a multi-stage question.

Once the survey is complete, you tally the results out of 100 – the higher the score the better. Here are some reference ranges based on the research used to validate the tool:

Note the tool must be used with the advice from a health care professional who has performed an appropriate evaluation where diagnostic imaging may have been used in forming a clinical impression.

Who can be Develop Jumper’s Knee

It is common in jumping sport athletes participating in basketball, and volleyball, but less common in athletes participating in soccer, weightlifting and alpine ski racing.

• 20% of visits to a sports injury clinic for knee pain are related to jumper’s knee or patellar tendinopathy
• 45% of Elite volleyball players experience PT[6]
  • Outside hitters and middles are at greater risk[7]
• 32% of Elite Basketball players experience PT
• 11% of Recreational basketball players experience PT
• Jumpers’s knee is more common in males than females (nearly twice as much)[7]
• Bilateral PT is less common than unilateral PT and it appears it is caused by different mechanisms

Click here for references

Hurts when you hit your spike in volleyball or serve in tennis?

Done your rotator cuff exercises a million times and still having problems?

Maybe you need to stop spreading your wings, maybe you need to stop being a gargoyle.

“Winging” is a commonly used term to describe the position of the scapula in relation to the shoulder and thoracic spine, where the inner or medial border of the scapula appears raised off the thoracic spine so that it is almost coming round to the front of the body to look like……wings.

Note the reduced visibility of the medial borders of the scapula in pictures one vs. three.

Winging occurs when you have reduced strength endurance and neuromuscular control of the primary stabilisers of the scapula (rhomboids, middle & lower trapezius, serratus anterior) and is often accompanied by over activity and preferential use of the accessory movers of the scapula (upper trapezius, levator scapulae, pec minor, anterior/middle/posterior scalenes). Many combinations of the above patterns can lead to winging, and this problem is very common when dealing with both overhead athletes (baseball, tennis, volleyball) or the everyday population dealing with postural syndromes as a result of their jobs READ SITTING!!!!!! (1)

But why is it bad to have wings?

RedBull makes it sound like an amazing thing to have.

The job of the scapula is to position the shoulder joint so that we can create optimal force vectors and keep the shoulder stable (Paine, 2012). Consider the scapula like the base of a pyramid. You want your base to sit as flat, or “flush” with the surface it’s resting on as possible in order to be as stable as possible and stop the structure from toppling over. To borrow an analogy from Mike Reinold’s online shoulder program (2), the scapulo-thoracic humeral joint is like a seal balancing a ball on its nose. Rather than the traditional golf ball-tee analogy, the shoulder complex needs dynamic stability due to its ever changing position.

If your scapula is winging, it is basically supporting the rest of the pyramid (shoulder and arm) by balancing on an edge, rather than a flat surface, and given that the stability is dynamic and very tough to control anyway, why would you want to start from a more unstable position. All this does is pass the stress up the chain into the rotator cuff leading to a cuff tear or tendonopathy or in a worse case scenario, a labral tear. An injury to the biceps-labrum complex comes about due to weak scapula stabilisers because the biceps has to take over the job of decelerating the shoulder during throwing or hitting. At this point the biceps is essentially trying to lift the labrum off the glenoid (pull the shoulder cartildge off the bone). If the cuff somehow survives, into the elbow the force will go, increasing the risk of a Ulnar collateral ligament (UCL) tear and the long and painful process of Tommy John surgery.

If you end up with either of these problems (labral tear or Ulnar collateral ligament tear) and you wish to continue playing your sport, surgery is going to be your only option.

But how to you fix winging? Particularly when dealing with an overhead jumping athlete?

The overhead jumping athlete is a unique athlete that needs high levels of vertical power to be successful. But they also need tremendous shoulder stability and force tolerance in order to avoid injury from repetitive hitting of the volleyball.

I’ve been thinking a lot lately about how I go about improving shoulder stability, and more importantly, how do I fit it into an athletic development program? At FITS our athletic development programs are designed to do just that, develop athleticism-make the athlete run faster, change direction quicker and jump higher than the opposition while also preparing their body for the rigors of their sport to ensure they don’t get hurt. But to do this takes time, and chasing a 40 inch vert is a much sexier reason to train than improving the dynamic stiffness of your shoulder, even if you’re an overhead athlete.

