The MONaSh TEndon ReSearch group, otherwise known as the MONSTERS on twitter (@tendonresearch), are a tendon research group from Monash University that have contributed some great insight into the mechanisms, prevention and rehabilitation of tendon injury. I have had the privilege of meeting and working with some of the great minds behind this group including Jill Cook, Sean Docking and Ebonie Rio. If you ever get the chance to get along to one of their tendinopathy courses you will not be disappointed, it is a fantastic combination of evidence based expertise and practical applications. This semester Sean presented to the students of the Masters of High Performance Sport on the current best practices for prevention, management and rehabilitation of achilles and patella tendinopathy, providing a great insight into what we know works and what we need to keep an eye our for.
ONCE A TENDON ALWAYS A TENDON
Tendinopathy is a common injury affecting people of all populations, the most common presentations are:
- Older Populations: Achilles, Rotator Cuff, Lateral Epicondylitis, Gluteal Medius
- Younger Populations: Patella, Adductor, Hamstring
The clinical presentations of tendinopathy usually develop after a sudden increase in load (exercise), which may have been a result of volume, intensity or frequency of training. This can result in pain, decreased exercise tolerance and a reduction in function (Cook & Purdam 2009). The main clinical features include:
- Focal localised pain, approx 1cm diameter (doesn’t move or refer)
- Pain is load dependent, therefore if greater load administered it should be more painful e.g. Single leg calf raise vs Single leg hop
- Pain worse 24hrs after load
There is still some debate over the current pathogenesis and primary aetiology of tendinopathy, however, Sean spoke about the histological features and comparisons between a normal tendon and abnormal tendon, illustrating the changes that occur at a cellular level. Sean highlighted the major issue for individuals suffering tendinopathy is the loss of collagen architecture and integrity as a result of tenocyte activation (rounding) and infiltration of large proteoglycans resulting in increased water, blood and nerve vessels. These cellular changes are a response to a cell driven pathology, not an inflammatory condition, which unfortunately means the changes cannot be reversed, reminding us that ONCE A TENDON ALWAYS A TENDON (good or bad).
TENDON CONTINUUM – A PATHOLOGY MODEL
In 2009 Jill Cook and Craig Purdam proposed a continuum for tendon pathology that has three stages, as it is a continuum there is continuity between stages:
- Reactive Tendinopathy
- Tendon Dysrepair
- Degenerative Tendinopathy
As you can see in the image load is the primary stimulus that drives tendon pathology forward or backward along the continuum, therefor it is imperative to know how to identify the stages of the continuum and possible management.
REACTIVE -> short-term adaptive response to load, usually as a result of sudden unaccustomed physical activity resulting in thickening of a portion of the tendon, increased stiffness and reduced stress. Able to return to normal tendon if load sufficiently managed. Common in young jumping athletes or from a direct blow to tendon. The image below demonstrates the collagen structure in a normal tendon (Picture A), while in Picture B the collagen structure is disorganised with a greater amount of cells present within the tendon.
TENDON DYSREPAIR -> Attempt at tendon healing, similar to reactive tendinopathy but has sustained some cellular matrix breakdown (collagen disorganisation), possibility of increase in vascularity and neural ingrowth. If load is poorly managed in the reactive stage the tendon will progress to tendon dysrepair, this is commonly seen in chronically overloaded youths but is possible in the older population. Some reversibility is possible with load management and exercise prescription.
DEGENERATIVE TENDINOPATHY -> Result of chronic matrix and cell changes, areas of cell death and large areas of matrix breakdown and little collagen. Infiltration of vascularity and neural ingrowth is abundant, little capacity for reversibility of pathological changes at this stage. Primarily seen in older populations or elite athletes with chronic overload. Clinical history of repeat bouts of tendon pain, resolving slightly but returning due to load changes. Possibility of reactive on degenerative, which is a flare up of the ‘normal’ part of the tendon around degenerative tissue, most likely where the tendon is absorbing load.
Previously the only options for imaging we have had has been US and MRI, which both have good to excellent accuracy and sensitivity, however, both still have a highly subjective interpretation. Fortunately the development of the UTC-Tracker (Figure 1 & 2) originally used in horses has been an innovative technique for quantifying tendon structure of the patella and achilles.
