Podcast Review: Tendons

I wonder if anyone else does this, subscribe to podcast channels and store them on your phone in an attempt to convince yourself that you’re doing CPD, but never get round to listening to them? I’ve also been known to do this with articles, printing them out then cluttering mine & my colleagues desks but never reading them.

Well I decided to catch up on a few podcasts and start listening to them in the car on the way to work. Flicking through the different channels I subscribe to, I saw 2 separate discussions about tendons. So I thought I would listen to both in succession and see what similarities or differences the experts had. These aren’t necessarily the only podcasts to talk about tendons, just 2 I had on my phone:

1) Physioedge #23: Lower Limb Tendinopathies with Dr Peter Malliaris (here)

2) The PhysioMatters Podcast session 6: Achilles Tendons with Seth O’Neil (here)


Revision time: 

Before we start, a quick opportunity to revise some key topics discussed below. Figure 1 demonstrates Cook & Purdhams continuum of tendinopathies.

Tendinopathy continuum
Figure 1: Cook & Purdhams Tendinopathy Continuum (click image for article)


Difference between Achilles and Patella Tendon:

A particularly interesting theme throughout the podcasts was the difference between Achilles and Patella tendon pathologies. None of the podcasts openly said “lets start addressing different tendons with different management” but they pretty much edged that way.

Malliaris was careful not to align himself with any particular “recipe” for tendon treatment, but did say that if he were to prescribe a protocol, he would use a different one for Achilles than he would Patella tendons. Later in the podcast, he explains his theory on not loading the patella tendon beyond 70 – 80 degrees knee flexion, explaining that there is no benefit to heavy loading into the end range for tendons… except the achilles tendon. This makes sense, if we understand that tendinopathies are a reaction to a combination of tensile and compressive loads. For the patella tendon to be lengthened, with the knee in full flexion, the patella will be acting as a fulcrum on the tendon tissues. However, when loading the achilles in a lengthened position the calcaneous doesn’t cause as much compression on the tendon (excluding Haglund’s deformity).

A quick cameo from a third podcast (BJSM Apophyseal injuries in children and adolescents with Dr Mattheiu Sailly, here) but interestingly discusses different processes between Osgood-Schlatters and Severs disease, with less tendon involvement seen in Severs. Could this paediatric presentation be similar in adult tendinopathies?


Is there a benefit to deep squats with a tendinopathy?

Exercise management:

While on the topic of lengthening tendons and putting them under load, it seems apt to discuss the one exercise method that goes hand in hand with tendons, Eccentrics.

“Eccentrics are not essential – Dr Peter Malliaris”

Malliaris comes across as a big fan of eccentrics. They are a useful method of increasing time under tension (TUT) and applying a heavy load, however they do not have to be a part of every program!

If a patient is unable to perform an isometric exercise, don’t even bother attempting an eccentric exercise as they will lack the quality throughout the movement. Another example would be a program designed for a player in mid-season. In these circumstances, it could be better to provide high load isometric exercises. O’Neill supports this theory for mid-season. While we accept that eccentric exercises will help the tendon, remember that they will also fatigue the muscle and therefor could impact on performance.

It is also important to recognise the stage of tendinopathy (see Figure 1). While a degenerative tendon can be treated quite aggressively in order to increase stiffness, however most athletes are likely to present with a reactive tendinopathy. In these cases, the cellular matrix is generally intact so the management can afford to be less aggressive. In these cases, activity modification to acutely lower the load would be beneficial and combined with isometrics, which Malliaris believes have an analgesic effect.

With any program for tendons, it is important to continuously monitor pain responses. A short duration of pain following activity suggests a stable tendon, however pain for a couple days suggests a very reactive and unstable presentation. O’Neill quotes a theory based on Delayed Onset Muscle Soreness (DOMS) as the characteristics of tendon pain and DOMS are strikingly similar. He explains that fascia seems to be a source of pain as opposed to the contractile tissues. The paratenum contains most of the nerves and the structures here will suffer from the delayed onset soreness. Much like actual DOMS, the tendons respond well to loading. O’Neill uses the analogy of going for a gentle jog when you have DOMS in your legs, and feeling a bit better afterwards.Over time, changes in both central and peripheral sensititsation may cause the heightened peripheral sensitisation we see with chronic loading – hence part of our management is activity modification.


Moving on from mid-season management, Malliaris discusses the off-season and the tendency of athletes to put their feet up for a few weeks after a gruelling season. This would be detrimental to a problematic tendon and as soon as they resume intense pre-season training you will spend the whole pre-season fighting fires with a reactive tendon. Therefore prescribe off-season tendon programs that include jumping, hopping, running drills to maintain control of the tendon.