When you come from a therapy back ground as I do (even though I trained as an exercise physiologist first my first experience with elite sport was on the therapy side) the exercises you learn to develop scapula control include rows, shrugs, band exercises such and ER and IR but what I’ve come to realize more and more is that these aren’t enough when dealing with uninjured elite athletes. I’ve written about this before in my article about shoulder stiffness But have continued to think about it and learn both by observation and reading, what follows are some more thoughts on how I think we can be as efficient as possible in our athletic development programs to achieve the desired athleticism changes, as well as develop scapula control in the overhead jumping athlete.

The first thought I had is what about the use of gymnastic tasks to develop scapula control? Gymnasts after all, have better body control than any athlete on the planet, so why not add some of their training techniques to other sports? I’m not talking about crazy tumbles and reverse 2.5 in the pike position. But what about something like a hand stand? It forces the athlete to bear weight through their arms, which I’m a big fan of, even just to hold still there is a constant sway from gravity which is like adding perturbations or rhythmic stabilizations and it can be progressed to walking or push ups and regressed by adding a spot or using a wall. Plus, I believe it would add an element of fun to training, and I believe training has to be fun every now and then to keep the athletes on board and mentally involved.

You cant tell me this little guy doesn’t have good scapula control to do these things?

I also read recently an article from Jeff Cubos on his use of kettle bell exercises to develop not just whole body control and movement quality but scapula control in particular, another example of how we dont have to be stuck with just band exercises to improve scapulo-humeral stability. Click here to read Jeff’s article.

My second thought on an unusual, but still effective way to develop scapula control is using Olympic lifts-specifically the Snatch. I know a lot of people are probably already preparing their arguments against me right now, but hear me out.

The overhead athletes we deal with a FITS come from tennis and volleyball. Both high powered explosive sports, but volleyball in particular needs the added element of a big vertical jump to be successful, and one of the essential tools needed to develop a high vertical leap is Olympic lifting. So a while ago I was watching our elite beach volleyball athletes train and they were doing Snatch, and watching it I began to think about what a perfect exercise it was for them:

To do it well you need explosive leg power, motor coordination and timing to accelerate the bar and scapula stability to make the catch.

But more accurately, to make the catch well, you need the ability to hold a neutral spine, which you can’t do if you don’t have thoracic mobility and scapula stability, you can’t do it if you can’t hip hinge properly, and finally you have to put all one things together to make the catch overhead. So really rather than injuring the athlete, as long as you ensure they are adequately prepared to do the task, you are actually enhancing all elements of their dynamic stability, particularly their scapula control (2).

The other element of this exercise that I’ve come to really love to improve scapula stabiliser strength is the dead lift portion. While deadlifting myself recently, I found that I had trouble maintaining a neutral spine during the initial phases of the lift because I had trouble holding the bar and stopping my scapula from winging out and rounding my thoracic spine. This shocked me as I have always worked on my posterior chain strength, and thought I was quite strong in this regard…….how wrong I was. This to me is important because while we need scapula stabiliser endurance, we must (for high velocity over head sports) be able to produce and thus tolerate, an extremely high level of force.

So why wouldn’t we use the Olympic lifts? It does everything we need to improve the athlete in one exercise, rather than having to do a whole gamete of different things, making us more efficient in our training programs.

Now we have a program that might include some handstand or rings exercises as part of our dynamic warm up, Olympic lifts particularly the Snatch as our primary quality, some energetics and some trunk stability exercises to finish. This nails all of our 5 site integrity in sufficient volume and intensity, but more importantly in an acceptable time frame for the athlete and coach.

Next up, Thoracic Mobility: Stop being a hunchback.

1. Reinold.M, Escamilla.R, Wilk. K. Current Concepts in the Scientific and Clinical Rationale Behind Exercises for Glenohumeral and Scapulothoracic Musculature. Journal of orthopaedic & sports physical therapy | volume 39;2, February 2009.

2. Mike Reinold Online Shoulder Course: Clinical Examination of the Shoulder Joint Complex.

3. Wilk.K, Macrina.L, Reinold. M. NON-OPERATIVE REHABILITATION FOR TRAUMATIC AND ATRAUMATIC GLENOHUMERAL INSTABILITY. NORTH AMERICAN JOURNAL OF SPORTS PHYSICAL THERAPY. FEBRUARY 2006, VOLUME 1;1

4. Laudner.K.G, Stanek.J.M, Meister.K. Differences in Scapular Upward Rotation Between Baseball Pitchers and Position Players. The American Journal of Sports Medicine, Vol. 35, No. 12. 2007.