The UTC (Ultrasound Tissue Characterisation) is a precision instrument that moves the ultrasound probe automatically across the region of interest, e.g. along a tendon’s long axis, collecting transverse images at even distances of 0.2 mm over a length of 12-20 cm. These images are stored real-time and a 3-D image is created that can be used for tissue characterisation and quantification of architecture and integrity of the collagenous matrix. Sean is an expert in the application of UTC and works with multiple professional sporting teams to help diagnose and manage lower limb tendon injuries. For further information about the use of UTC and its benefits visit http://www.utcimaging.com/home-human/.
Sean highlighted some possible risk factors for tendinopathy, which are important to identify in the prevention of a tendon injury:
- Gender: higher risk in males and postmenopausal women
- Genetic Predisposition: COL5A1 gene associated with achilles tendinopathy, possibly due to collagen changes
- Adiposity: waist circumference > 83cm
- Acute vs Chronic Load: what have they done before? What are they planning on doing?
As I mentioned earlier, load is the major concern for tendon injuries, which makes it important to define different forms of physical activity dependent on their tensile load:
LOW LOAD= Slow strength movements, Cycling, Rowing, Swimming
MODERATE LOAD= Straight line running, Slow skipping
HIGH LOAD= Plyometrics, Agility and Change of direction, High speed running
Quantifying and managing load is an important aspect of injury prevention and rehabilitation in high performance sport. Rosengarten et al (2014) reported that tendon structure on a UTC scan in asymptomatic AFL athletes changed as a result of high tensile load (AFL game), the results demonstrated that cell response to high tensile loads may take up to 72 hours before returning to normal. This is important information when scheduling training sessions or rehabilitation sessions to help limit or manage possible tendon damage, Sean and the MONSTERS group recommend a rolling 3 day cycle (High-Low-Moderate).
One very important bit of advice Sean had was always remember TENDONS HATE CHANGE. Change can be related to load (frequency/intensity/volume), training surface, footwear, inactivity (illness or surgery) and/or equipment, this is an important factor when considering athletes who may be at risk and programming injury prevention.
WHAT TO DO IF THEY GET ANGRY
PHASE 1-> Identify and adjust the load that is causing the problem.
PHASE 2 (LOW LOAD)-> Pain reduction via ibuprofen and corticosteroid if in reactive stage, best form of pain reduction at the present time is Isometric muscle contractions. The Isometric contractions can be built up 30secs – 60secs x 3 – 5 sets up to 5/day. Primary goal is to reduce morning stiffness and pain during tensile load. Approx 2 weeks.
PHASE 3 (LOW LOAD)-> Tendon pain <3-4/10 VAS and stable. Intro of slow heavy isotonic (concentric/eccentric) exercise (4 up/4 down), 4 x 6-8 reps. Every 2nd day, retain phase 2 exercises. Approx 2-4 weeks.
PHASE 4 (MOD LOAD)-> Pain is stable in morning <1/10, muscle symmetry, >25 calf raises (achilles) or 1.5X BW leg press (patella). Power development, faster eccentric portion and increased speed, every 3rd day, retain phase 2 & 3 ex. Monitor 24-48hr response. Approx 2-4 weeks.
PHASE 5 (HIGH LOAD)-> Sports specific training, elastic loading (plyometrics). Retain phase 2-4 ex, every 3rd day high load exercises. Return to sport at modified loads. Monitor 24-48hr response.
It is important that once the rehabilitation phases are complete that maintenance programs remain in place to continue developing the athletes isometric and isotonic strength and reduce the risk of re-aggravation. Tendons take time to adapt to load so listen to them, when they get angry the main focus should be calming them down and slowly reloading, at the end of the day all tendons want to do is find their HAPPY place.
For further information about tendinopathy be sure to follow some of the experts in the field on twitter Sean Docking (@SIdocking), Ebonie Rio (@tendonpain), MONSTERS (@tendonresearch) and Jill Cook (@ProfJillCook).
Cook J, Purdam C (2009) Is tendon pathology a continuum? A pathology model to explain the clinical presentation of load-induced tendinopathy. Br J Sports Med 2009;43:409-416
Rosengarten S, Cook J, Bryant A et al (2014) Australian football players’ Achilles tendons respond to game loads within 2 days: an ultrasound tissue characterisation (UTC) study. Br J Sports Med 2014; Online First