“True tendon problems tend to be aggravated by a Stretch Shortening Cycle – Seth O’Neill”


In his exercise programs, Malliaris ensures that the Stretch Shortening Cycle (SSC) is as long as the “slower exercise” phases. However, these do not have to be done in simaltenous blocks. The SSC exercises should be incorporated as early as possible, providing the movement patterns are fluid and symptoms are under control (again, its important to understand and recognise a reactive or degenerative phase tendinopathy).


“Patella tendinopathies love intensity and loves load”



Tendon management remains a complex and daunting task for physiotherapists, yet in an age where we promote individualised management of injuries we still seem keen to follow a “recipe” for tendon management. Both podcasts discuss the importance of treating the individual, with reference given to their demands and tailoring programs to suit them. However, we seem happy to discuss “tendons” as a whole. Hamstring management has its own niche, at the same time we don’t treat all ligament injuries like an ACL. Should we start discussing individual tendons separately? As mentioned at the top, Malliaris changes his stance on loading through range when managing Patella tendons and Achilles tendons. We have only discussed these two tendons, without any reference to the rotator cuff, the hamstring tendons, flexor and extensor complexes in the forearm – all of which have different roles and demands.

What is exciting is the amount of research going into tendons and our understanding is evolving very quickly. Since my short time of being a physio, we have dropped “itis” and introduced “opathy”; eccentrics fell out of favour recently and Alfredssons protocol has been dissected and critiqued to death, yet now, with the support of Malliaris and O’Neill (amongst others) we feel comfortable using eccentrics again, but as part of a bigger program.

I highly recommend listening to the above podcasts and subscribing to their channels, they are a hugely resourceful… resource!


Yours in sport


Case study: “Bulls Eye Lesion”

Every now and then in clinic you come across an injury that doesn’t quite fit “the norm” in terms of its recovery and management. I know every injury should be considered unique and every individual managed differently, but I thought I would share the management of this particular injury as it did prove tricky, we did fail a couple of times but eventually we got it just right.



This case study revolves around an 18 year old central midfielder, skeletally mature (no increase in height throughout the year / evident secondary sexual features) with a regular playing and training history prior to this injury. The presentation started in the autumn, after a complete pre-season and a good few weeks of competitive season underway. The player was in & out of training with a niggling groin / quad but with nothing substantial showing in assessment (the benefit of hindsight would be a very good money earner for any clinician that could harness it and set up a course!)

Towards the end of an under 21 game, the player was visibly struggling with pain at the top of his thigh, unable to sprint or strike a ball but 3 subs had been made, so he was inevitably staying on the pitch. At the end of the game, there was pain on palpation of the proximal rectus femoris and sartorious region. At this stage, there was nothing more to assess – there was no point, we would only aggravate something without actually learning too much more.  He presented the next morning with visible swelling in a small pocket of proximal thigh, palpable crepitus and pain with straight leg raise at 20 degrees.


Review of anatomy

The rectus femoris is a long fusiform muscle with TWO proximal attachments. The Direct Head attaches to the AIIS and Indirect Head attaches to the superior ace tabular ridge and the joint capsule. It has a long musculotendinous junction, as such can execute high velocity shortening as well as coping with significant length changes – remember it is a two joint muscle crossing both the hip and knee, with an action like kicking it must cope with hip extension coupled with knee extension during the pull-back of the kick, so both ends of the muscle are undergoing an eccentric load (Figure 1). The muscle structure itself is made up of mostly type II fibres so this high eccentric load makes the muscle quite prone to injury (Mendiguchia et al 2013 source).

Figure 1: Demonstrating the demands on rectus femoris during a kick


“Bulls eye lesion”

The term “Bulls eye lesion” was coined by Hughes (1995 source) following the presentation of injury on MRI (Figure 2). The high signal signs around the tear of proximal injuries. Occasionally this causes a pseudocyst, thought to be the serous fluid in the haematoma.

Figure 2: MRI scans highlighting a “Bulls-eye lesion” presentation

Predisposing factors to a proximal tear include fatigue, insufficient warm up and previous injury. From this case, we know that the pain started at the end of the game with the player in a fatigued state, and there was a history of niggling pain on and off for a couple of weeks.



