Outcome measures: An observation and a reflection

Sports science and strength & conditioning practice is built on a foundation of identifying a problem, testing the problem, applying an intervention and then re-testing to ensure progression. Athletes will buy into fitness testing, injury prevention and subsequent high performance behaviours if they are given the impression that their coach and medical team know what they are doing and things are done with a purpose (Kristiansen and Larsson, 2017). This begs the question whether coaches can justify and clinically reason their battery of performance tests.

When applying a performance measure, understanding of the underlying kinematics is essential to understand the validity of the test to the desired outcome. The OptoJumptm is a valid tool in assessing a reactive strength via  drop jump (Healy et al., 2016) however what components of the jump is the coach wishing to address? The validity of the tool is the not the same as the validity of the test. For example, reactive strength index (RSI) can be influenced by a reduced contact time (stretch shortening cycle via the musculotendinous unit) or via total jump height (power output throughout the lower limb and nervous system) or a combination of both (Healy et al., 2017). Understanding these mechanisms may influence the instructional bias of technique given by the coach in order to test what is desired.

With complexities over a test like an RSI to something seemingly obvious like a jump, testing for broader components of fitness and multiple movement patterns is much more difficult.

The Yo-Yo intermittent recovery test (IRT) is reported to be a valid measure of fitness and correlates to match performance in football (Krustrup et al., 2003). However, this is an example of a fitness capacity test and in fact correlates to fitness capacity in a match scenario. In field based team sports, there are a large number of variables and complex interactions that all contribute towards “performance” as an outcome (Currell and Jeukendrup, 2008). Krustrup’s conclusion was based on correlated Yo-Yo IRT results to high speed running in a game (>15km.h-1) with a strong correlation (r=0.58). Overlooking the methodological accuracy of this (pre-GPS, using VHS locomotive assessment retrospectively), the correlation is between two differing metrics. Where the high speed running was recorded over 90 minutes of varying intensities and periods of effort (12 players across 18 different games), the Yo-Yo IRT covered 1.7km in a mean time of 14.7mins with incremental increases in pace dictated externally. For a test to be considered a valid indicator of performance, it should meet the same metabolic demands as the sporting activity (Currell and Jeukendrup, 2008). The Krustrup paper does not make this comparison, instead analysing physiological markers from rest to exhaustion during the Yo-Yo IRT, not exhaustion markers in comparison to game data.

Perhaps semantics, but in fact there should be differential terminology to distinguish “fitness performance” from “athletic” or “sporting performance.” It should be considered that sporting performance is influenced by a large number of uncontrollable and non-modifiable factors that would make any comparison of validity and reliability to outcome measures unfair. Essentially, recreating a competitive environment is near impossible. This raises the question whether we are exercising just to improve test scores or, closing the loop and relating exercises to performance? Does raising the envelope of one, consequently improve the other? Something that we should not only be asking ourselves, but a question we could come to expect from coaches and athletes a like.

Oriam

Does the research answer this?

It has been suggested that stronger athletes produce faster sprint time, quicker change of direction speeds and higher vertical jump scores when compared to weaker athletes of the same sport (Thomas et al., 2016). Squat jump (r = -0.70 to -0.71) and counter movement jump (r = -0.60 to -0.71) demonstrate strong correlations to change of direction speed (Thomas et al., 2016). Peak force during isometric mid thigh pull was significantly correlated to 5m sprint time (p <0.05) however this correlation was only moderate (r = -0.49). But again, does this correlation transfer into performance if the testing protocol doesn’t accurately mirror sporting performance?

Sprint times over 40m have been shown to decrease following an acute bout of heavy loaded squats, hypothesised to be due to post activation potentiation (Mcbride et al., 2005). Higher squat strength scores also correlate with sprint times over 0-30m (r= 0.94, p=0.001) and jump height (r = 0.78, p=0.02) (Wisløff et al., 2004). Importantly, we know sprint performance tests have demonstrated construct validity to the physiological requirements of a competitive field based game (soccer) (Rampinini et al., 2007), which is ultimately what we are aiming to do; relating performance testing to physiological and metabolic markers from a given sport.

The addition of a jump squat exercise into a training program may help improve 1RM squat and 1RM power cleans (Hoffman et al., 2005). So perhaps yes, there is a perpetuating loop between exercise, tests and performance but the link between them all may not be tangible or direct.

