Managing patella tendinopathy in powerlifting Pt.1 - Understanding Tendinopathy

Posted on 29th Jun 2019
by Josh Chuah

Tagged as: powerlifting, tendinopathy, patella, knee





Imagine having over 90% of your 1 rep max squat on your back – In that particular moment, the focus should really be on cues aiming to maximize efficiency, positioning and force production. Instead, you’re worrying about what your knee would feel like when you hit the bottom of your squat and you’re anxiously waiting for the pain to come on – it’s not a very nice experience, and definitely not ideal especially when working with higher percentages.

 

Tendinopathy can be one of the most frustrating injuries to deal with – As someone who has previously dealt with both hamstring and patella tendinopathy, I can attest to the huge toll it takes on one’s physical and mental well-being. The constant battle between not wanting to lose strength and the need to properly rehab the issue usually leaves the athlete feeling drained and unmotivated. If that sounds familiar to you, the next 2 posts may be helpful.

 

Understanding tendons, tendinopathy, what it is and why it happens is essential to the rehabilitation process. I’ll aim to keep this whole post fairly simple and basic; However, if that doesn’t interest you, feel free to wait for the second post with practical recommendations of how to effectively manage tendinopathy in training.

 

Tendons - What are they? What do they do?

Tendons are made up of fibrous connective tissues (A.K.A collagen) that attach muscle to bone. (e.g. Patella tendon, Achilles tendon) They are designed to tolerate considerable amount of loads and function to transfer tensile loads between the muscle and bone which it inserts into, in order to produce movement.

Due to a tendon’s elastic property, it provides a mechanism to store and release energy (stretch-shortening-cycle) during activities such as hopping, running, and bouncing out of a deep squat. This particular mechanism has been shown to serve a protective role for the muscle it attaches to, sparing the muscle from large tensile forces whilst prolonging the muscle’s ability to maintain optimal length tension relationships. At the same time, muscles act as a buffer to the tendon, meaning that the better your muscles are at handling load, less stress will be placed on the tendon. (1) Simply put, stronger muscle = happier tendon.

 

Understanding tendon response to load

 

The above is a schematic representation of collagen synthesis and degradation following mechanical loading of normal tendon tissue (e.g. squatting, sprinting, jumping).(2)

  • The green line represents an acute increase in both collagen expression and collagen protein synthesis that peaks around 24 hours post exercise and remains elevated up to 70-80 hours

 

  • The dark purple line represents the degradation of collagen that is occurring simultaneously. The degradation of collagen is said to occur earlier on and to a greater extent compared to collagen synthesis. Note: This is a normal tendon response to loading

 

  • The light purple line represents the net balance of both collagen protein synthesis and collagen degradation. There is a negative net balance in collagen levels (catabolic) up to 18-36 hours after exercise, whereas the balance is positive after that for up to 72 hours (anabolic).

 

Understanding the tendon’s response to load is critical, as tendinopathy can potentially arise as a result of an imbalance between collagen matrix synthesis and breakdown.

Tendons require enough time between loading to allow for positive adaptation to occur (>36 hours). Spending too much time in a negative net balance (degradation>synthesis) as a consequence of insufficient rest, continual high periods of loading especially consecutive days may leave the tendon vulnerable to injury. (2) Practical implications of timing your rehab protocols according to the tendon’s response to loading will be covered in the next post.

 

Note: There are groups of people that are at a higher risk of developing tendinopathy than others, a variety of other factors exist that can contribute to the development of tendinopathy but I’ll leave that for a future post. My point is, some people are more vulnerable than others and not everyone will develop tendinopathy.

Furthermore, the relationship between tendon pathology and pain is complex and unclear. Tendon pain can occur in people without actual structural tendon changes, and people with structural tendon changes do not always have tendon pain. Research do suggest that the presence of tendon pathology via imaging is a risk factor of developing tendon pain.(3)

 

Tendinopathy

So what exactly is tendinopathy? Dr. Jill Cook, a leading researcher in this field, describes tendinopathy as “an overuse tendon injury in the upper or lower limb that can result in pain, decreased exercise tolerance of the tendon and a reduction in function. Structurally, the tendon is less capable of sustaining repeated tensile load”. (4) It is worth mentioning that the role of inflammation in tendinopathy is debated, more high-quality research is required to better understand inflammation’s role in tendinopathy. (5) However, if it interests you and you would like to read more in-depth into whether or not inflammation is a key driver of tendinopathy, the article is linked below in the reference list.

 

Development of tendinopathy and the Acute : Chronic Workload Ratio

If you’ve managed to get this far into the post, you would notice how many times the word “load” has been mentioned. Development of tendinopathy is almost always caused by too much OR too little load. As mentioned above, keep in mind that there are many contributing factors that can play a role in the development.