5. Paine. R. ASMI Injuries in Baseball Conference, Birmingham Alabama, 2012.

No program is superior to another program in all contexts. Careful consideration to the following factors will determine if a program will “optimally” work for each context / situation. Failure to appreciate these factors will lead to adoption of cookie cutter based training or worse cookie cutter INJURIES. I’ve seen a lot of this and we can do much better than that J. Let’s take our time and build sound programs that are individualized. But more importantly, let’s ensure that we always practice sound movement based training that addresses factors such as:

• Breathing and posture (yes that means how you sit at your desk…)
  
• Mobility: thoracic, hip, ankles
  
• System Stability with Neutral spine control: hip abduction, planks, side bridges,
  
• Basic movement patterns: squat, lunges, presses, pulls, carries,
  
• Basic speed patterns: hops, jumps, changes in direction, sprints and accelerations
  

Addressing these factors will get you closer to your goals, while helping you prevent injuries – particularly those suffered while sitting
J. Note, there are many activities that can work to make you more “fit”. Being physically active and adopting a health active lifestyle is the goal. Don’t think that I’m bashing boot camps or personal trainers. Many do a wonderful job. I just wanted you to consider that there is an optimal way to train for each individual given their unique goals and their circumstances – see major considerations below. Note if your goals are general there are many methods that can work.If you’re enjoying yourself and being physical active then who am I to say otherwise. Just make sure that you are moving well.

Major Considerations that will determine the success of YOUR program!!!

• Injuries – if you’re injure you must seek the assessment of a health care professional
  
• Existing Movement Qualities | motor coordination | Deficiencies | Movement awareness
  
• Training Status (Competition, off-season)
  
• Time Frame
  
• Training Readiness and Neuromuscular Development | Age Appropriateness
  
• Sport Needs Analysis
  
• Individual Needs Analysis | Competition Schedule | Personal variables – extracurricular activities | Lifestyle | etc…
  
• Training Residuals
  
• Training History
  
• Energy Supply – lack of sufficient energy supply (and substrate availability) for concurrent performance of diversified workloads. For example, performing repeat sprints followed by heavy bench press
  
• Cellular Adaptation – each pathway (i.e. mitochondrial biogenesis, myofibril protein synthesis, etc.) uses a separate pathway of biological adaptation
  
• Post-exercise recovery – “Because different physiological systems require different periods of recuperation, athletes do not get sufficient restoration.
  
• Compatibility of various workloads – this impact is related to energy supply, technical complexity +/- neuromuscular fatigue
  
• Mental Concentration
  
• Mindset
  
• Sufficiency of training stimuli for progress – Progress of high-level athletes demand intense focused workloads
  
• Rest and Recovery
  
• Biochemical and Nutrition
  

Before we get into any detail about the T-spine, what can go wrong, and how to fix it, lets define it.

The thoracic spine is the section in the middle of your spine that is primarily located between your shoulder blades. It consist of 12 bones below the 7 cervical, and the 5 lumbar and the 5 sacral vertebrae.

With technology advancing daily, (I’m writing this on my Ipad at this moment) we as therapists are encountering more and more thoracic spine problems, particularly one’s involving posture. Everyday more and more people are becoming hunchbacks. Desk jobs, long hours at the computer, laptops, smartphones, reduced exercise, all of these things are breeding a race of hunchbacks intent on world domination.

This epidemic is involved with problems including but are not limited to:

• Winging of shoulder blades
• Reduced shoulder external rotation, changing your throwing/hitting/serving mechanics leading to rotator cuff tendonopathy/tears/impingement/Labral Tears
• Neck pain/headaches
• Thoracic Outlet Syndrome (TOS)
• Rib position and difficulty breathing

Hunchbacks and winging of the shoulder blades:

The thoracic spine plays a major role in stability of the scapula (shoulder blades) which play a major role in stability of the shoulder. This will be explained more in an upcoming post "Gymnastics, Olympic Lifting and Shoulder Stability: Stop being a Gargoyle". In short, slumping (being a hunchback) leads to lengthening and inhibition of the scapula stabilizers and fascial system e.g. rhomboids, lower trapezius which allows the shoulder blades to round and tilt off the thoracic spine (Wilk, et al. 2002). Repeated time in this position reduces thoracic spine mobility, leading to the hunchback posture becoming normal.