But how do we translate all of these statistics and data sets this to a non-scientific population, as a lot of our athletes are? I’ve developed the following analogy to try and help with this.

 

Solar system analogy:

If we consider that “athletic performance” is the main focus of any intervention, much like the sun at the centre of the solar system. This is the bright light that everything revolves around; media, finance, fan base and support and so on. It could be argued that any intervention we have as coaches will never truly replicate “athletic performance” but should be influenced by it. This influence works both ways, positively and negatively. For example, if we maximally test an athlete before a competition, this will likely have a negative impact on “athletic performance”. Conversely, if we were able to collect data that informed a training program to improve athletic performance, despite not actually replicating “athletic performance” it would (hopefully) have a positive impact. For example, a football game is determined by so many uncontrollable variables that can not be replicated in a gym, but we might identify that a player needs to improve their 5m sprint time which in turn, will benefit performance.

Figure 1 solar system
Figure 1: An analogy depicting the relationship between “athletic performance” and controlled interventions / measures. The skill of the coach is identifying which outcome measure or intervention is going to have the greatest influence on athletic performance.

Let’s consider our potential interventions to be orbiting the sun (Figure 1). There is an interaction between the planets and the sun via gravity but they do not have a direct overlap, where the planets do not collide with the sun just as an outcome measure does not truly match sporting performance. We know that larger planets have a greater influence, so as coaches, we are trying to affect the level of positive interaction with “athletic performance”, the gravitational interaction. By influencing links between exercise intervention and outcome measures, we can affect the size of these planets. In turn, this will have a greater interaction with the centre of our solar system, “athletic performance” (Figure 2). Much like the universe, there will be many different solar systems just as there are different sporting codes and contexts, so the skill lies in identifying the most influential planets in your solar system.

figure 2 solar system
Figure 2: The impact of enhancing an intervention or measure on sporting performance, in this case there has been a greater focus and development of the blue “planet” which has changed the interaction with the “athletic performance”

 

A clinical reflection:

For long term injuries, I utilise a continuum to guide return to play (train / play / perform), often these stages are guided by outcome measures linked to goals and aims for stages of rehab. Typically these tests are scheduled in advanced and often follow a planned “de-loading” micro-cycle. This helps with continuity and, as much as you can in sport, standardisation of the test.

A recent case study found me questioning my judgement and to a degree, wondering if my intrigue and curiosity about my rehab plan drove me to test out of sync with the schedule, instead of doing the test for the athletes benefit.

Following a good period of return to train, the proposed testing date previously scheduled clashed with a squad training session. Observational assessment suggested the athlete was coping well with the demands of training and it seemed counter-intuitive to pull them out of training to undertake some tests. A few weeks later, a gap in the daily schedule presented an opportunity to re-test. The test scores were down compared to the previous month, most likely because the athlete had trained in the morning and trained the 4 out of the last 5 days in some capacity. In previous tests, the athlete had come off of a de-load week and tested the day after a day off.

The result:

The athlete began to question their ability and availability to train. They were visibly knocked in their confidence given a drop in scores, despite me being able to rationalise why this could be. Having had the opportunity to feed my own interest and try to prove to myself that a rehab program had worked, the outcome was much worse. I threatened the confidence of a long term injury returning to training, potentially adding doubt and hesitation to their game and I did not get the results I was expecting.

On reflection, given their time out through the season so far, I should have stuck to protocol and tested on the scheduled day (one training session was not going to increase their chances of availability).. or, not tested at all. Instead, i shoe-horned some testing into an already busy schedule. What did I expect given the current level of fatigue?!

Image result for reflection

Previous results had reached a satisfactory level to return to train and I was now chasing the final few percentages available. To give them confidence? Probably not, as they were training and enjoying the return to train. So perhaps it was just to give myself confidence. An interesting lesson learnt, mostly about myself.

 

Yours in sport,

Sam

Compex doesn’t have to be complex

compex

I should probably start by acknowledging that there are other muscle stimulation devices available… but I’m not employed by Compex, I just have some very good experiences using their product. This blog was borne out of frustration of seeing Compex machines gathering dust in treatment rooms or being used ineffectively as passive, plinth based modalities. I think a lot of people are missing the trick, you need movement!