 

So how do we figure out what is too much or too little load? How do we decrease the risk of developing tendinopathy? The “Acute : chronic workload ratio” is probably the closest thing we have at this stage that can answer that question.

 

The “Acute : chronic workload ratio” proposed by Dr.Tim Gabbett is a great method used to monitor an athletes training load history and current training load. (6) Although this research has not been done exclusively on tendinopathy or barbell sport athletes, the information is still applicable, valuable and easily adaptable to the condition.

 

External load (Acute and chronic workload)

  • Acute workload is typically calculated as the total training load in the past 7 days. This is a representation of current workload demands/fatigue.
  • Chronic workload is typically calculated as the average weekly training load in the past 4 weeks. This is a representation of how physiologically prepared you are/fitness.
  • The acute:chronic workload ratio is then calculated by dividing the acute workload (fatigue) by the chronic workload (preparedness/fitness)

 

Using squats as an example

o   Acute workload – 8,640 total volume (x2 squat sessions in the past week - For simplicity sakes, lets just say the sessions consisted of 180kg for 4x6 per session)

o   Chronic workload – 7,350 average total volume in the last 4 weeks

o   Acute:chronic workload ratio – 8,640/7,350 = 1.17 (optimal)

 

Internal load (Individual’s physiological response to external load combined with psychosocial factors)

In addition to external training load, it is important to consider an individual’s response to the training stimulus - As an identical training stimulus can produce a vastly different internal load in 2 athletes, which plays a big role in injury risk.

For example, an 80kg well-trained athlete with a 1RM squat of 200kg squatting 140kg for 3x10 vs an 80kg not so well-trained athlete with a 1RM of 170kg squatting 140kg for 3x10 after 2 weeks off training. I’m sure you could guess which athlete would be the one struggling.

Rate of perceived exertion (RPE) should be quite a familiar tool for most powerlifters to track how hard each set and each session was, and it should go hand in hand with tracking external load. If you’re not familiar with how to apply RPE in training, this article by the great Mike Tuchscherer will give you a good run-down - RPE

 

What do I do with these numbers? What does it have to do with tendinopathy?

 

Research investigating the relationship between week to week training load and the influence it has on injury risk suggests that excessive and rapid spikes in acute training load are responsible for a large percentage of non-contact soft tissue injuries. This has been a consistent finding across a variety of team sports. (6)

The bottom line is: If you haven’t prepared your body to handle required demands, there is a higher risk of developing tendinopathy or just getting injured in general, if you constantly expose yourself to excessively high loads without sufficient recovery.

 

The acute : chronic workload ratio values and the significance are listed below:

  • <0.80 (Undertraining, higher relative injury risk)
  • 80-1.30 (Optimal, lowest relative injury risk)
  • >1.50 (Danger zone, highest relative injury risk)

 

To close..

 So there you have it – the very basics of understanding the development of tendinopathy. A few key takeaway points:

  1. Load is king – Manage your load well. Too MUCH or too LITTLE load can increase your risk of developing tendinopathy.
  2. Avoid spikes in loading. If you’re going away on a 6-week holiday, there is no doubt that you will be de-trained. Don’t jump straight back where you left off and expect your body to be in the same condition as before.
  3. Get into the habit of tracking your load (External and internal)

 

The next post will cover practical recommendations of managing patella tendinopathy in off-season training vs competition prep. This will be particularly helpful if you’re currently experiencing symptoms. However, management should be individualized for each athlete, this post is not meant to replace a consult. If you’re currently experiencing worsening, persistent symptoms, it would be a good idea to seek help.

 

Stay tuned!

 

 

Reference

  1. Roberts TJ, Konow N. How tendons buffer energy dissipation by muscle. Exerc Sport Sci Rev. 2013;41(4):186-93
  2. Magnusson SP, Langberg H, Kjaer M. The pathogenesis of tendinopathy: balancing the response to loading. Nat Rev Rheumatol. 2010;6(5):262-8
  3. Patellar tendinopathy: clinical diagnosis, load management, and advice for challenging case presentations (Malliaras P, Cook J, Purdam C, Rio E. Patellar Tendinopathy: Clinical Diagnosis, Load Management, and Advice for Challenging Case Presentations. J Orthop Sports Phys Ther. 2015;45(11):887-98
  4. Cook JL, Purdam CR. Is tendon pathology a continuum? A pathology model to explain the clinical presentation of load-induced tendinopathy. Br J Sports Med. 2009;43(6):409-16
  5. Dean BJ, Gettings P, Dakin SG, Carr AJ. Are inflammatory cells increased in painful human tendinopathy? A systematic review. Br J Sports Med. 2016;50(4):216-20.)
  6. Gabbett TJ. The training-injury prevention paradox: should athletes be training smarter and harder? Br J Sports Med. 2016;50(5):273-280.

 

 

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