Hunchbacks and rotator cuff tendonopathy/impingement:

A sustained hunchback posture WILL affect your ability to lift your arm above your head. Try it now, slump forward in your chair and lift your arm as high as you can. Now, sit up with perfect posture and lift your arm again, higher right? If you maintain that first position, every time you lift your arm you are rubbing the tendons of your rotator cuff against the underside of your shoulder blade. This wears on the tendon leading to irritation (tendonopathy) or even leading to a tear. Now there are many other causes of these conditions, but I can guarantee you, that when treating them, or training to prevent them from happening, if you don’t address mobility in the thoracic spine and rid yourself or your patient or athlete of their hunchback posture, you wont rid yourself of the tendonopathy or improve the function in presence of a tear (Lewis, Wright, Green, 2005).

Hunchbacks and neck pain/headaches:

This is another indirect effect of having a hunchback posture, but like the one’s mentioned above, very common and very problematic for the person suffering from it. If you are in the posture position mentioned above, and as mentioned the stabilizers of your scapula are getting longer and more inhibited every day, imagine what is happening to the muscles at the bottom of your neck that lead up to your head. They are displaying the opposite pattern, they are getting shorter and more facilitated (tighter and more active). This is known as the upper cross syndrome and was described by Professor Janda many years ago. These facilitated muscles around your neck squeeze tighter and tighter leading to neck pain, or affecting the nerves that supply your head causing headaches, or perhaps more troubling problems such as blurred vision and dizziness (Cleland, Childs, Fritz, Whitman, et al. 2007).

Thoracic outlet syndrome (TOS):

While the nerves that supply the muscles and skin/sensation to our arms originate from the cervical vertebrae (see above diagram), because of the interactive, linked nature of our musculoskeletal system the cervical vertebrae are heavily influenced by the thoracic spine. As we can see in the diagram above, the last few cervical vertebrae have nerves that supply the triceps and hands, located very close to the first few vertebrae of the thoracic spine (Norlander, Nordgren, 1998). This, coupled with the dysfunctional movements of the shoulder outlined above can also lead to nerve entrapment causing altered sensation or weakness at some point along the arm, these symptoms as often diagnosed as thoracic outlet syndrome (TOS). Thoracic spine stiffness will also affect the fascial (soft tissue) system as outlined above in “winging”, this too can lead to nerve entrapment and altered sensation or weakness in your arms.

Difficulty Breathing:

The thoracic spine has a direct relationship to the rib cage (which houses your lungs), for every rib we have (12) we have one thoracic vertebrae (12). Because these two structures are joined directly, dysfunction of one will affect the other. So if you have a stiff thoracic spine with poor mobility, your ability to expand your rib cage and position your scapula as well as take a deep breath will be limited (Shaw, 2012). As mentioned above in “winging”, your ability to position your scapula directly affects your shoulder and thus decreased thoracic mobility can lead to shoulder problems indirectly. Similar to the exercise above where you lifted your arm above your head in a slouched position, try returning to that position and trying to take a deep breath. Now try it in an upright posture……much deeper right? Imagine trying to complete an endurance of repeat power exercise such as basketball or tennis, it’s tiring enough without being unable to get maximum oxygen to your system because you cant take a deep breath. Decreased thoracic mobility also affects the your fascial (muscle & soft tissue) system in the ways mentioned under winging, which further reduces your ability to breath correctly.

More detail on breathing and its implications for the musculoskeletal system will be available in an upcoming post: “Breathing – Chances are you’re doing it wrong”

How do I fix these problems and/or stop them happening (again)?

Other than manual therapy (manipulations/adjustments, joint mobilisations or soft tissue release), there are many exercises that can be used to increase or maintain mobility within the thoracic spine.

Using these,  you will improve your thoracic spine mobility in flexion and extension. Extension is very important to allow you to retract and depress the scapula, which as we mentioned above is key to positioning of the scapula, which is key to not injuring your shoulder and also improving your velocity on your throw/serve (Shaw, 2012). It is extremely important not to forget about the small rotation component at this area of the spine. Because our bodies are 3 dimensional, we must address them in 3 dimensions, and just improving forward and backward (flexion/extension) movements of the thoracic spine will not allow full mobility, you must address rotation as well (Willems, Jull, Ng, 1999).