While I am an advocate of its use clinically, I  want to disclose that using a Compex will not make a bad exercise good. It is a bolt-on to a rehab program and is something that can make a good exercise great. That is key. The clinical reasoning, exercise selection and placement of the stimulation all underpins an effective application, so before rolling it out to all athletes or patients make sure you can reason why it has a place in your practice.

Its all about progress

Like with any intervention, the clinical reasoning behind the application of muscle stimulation can influence its use at different stages of injury and rehabilitation. In the acute stages, it is believed that muscle stimulation may modulate pain. For an interesting read on the use of electricity and pain throughout the centuries, click here. However, as we understand more about optimal loading and mechanotherapy, we probably need to limit the time an athlete sits on the plinth watching the latest Mannequin Challenge on their smart phone while their quad twitches. It is worth considering that a Compex placed on a dead body would still cause it to twitch. The key is to get them moving and use the Compex to either facilitate movement or provide an external load. Interesting that we can use the same machine and the same settings to either regress or progress an exercise… the key is in the exercise selection.

Consider the tissues

Muscle injury: It should be pretty obvious that placing a muscle stimulation device, designed to promote contraction of muscle, on a contractile tissue with a tear or micro-damage could have negative consequences. For a second, lets forget the Compex. Respect the pathology and consider if you really need to lengthen or contract that muscle to load it. Is there a way you can work that tissue as a synergist perhaps? If the hamstring was injured in the sagital plane, can we move through coronal (frontal) planes and still load the hamstring? This could possibly be a slight progression on an isometric exercise and shouldn’t change the length of the muscle that may cause pain or further damage. Certainly more beneficial than sitting on the treatment bed though. So now consider how muscle stim may benefit this stage of injury. It could possibly help with any inhibition due to swelling or pain, perhaps be used to add an increased load to unaffected tissues that you may not be able to load otherwise.

As the healing progresses and the level of activity increases, it is quite common that we see some deficits in muscle function, especially after a long acute phase (if that isn’t a paradox?! Think post surgery or fixation). A good example is post ankle reconstruction, where you have worked on regaining plantar / dorsi flexion but when you ask the athlete to do a heel raise, it’s quite an effort. It may be appropriate to use the Compex here as a little crutch to facilitate movement and contraction. But the key thing here is it is not our cadaver that we causing a contraction in, the athlete is consciously initiating the movement. (Previous blog on internal and external cues here).

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Now promise me if the Compex hurts, you will turn it down. OK?
Progressions by all definition, progress. So after working through isometric and concentric exercises, the program may require some eccentric load. This is worth trying yourself before asking a patient to do it, because a very simple exercise like a TRX squat that may have been cleared earlier in the program can dramatically increase in work with the addition of Compex. Consider a quad injury. The Compex has two phases of a cycle, a fasciculation phase that causes visible twitch and a long contraction phase (depending on the setting, the length and intensity of the contraction change). After one or two cycles for familiarisation, instruct the athlete to work against the contraction – so when the Compex wants to promote knee extension via a quad contraction, sit back and encourage knee flexion. Try this yourself for 6-8 reps and feel the fatigue induced, it usually surprises people. Again, make sure you can reason WHY you are doing this. This is usually a good bridge for someone who needs to step up their program but maybe can’t tolerate external load (confounding injuries, instability of joints, lack of technique etc etc.)

Joint Injuries: In comparison to a muscle injury, your application of Compex may be more aggressive. Because you are unlikely to affect a non-contractile tissue with the stimulation, you may use the eccentric reasoning to help reduce atrophy rates following a intracapsular injury like an ACL. Ensure you know the available range first of course.

With these injuries, the external stimulation may help with inhibition, improve proprioception lost by the ligament or capsule or it may provide stability to the joint by increasing the available contraction. Again, there will be a time and a place and it requires the clinician to reason through the application, but this may be a great addition to a program that is becoming stale.