The initial management of this injury was relatively routine, revolving around the POLICE guidelines (see Cryotherapy Blog). By day 2/3 we were addressing pelvic control exercises & posterior chain assessments. By day 5 we could achieve pain free stretching of the hip flexors and were using “Compex” to achieve isometric contractions of the quad while the player did upper body exercises.  After day 7 we were able to begin loading through a pain free range, working on co-contractions and concentric contractions of the quad.

To Speed up, you must be able to slow down – Bill Knowles

In the early-mid stages of rehab, we began working on movement patterns but at a painfully slow speed. Using the Bill Knowles mantra above, we progressed though different ranges of box step ups at slow pace to elicit a co-contraction of quads, hamstring and glutes (Figure 3). We slowly lowered the player through a Bulgarian split squat (Figure 4) to work on stability through range and we did some bridging variations (anti-rotational core) to encourage isometric control of the pelvis (Figure 5 – excuse the size 11 shoes taking up most of the picture!!).

Figure 6: a) Low box step up with knee drive
Figure 3: a) Low box step up with knee drive



Figure 6: b) medium box step up
Figure 3: b) medium box step up
Figure 6: c) High box step up
Figure 3: c) High box step up












Figure4: Bulgarian split squat (a & b) with progressive knee drive added later (c)
Figure4: Bulgarian split squat (a & b) with progressive knee drive added later (c)




Figure 5: Single leg bridge (a) with ipsilateral arm fall out (b) and contralateral arm fall out (c)
Figure 5: Single leg bridge (a) with ipsilateral arm fall out (b) and contralateral arm fall out (c)


By adding speed to the high box step up, we were able to switch the demand of the quadriceps to an eccentric action as the hip extends from a flexed position and the pelvis rapidly comes forward. We felt confident adding this eccentric component after we had cleared the player at a decent weight using the cable machine and a jacket to work though some deceleration work on the hip and knee (Figure 6).


Figure 6: Cable decelerations. a) start position b) end position with 3 sec hold. c to e) Dead slow step backs with weighted cable pulling posteriorly


The Bulgarian split squat was advanced by adding a knee drive at the top the squat, taking the back leg from a position of full hip extension through into hip flexion, a rapid concentric action. Following the model of exercise progression and regression (source) we added weight, removed the concentric component and decreased the speed again before building back up in a now weighted position.

The later stage of rehabilitation saw the player undertake more field based conditioning, working under fatigue whilst completing technical drills and building up his range of passing and shooting, all the while maintaining his gym program to supplement his rehab. This late stage rehab combined the expertise of the physiotherapy department, working alongside the strength and conditioning coach to discuss reps and sets of all drills and help periodise the weeks for the player and design the field based conditioning sessions; the sports science department was able to use GPS for all outdoor drills to help monitor load and provide up to date feedback on key information, in this case monitoring the accelerations and decelerations for the player in a fatigued state.

It was important that the stress elicited in this late stage was in line with the rest of the squad mid-competition. Rob Swire and Stijn Vandenbroucke (source) explain the importance of rehab being harder than the team training. This is because we have control over rehab, but no control of training so we must be confident that player won’t break down again in training!

The player returned just under 8 weeks later. He continued his gym program for another 4 weeks after his return to training and (touch wood) has had no recurrence of this injury since.



Knowing what I know now, I would be more cautious of this nondescript pain around the proximal thigh. The indirect head runs quite deep and typically presents as a gradual onset. The niggle the player was displaying a few weeks before was probably a worsening of this small tear, that when fatigued and put under a double eccentric load such as kicking or sprinting, was bound to “give” at some point.

I’m sure that reading this back, it seems pretty obvious that there was something wrong with the player initially. Again, another lesson learnt from this relates to the players age. He had not had a soft tissue injury prior to this, so his subjective history was vague and typically teenager-ish. Its important to remember that young players and professionals don’t necessarily understand their own body. If they play things down, its important that we as clinicians double check everything before we clear them and not just rely on their feedback alone.


I hope you find my reflections useful


Yours in sport



The Osgood, the bad and the ugly

One of my best sources for recent literature is via a good friend of mine, Mr Jonny King (@Jonny_King_PT). Before he shot off to Doha to have his moment in the sun, he left a multitude of articles on my desk for me to read, one of which was a study looking at that persistent pest in my clinic, Osgoods Schlatters Disease (OSD).

OSD falls under the apophysitis or enthesopathy umbrella along with severs disease and Sinding Larsen Johansen disease amongst others. In our injury audit for the last season, these injuries alone accounted for 20% of our total injuries (u9-18s).

However, with a little bit of education to players, parents and coaches we feel confident that we can manage these numbers even better.