Below are some clips of exercises designed to improve thoracic spine mobility that you can try at home, in your local gym, or ask your therapist about the next time you see him or her.

If you are inexperienced with exercise please consult a registered healthcare professional before commencing exercise. FITS Toronto takes no responsibility for injuries sustained while trying any of the exercises contained in the clips below.

These include:

• Mobility exercises/stretches
• Strengthening exercises
• Compound exercises that target/require multiple areas of the body to work together.  

References:

• Norlander.S., Nordgren. B. Clinical symptoms related to musculoskeletal neck-shoulder pain and mobility in the cervico-thoracic spine. Scandinavian Journal of Rehabilitation Medicine 1998, 30(4):243-51

• JM Willems, GA Jull, JK-F Ng.

  An in vivo study of the primary and coupled rotations of the thoracic spine. Clinical Biomechanics Volume 11, Issue 6, September 1996, Pages 311–316

• Cleland.J, Childs.J, Fritz.J, Whitman.J, Eberhart. S. Development of a Clinical Prediction Rule for Guiding Treatment of a Subgroup of Patients With Neck Pain: Use of Thoracic Spine Manipulation, Exercise, and Patient Education. Physical Therapy January 2007 vol. 87 no. 1 9-23

• J.S. Lewis, C. Wright, A. Green Subacromial Impingement Syndrome: The Effect of Changing Posture on Shoulder Range of Movement J Orthop Sports Phys Ther Volume 35 Number 2 February 2005

• Kevin E. Wilk, Keith Meister and James R. Andrews. Current Concepts in the Rehabilitation of the Overhead Throwing Athlete. Am J Sports Med 2002 30: 136.

• Nathan Shaw, ASMI Injuries In Baseball Conference 2012.

For more information contact:

FITS TORONTO
300 Campbell Ave, Suite 208
Toronto, Ontario
M6P 3V6
416.628.4333
info@fitstoronto.com

Here’s a list of a several ideas to think about…we’ll explain more in a future blog post!

• Injuries – if you’re injure you must seek the assessment of a health care professional
  
• Existing Movement Qualities | motor coordination | Deficiencies | Movement awareness
  
• Training Status (Competition, off-season)
  
• Time Frame
  
• Training Readiness and Neuromuscular Development | Age Appropriateness
  
• Sport Needs Analysis
  
• Individual Needs Analysis | Competition Schedule | Personal variables – extracurricular activities | Lifestyle | etc…
  
• Training Residuals
  
• Training History
  
• Energy Supply – lack of sufficient energy supply (and substrate availability) for concurrent performance of diversified workloads. For example, performing repeat sprints followed by heavy bench press
  
• Cellular Adaptation – each pathway (i.e. mitochondrial biogenesis, myofibril protein synthesis, etc.) uses a separate pathway of biological adaptation
  
• Post-exercise recovery – “Because different physiological systems require different periods of recuperation, athletes do not get sufficient restoration.
  
• Compatibility of various workloads – this impact is related to energy supply, technical complexity +/- neuromuscular fatigue
  
• Mental Concentration
  
• Mindset
  
• Sufficiency of training stimuli for progress – Progress of high-level athletes demand intense focused workloads
  
• Rest and Recovery
  
• Biochemical and Nutrition
  

Without question there are many methods to skin the cat! But there are principles that must be maintained! We must build a solid foundation of movement qualities. Failure to properly develop these foundation qualities means we limit our ceiling of development.

So why do we care?

Let’s first begin by describing potentiation which is the pairing of exercises to potentiate / enhance the performance of the second exercise. Typically the second exercise is vertical jump or sprint. Typically the first exercise will be either a high velocity exercise (i.e. plyometric jump), or high load (heavy loaded back squat) to facilitate the potentiation.

Potentiation is a huge factor to enhance performance testing, particularly when millions of dollars on the line for example during combine testing (NFL, NBA, NHL, etc.) I’ve known several athletes who have catapulted into the first round, because of their combine results. This doesn’t mean that better testing results means better sport performance. It just means they were more “athletic” for the given tests. This makes them more attractive and thus selected higher – everybody loves athleticism all things being equal. So understanding how to get every last drop of performance is critical, just like tapering and nutrient and supplement timing. In fact we’ve seen athletes perform hip flexor stretches just prior to their vertical jump tests in the belief that it will enhance sport performance…more on this another time J.