Tendon injuries: The use of the Compex to enhance an isometric contraction or to create an eccentric contraction may be a great addition for an in-season tendinopathy as a way of managing load. The timed contraction allows clinicians to monitor Time Under Tension (TUT) which is essential for tendon management. If considering a High-Medium-Low frequency through the week, a pain free exercise that is used on a Medium day can become a High load exercise with the addition of an externally generated contraction. But consider the two things that aggravate a tendon, compression and shear. Appropriate exercise selection and range is going to be crucial, that being said, it may be that the addition of stimulation to the quads actually reduces shear through the patella tendon by changing the fulcrum of the patella (no research to back this up, just my musings).

musing
I really like Geckos. I found this Gecko a musing
Conclusion:

I think there are many options out there to enhance rehabilitation by considering the diversity of muscle stimulation. But I want to repeat for the hundredth time, it is the exercise selection that is key. The addition of a Compex will only amplify that choice.  For the patient, it adds a bit of variety to a rehabilitation program and for the clinician it is another tool to help with optimal loading of a healing tissue or structure. I am a big fan of weight training (don’t let my chicken legs fool you) but there are injuries or athletes that for one reason or another are unable to tolerate weights. This is one tool in a very large and overused metaphorical tool-box that may bridge that gap between body weight exercises and weighted exercises. I also believe there is great benefit when complimenting this with Blood-Flow Restriction Exercise or Occlusion training… but that’s another blog.

As always, thoughts and opinions are welcome.

 

Yours in sport,

Sam

Case Study: Myositis Ossificans – Deadlegs aren’t just for the playground

Whether you call them a “dead leg” or a “Charlie horse” or a “cork thigh” chances are we have all had one. Mostly from the playground days where the bigger kids want to take pleasure in seeing you limp for 5 minutes. However when they happen in sport, with fully grown athletes running at full pace, a collision to the thigh can result in an injury much more serious than the one we associate with from childhood.

The reason I wanted to write this blog was that I worry  that thigh contusions are underplayed in the treatment room, potentially because we associate them with those school sports injuries that can be “run off”. This is a case study that I became involved with after initial management of the “dead leg” failed, and to this day is one I reflect on about how important initial management can be in saving severe stress in the long run. This is a case of a “routine” dead leg that is commonly seen in contact sports that resulted in 9-months of rehab to manage a secondary case of myositis ossificans.

What are we dealing with?

There are two types of “dead legs”

  1. Intramuscular: blunt force trauma to the muscle that results in a haematoma, in this scenario the epimysium remains in tact and the bleeding is contained within the muscle compartment.
  2. Intermuscular: the epimysium surrounding the muscle is broken along with the damage to the muscle tissue, the resulting haematoma spreads outside of the damaged muscle.

The intermuscular hematoma by far looks the worst, it’s the one where the whole thigh goes black and blue and looks pretty nasty. However, clinically these ones tend to heal quicker and they look a lot worse than they feel. The problem with the intramuscular haematoma is that because it is contained, the pressure can build up and become more painful. It is generally more debilitating as a result, with larger loss of range and more pain. It also doesn’t provide that visible diagnosis as very often you just get a small sign of bruise on the skin from the impact – this is where it can get dangerous as we like to be able to see injuries (hmmm something about invisible injuries and under diagnosis.. concussion?). We have discussed acute management before (here) but with dead legs, it is always worth monitoring for a few days and hoping that the leg goes black and blue.

fig2

In the first few days, range is a good indicator. On day 1 after the injury, if they are unable to achieve >90 degrees knee flexion, the prognosis is generally longer. For a bad intramuscular contusion, you could be looking around 6 weeks. This is where the coaches tell you it’s just a dead leg and they’ve had worse. But, it is structural damage to the tissue resulting in bleeding and should be given the same respect you would give to a tear. (Muscle injury classification via the Munich Consensus here).

Myositis Ossificans (MO):

MO is the formation of heterotrophic bone within the muscle following trauma (here) essentially following failed healing the body begins to lay down bone in an attempt to add stability and structure.

Case study:

The following case study is an example of an academy player, where an initial intramuscular trauma to the muscle was accelerated back to activity resulting in a 17cm tear of vastus lateralis (VL), consequently being diagnosed with MO that was estimated to be 3cm thick and of equal length to the tear.