We are very lucky to be part of an in depth, ongoing study with the brilliant and very knowledgable Jenny Strickland at the University of Greenwich. With her guidance and protocol, we are bringing the days spent on the treatment table down considerably, but ideally we want to learn about these conditions to help prevent them in the first place.

What do we think we know?

OSD is a growth related condition, we think it can be attributed to high levels of activity during periods of growth. Unlike an adult presentation of a tendinosis, the condition affects the soft cartilaginous junction between the patella tendon and the immature anterior tibial tuberosity (ATT). (See my previous blog for the BJSM about differences between adult and Paeds injury management here).

Figure 1
Demonstrating the close relationship between the enthesis, the patella tendon, the infra patella fat pad and the physis of the tibia.

Historically OSD has been labelled as “growing pains” (a genuine medical entity, but no clinical similarities to OSD) and sufferers of the condition may well have been told to “just get on with it” or that “you’ll grow out of it”. Unfortunately this attitude still exists amongst some parents and, regrettably, GP’s – we see first hand evidence of this in our academy. When I first started in my role, I was guilty of just sitting a lad on the plinth with some ice, telling him to rest for a few weeks and we’ll see how we go.

OSD can almost certainly be attributed to growth spurts, where high levels of cellular activity in the growth zones of bone can’t be matched by the attaching muscles, resulting in traction on the inherently weak enthesis. Usual subjective presentation is that of an ache during, or more prominently, after activity. Gradually pain has been worsening over a period of days or weeks. Eases with rest. However, occasionally we see examples of players that have been kicked or landed on their knees in acute incidents but will display all the characteristics of OSD. But this doesn’t fit with our understanding of growth and traction…

Sailly et al (2013) looked at symptomatic adolescent male athletes competing in elite sport and using Doppler ultrasound they compared the ATT complex to gauge different stages of maturation. Within these stages of maturation, they could attribute pain scores from symptomatic athletes to determine the more vulnerable stages of growth (figure 2 below). The best descriptions for these stages that I have heard are from Sid Ahamed on his Adolescent Injuries course. He describes the enthesis as a continuum that develops with maturation from a stable state to an increasingly unstable state as the cartilage calcified with age.

Figure 2
Classification system of the maturation status of the ATT from stages 1 to 4. ATT, anterior tibial tuberosity; B, bursa; FP, fat pad; HC, hyaline cartilage; M, metaphysic; O, ossicle; P, physis; PT, patellar.

In Sailly’s study they found that no players reported pain during the “stable” first phase but increasing scores of VAS in stage 2. As the enthesis calcified and unites in stage 3 and 4, the numbers decrease again.
So what is happening in this 2nd stage of maturation? The use of Doppler ultrasound opens some new theories. In these symptomatic stage 2 patients, there was Doppler activity within the pre-patella and deep infra patella bursa, indicating the presence of neo-vessels within these structures. Recently, Seth O’Neil (physio matters podcast) explained that most of these pain inducing neovascular structures are actually present in peritendon & surrounding tissues like the bursa, fat pads and fascia. Maybe the same is true with the adolescent population.
The synovium that surrounds the enthesis is highly prone to compressive forces and as such, prone to inflammation. In the developing ATT, the patellar ligament attaches to the tibial tubercle but also to the physis of the tibial growth plate and to the periosteum of the metaphysis of the tibia (see figure 1 at top) . Sailley et al propose that this anatomical area is not only prone to traction that we normally associate with OSD, but also compression. Perhaps this explains the sudden onset OSD in the clinic alongside those rumbling insidious case loads.



As I mentioned, we now follow the Strickland protocol at our club in terms of treatment, but I still believe the key is in prevention rather cure. We regularly discuss loading with our coaches at every age group. If you consider that most of our players at school boy level will also play and train for their school, probably be selected for other sports such as cricket and rugby and will generally tear around everywhere at 100mph. Basically their day consists of sprinting, jumping, bounding and kicking. Consider the load on those immature structures (both compressive and tensile). As part of a warm up, does that player then need to do a series of hurdle drills or jumps? Could they not spend their conditioning sessions doing low impact movement patterns, balance & proprioception, or co-ordination drills for their newly elongated and uncontrollable limbs? Perhaps every now and then having a training session where the lads don’t have to strike a ball? Like basketball maybe, where you teach spacial awareness and evading the opponent? Or placing a technical bias on the session and reducing the pace?
If we can help coaches, players and parents understand that modifying activities and occasionally, resting, is the best thing in the long run for all parties, I think we will continue to see a drop in training / matches missed due to OSD.

Yours in sport