Understanding how to get the best out of your body is very important! Likewise understanding how potentiation works may lead to improved long-term training methods (see blog post Periodizing Training Residuals).

So let’s take a look at the study…

Subjects: Twenty men who could back squat a minimum of 2.4 times their body mass (3.7}0.7 kg・BdM-1)

Method:
All subjects participated in three conditions: control (CT), a 50% of 1-RM trial (50POT), and a 65% of 1-RM trial (65POT). One minute prior to each condition a maximal countermovement vertical jump (CMJ) was performed. One minute later the subject performed one of three conditions: CT condition, 50POT, or 65POT followed by vertical jumps at 0.5 min, 3 min, 5 min, 10 min, and 15 min post conditioning activity. A force plate was utilized to quantify displacement, peak power output, peak force, and the rate of

force development for each CMJ.

Results: There were no significant differences (p>0.05) in any of the performance measures quantified during the CMJ trials when comparing the CT, 50POT, and 65POT treatment conditions.

Important Consideration

• Lack of eccentric Stimulus. Smilios et al[2] demonstrated a significant potentiation of CMJ with ½ back squat @ 60% 1RM. The lack of eccentric component during the ¼ squat is a possible explanation why this study failed to demonstrate a potentiated effect.
• Depth of Squat
  and Loading Stimulus- 50 – 65% of 1RM was insufficient to elicit potentiation in this study however studies @ this relative intensity demonstrated potentiation but with an eccentric component and with a full back or ½ squat
• Timing of performance test – there was a trend where athletes demonstrated potentiation (although not statistically significant) 30s post conditioning exercise. After this period there was decaying potentiation.
• Individuality – 33% and 48% of 50%1RM and 65%1RM subjects displayed potentiation effect indicating an individual response that was not explained by strength when responders and non-responders were organized according to strength levels.

Implications

• It appears heavy loads > 85% 1RM are most effective at inducing potentiating effects [3-6]– proposed to be due to:
  • Recruitment of higher threshold motor units
  • Increased motor synchronization
  • Decreased alpha-motor neuron input
  • Decreased reciprocal inhibition of antagonists

Important Background Knowledge

Explanations for Post Activation Potentiation (PAP) or Strength-Power Potentiation Complex (SPPC)

1. Increased phosphorylation of myosin light chains (specifically the regulatory light chains (R-LC) allowing for an increase in the Ca2+ sensitivity of myosin-actin interaction, potentially increasing cross-bridge cycling rate.
2. Nervous system response which increase:
   1. Motor unit synchronization
   2. Desensitization of alpha-motor neuron input
   3. Decrease reciprocal inhibition of antagonists

Factors that effect SPCC (PAP) overall effectiveness

1. Initial strength levels of the individual. The stronger the individual the greater the potentiation
   1. Time frame between exercise and performance is largely predicted by the strength of the athlete – stronger athletes demonstrating potentiation in a shorter time frame than worker athletes.
   2. Squatting >2.0x body weight exhibit the greatest degree of potentiation
2. Overall state of fatigue. The lower the fatigue the greater the degree of potentiation.
3. Training history. Those that are more highly trained exhibit greater degrees of potentiation.

1.    Crum, A.J., et al., The Acute Effects of Moderately Loaded Concentric Only Quarter Squats on Vertical Jump Performance. J Strength Cond Res, 2012.

2.    Smilios, I., et al., Short-term effects of selected exercise and load in contrast training on vertical jump performance. J Strength Cond Res, 2005. 19(1): p. 135-9.

3.    Ruben, R.M., et al., The acute effects of an ascending squat protocol on performance during horizontal plyometric jumps. J Strength Cond Res, 2010. 24(2): p. 358-69.

4.    McBride, J.M., S. Nimphius, and T.M. Erickson, The acute effects of heavy-load squats and loaded countermovement jumps on sprint performance. J Strength Cond Res, 2005. 19(4): p. 893-7.

5.    Kilduff, L.P., et al., Postactivation potentiation in professional rugby players: optimal recovery. J Strength Cond Res, 2007. 21(4): p. 1134-8.

6.    Jo, E., et al., Influence of recovery duration after a potentiating stimulus on muscular power in recreationally trained individuals. J Strength Cond Res, 2010. 24(2): p. 343-7.

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