Timeline:

  • Day 0 – initial impact to right VL via collision in training, had to be removed.
  • Day 1 – “able to squat and lunge but pain on a stretch”. Player expressed determination to train and so was allowed to.
  • Day 2-3 – continued training
  • Day 5 – Removed from training with “cramp / DOMS” in right leg.
  • Day 8 – Sudden loss of power with running and kicking, removed from training.
  • Day 30 – returned to training
  • Day 31 – played in a competitive game but substituted by manager after 25 minutes due to inability to run. Assessed by doctor and head physio. Visible contained swelling in VL, palpable solid mass, loss of range and pain on contraction of quads. MRI scan demonstrates a 17cm longitudinal tear of VL. Suspicion of MO so sent for ultra sound scan which was confirmed, absent from full team training for 9 months.

Intramuscular haematoma
Contained haematoma within the vastus lateralis muscle after 30 days of continued training post-initial injury
Management:

Surgical excision of MO is only really reserved for persistent cases that don’t respond to conservative treatment (here). A collective decision was made that we should try to reduce any form of load that may stimulate further bone growth. As a result, the player was removed from all activity of the lower limbs, no soft tissue therapy to the quads and at this stage no stretching of the affected tissues.

It is neither healthy nor beneficial (or fun!) to completely rest when you are used to training 6 days a week. Credit should go to Will Abbott (@WillAbbott_) for his contribution to the maintenance of the athletic profile for this player. A periodised program was designed to maintain metabolic and cardiovascular systems, strengthen the upper body and completely unload the lower body.

Screen Shot 2016-06-19 at 9.02.28 AM
A periodised model to demonstrate maintenance of unaffected systems with complete lower body unload (designed by Will Abbott)
The program included swimming, with multiple floats between the legs to reduce the temptation to kick. All gym based activities were performed seated or with legs supported when lying to reduce axial load through the legs during upper body lifts. Upper body metabolic sessions were implemented via high intensity interval training, with small rest periods to help maintain specific anaerobic demands relating to the sport. This was done using medicine balls, ropes, boxing pads.. anything to reduce the monotony of daily upper body training.

Each month was broken down further (as shown below), with follow-up ultra sound scans every 4 weeks. After the first 4 weeks, we observed a 2.5cm reduction in length which consolidated our thought process to continue de-loading. With limited exercise potential and treatment for the leg, we ran half days and 5 day weeks to help maintain a positive psychological presence.

Screen Shot 2016-06-19 at 9.02.58 AM

This was an opportunity to increase muscle mass in the upper body, an opportunity that would not have been possible during season if the player continued to play and train. This allowed a clear progressive pathway for increased lean mass with the following phases:

Hypertrophy –> Max strength –> Strength / power conversion –> Power

While the conditioning phases were as followed:

Aerobic base –> Max aerobic –> Supra max aerobic

There was a decrease in calcicific mass every month, although the rate of this varied each time. By the end of month-4, the mass had completely reabsorbed which meant the reintroduction of load to the lower libs.  By this point, the end of the season was 6 weeks away and therefore no realistic opportunity to play again this season, so the decision was made to start physical preparation for the following season.

Screen Shot 2016-06-19 at 9.03.30 AM
An example of the lower body periodisation
The lower body gym program was tailored as followed:

Strength endurance* –> Strength –> Max strength –> Strength & power complex training

(* This was probably more “re-introduction to the gym” rather than true strength-endurance. But this phase would have served as a gentle hypertrophy phase given the 4 months of atrophy)

Before undergoing a linear outdoor session progressing from general preparation to sport specific drills with Tom Barnden (@barnden_tom). The player completed a full pre-season and no recurrent symptoms to date.

Conclusion:

Hopefully the lengthy timeline of this case study demonstrates the importance of giving each individual injury the respect it deserves. While I hope the management is interesting, the key discussion point is how do we approach “dead legs”? Should there be better education to athletes and coaches about the magnitude of injury? Essentially given the tissue damage, are they a tear? If an A4 piece of paper represented a muscle, and we tear down the middle (strain) or poke a hole through the centre of the page (blunt force trauma), that page is still affected and unable to serve as an A4 piece of paper. Why does the mechanism of damage change the management of injury? Given any loss of range or function following a blunt force trauma, always consider the magnitude of potential damage; monitor swelling, bruising and pain and have adequate timelines in the back of your mind – don’t rush to a diagnosis / prognosis on day 1. There will be times where there is impact and initial pain but full range and full strength – this is where our pitch-side assessment and reasoning comes in (here).

Yours in sport,

Sam

Clinical Updates from ISHA 2015 (International Society for Hip Arthroscopy) Conference – Ben Matthew

We are delighted to host a blog from fellow physiotherapist and twitter geek, Ben Mathew (@function2fitneswho discusses his take home messages from last years International Hip Conference in Cambridge. Ben discusses some brilliant considerations for when conservative treatment just doesn’t work, which compliments nicely with a recent blog we wrote on trying to manage hip pathology in-season (here). Some of the points I particular like relate to the rehab after surgery. Thats enough from me…Thanks very much to Ben.

 

Clinical Updates from ISHA 2015 (International Society for Hip Arthroscopy) Conference – September 2015, Cambridge

 hip

Conditions like Femoro-acetabular impingement (FAI) and Acetabular Labral tears (ALT) are being recognised as the leading cause of hip and groin pain in the active population and has gained increasing attention over the past decade. In the past, these pathological process simply went undiagnosed. Surgical management, especially hip arthroscopy, can be a viable treatment option, especially when conservative management has failed.

Leading hip surgeons, researchers, health economists and expert physiotherapists came together for the ISHA conference at Cambridge (24 – 26 September, 2015) to discuss the latest developments and research findings in this rapidly evolving clinical speciality. I was fortunate to be there and to gain the up-to-date understanding of the complex hip and groin area, and also to listen to some top speakers. It is difficult to summarise a 3 day seminar in a short post. However, I have tried to cover some key clinical points, which might be useful for therapists, involved in hip and groin rehab. I have divided this post in three areas

 

  1. Clinical Examination of Hip Related Groin Pain
  2. Management of Post-op Hip Arthroscopy Patient
  3. Key References which were mentioned in the lectures

 

Clinical Examination of Hip Related Groin Pain

  1. Examination of Chronic hip and groin pain is challenging. It is important to have a thorough subjective assessment as part of the screening process. Some of the key subjective questions specific to the hip region are
  • Childhood hip disease like Perthes, SUFE, Dysplasia (These patients are at a high Risk of secondary Osteoarthritis)
  • Lower Limb Fractures and History of Stress Fractures
  • Mechanical Symptoms like Clicking, Locking and Catching with pain (Highly indicative of ALT)
  • History of Steroid Use (linked with Red flag Pathology like Avascular necrosis)
  • Multi-joint Pain and Presence of Generalised Ligamentous Laxity (linked with capsular laxity and ligamentum teres injuries)

 

  1. Use of Patient reported Scales such as the HAGOS Scale and iHOT 33 were encouraged to be used as part of the screening process, to assess the physical, functional and psychological effect of chronic hip pain.

 

  1. The most provocative movements for FAI and ALT are prolonged sitting, deep squat, getting in and out of car, kicking and twisting movement. Movements which involve deep squatting or loaded rotation are usually painful in this cohort. If the patients have significant early morning stiffness, there could be an element of early osteoarthritis.

 

  1. Functional testing is an important part of the objective examination. Tests such as Overhead squat, Lateral step-down and Single leg squat are impaired in chronic hip and groin pain. The most common compensation is excessive hip adduction and hip internal rotation. These impairments could be due to pain, motor control deficits or weakness. If the patient can consciously correct it, it is most likely to be motor control deficit.

 

  1. It is very common to have co-existing pathologies with chronic hip pain. Some common conditions are low back pain, SIJ pain and Pubic overload syndrome

 

  1. There is no specific tests to diagnose for FAI or ALT. A combination of the FAIR (Impingement test) and FABER is useful to rule out articular hip pathology. The FAIR test is not specific for FAI, but indicates internal derangement of the hip.

 

  1. Strength deficits are very common in chronic articular hip pathologies. It can be bilateral. The most affected groups are hip abductors and hip external rotators.

 

  1. A very useful tip to differentiate between hip related groin pain and adductor related groin pain is by isometric strength testing, using hand held dynamometer. There is reduced adductor to abductor ratio in the adductor related groin pain group than hip related groin pain.

 

  1. The most important objective marker is the range of medial rotation. Generally, patients with FAI tend to have internal rotation less than 15 degrees. Patients who have less than 10 degrees of internal rotation tend to do poorly with conservative management.

 

  1. Excessive ROM in internal rotation and external rotation can be indicative of structural variations such as dysplasia or capsular laxity, which is very common in the dancing and martial arts population.

 

Post-op Hip Arthroscopy Hip Patients Management 

  1. There is lack of consensus on these variables following hip arthroscopy (Weight bearing status, Use of CPM, timing for manual techniques, guidance of soft tissue work, Use of brace). Therefore, it is important to liaise with the surgeon on clear guidance and precaution for optimal rehab following hip arthroscopy.

 

  1. Some suggested time-lines for different types of procedures in hip arthrscopy in the conference were
  • Bone Reshaping / Osteoplasty   –   Immediate WB with crutches as tolerated
  • Labral Debridement / Repair       –   Immediate WB with crutches as tolerated
  • Cartilage Procedures / Microfracture – 6 Weeks NWB
  • Capsule Procedures / Plication          – 6 Weeks NWB

 

  1. The incidence of post-op complications are very low, around 0.5% for major complications. Most post-op issues are soft tissue inflammation such as psoas tendinitis.

 

  1. Most patients symptoms tend to flare-up after 3-4 weeks, following hip arthroscopy, when they start weaning off crutches and increasing activity. It is important that patient are informed that it is a very slow process of rehab and loading should be gradual.

 

  1. Hydrotherapy is a very useful adjunct and can be started within 8- 14 days, once the sutures are out and the wound is healed.

 

  1. Exercises such as CLAM and Active SLR are best avoided in this cohort since it irritates the hip flexors and can lead to psoas tendinits which can be very painful and limit rehab progression. (See Sams thoughts on CLAM’s here)

 

  1. Regaining Hip extension is paramount in the initial stage. Manual techniques are best avoided in the first 3-4 weeks. Avoid excessive passive stretches during this period, when the capsule and labrum is vulnerable.

 

  1. Local stability of the small rotators of the hip is encouraged, in the initial stage, along with hip abductor training. Global movement training such as squats, step-ups and dead-lifts are not appropriate in the initial stages.

 

  1. Progression of patients should be criteria based, rather than time based. It is important to have a clear return to play screening process, before returning to contact sports. In this regard, it is similar to ACL rehab.

 

  • Around 82-87% of athletic patients are able to return to playing full sports following hip arthroscopy. The average time is between 6months – 8 months. The sport with the lowest success rate is rowing (not surprising, considering the excessive flexion in the sport)

 

I hope you found this summary of the conference useful and thanks for reading.

Any thoughts/comments very welcome.

 

Ben is MSK Extended Scope Practitioner in the NHS and also in private practice. He has a special interest in lower limb, running injuries and chronic hip and groin conditions. He is passionate about application of research in clinical practice and is involved in regular teaching nationwide on multiple lower limb courses. You can follow ben on Twitter@function2fitnes

Key References

  1. Adler(2015)- Current Concepts in Rehabilitation following Hip Preservation Surgery: Part 2. Sports Health. Published online – July 2015
  2. Agricola(2015)- What is Femoroacetabular Impingement? BJSM, Published Online – June 2015
  3. Bleakley et al (2015)- Hip Joint Pathology as a Leading Cause of Groin Pain in the Sporting Population: A 6-Year Review of 894 Cases
 Am J Sports Med published online May 11, 2015
  4. Elias- Jones et al (2015)- Inflammation and Neovascularization in Hip Impingement. Not just wear and tear. The American Journal of Sports Medicine, Vol. 43, No.8
  5. Frank et al (2015)- Prevalence of Femoroacetabular Impingement Imaging Findings in Asymptomatic Volunteers: A Systematic Review, Arthroscopy, Vol 31, No 6 (June), 2015
  6. Hammoud et al (2014))- The Recognition and Evaluation of Patterns of Compensatory Injury in Patients with Mechanical Hip Pain. Sports Health. Mar/Apr 2014
  7. Mosler(2015)- Which factors differentiate athletes with hip/groin pain from those without? A systematic review with meta-analysis, BJSM, Published online – July 2015
  8. Nepple at al (2015)- What is the association between sports participation and the development of proximal cam deformity? The American Journal of Sports Medicine
  9. Ross et al (2014)- Effect of changes in pelvic Tilt on range of motion to Impingement and radiographic parameters of acetabular Morphologic Characteristics. Am J Sports Med, originally published online July 24, 2014
  10. Zadpoor (2015)- Etiology of Femoroacetabular Impingement in Athletes: A Review of Recent Findings, Sports Med, Published Online: 22 May 2015

 

 

 

“Has the athlete trained enough to return to play safely?” Acute:Chronic workloads and rehabilitation – a guest blog by Jo Clubb

We are delighted to have the excellent Jo Clubb agree to write a blog for us. Admittedly, this blog is a little more high-brow than our usual ramblings, so thanks to Jo for adding some class to our library. Jo has recently broken into the American sports scene, working as a sports scientist with the Buffalo Sabres NHL, bringing with her expertise from her years in football (..soccer) in the UK (previously with Chelsea & more recently with Brighton & Hove Albion FC). What makes this blog extra special to us is that Jo already has an excellent blog page of her own that is read and commended worldwide (Sports Discovery – here). Jo demonstrates how & why sports science plays a massive part in return from injury in professional sport…

Introduction:

Training Stress Balance and the Acute:Chronic Workload Ratio are real buzz words in Sports Science at the moment. They also have important implications for the Physiotherapy and Conditioning communities in terms of rehabilitation and Return To Play.

This concept is derived from Banister’s modelling of human performance back in the 1970s (and then later added to by Busso in the 1990s) that put forward an impulse-response model to predict training load induced changes in performance. If we consider a single block of training, this stimulus will have a temporary negative influence represented as ‘fatigue’ but over a longer time frame will have a positive influence, represented as ‘fitness’. Performance will consequently be a product of the Fitness Fatigue relationship (see Figure 1). Within this theoretical model of Training Theory, it is suggested that with regular training stimuli we can manipulate these processes of fitness and fatigue via training load, recovery and overcompensation, to have a positive influence on performance (see Figure 2).

fig 1

Figure 1: Used with permission from Professor Aaron Coutts

 

fig 2

Figure 2: Used with permission from Professor Aaron Coutts

The Acute:Chronic Workload

Whilst this concept of training stress balance has been cited since these early, groundbreaking days, it has recently been developed into the acute:chronic workload ratio by Tim Gabbett and colleagues, which they suggest is the best practice predictor of training-related injuries (Gabbett, 2015).

It has previously been represented as a % for Training Stress Balance, but the focus now seems to be on utilising it in a ratio form, for example:

= Acute workload / Chronic workload

= 3000 (Au) / 4000 (Au) = 0.75

In this example acute workload is represented as the total load over the previous one week and chronic workload is the average weekly load for the previous four weeks, both utilising an arbitary unit (Au) such as session RPE.

So a ratio below 1, as per the above example, suggests the athlete is more likely to be in a state of “freshness”; their load over the past week has been less than their average weekly load over the past four weeks.

On the other hand a ratio above 1 represents that the workload over the past week has been greater than the average weekly load over the past four weeks, so they may be more likely to be in a state of “fatigue” and potentially less prepared for that workload. Recent research has suggested a ratio greater than 1.5 represents a “spike” in workload that is related to a significantly higher risk of injury (Blanch and Gabbett, 2015 here).

Training and Game Loads and Injury Risk

Tim Gabbett and his colleagues have collected consistent data within the training environment, statistically modelled the relationships between workload and injury risk, applied their model to help reduce injury risk in the training environment and published this data – for me this is the gold standard process of Sports Science and a method we should strive to replicate within each of our own environments. The relationship between workloads and injury risk has included just some of the following research:

  • Running loads and soft tissue injury in rugby league (Gabbett and Ullah, 2012)
  • Training and game loads and injury risk in Australian football (Rogalski et al, 2013; Colby et al, 2014)
  • Pitching workloads and injury risk in youth baseball (Fleisig et al, 2011)
  • Spikes in acute workload and injury risk in elite cricket fast bowlers (Hulin et al, 2014)
  • Acute:chronic workload ratio and injury risk in elite rugby league players (Hulin et al, 2015)

I can talk about this all day (and probably will in a number of other blogs); however the focus of this specific blog is on the application in the rehabilitation environment so I will leave it at that for now. If you do want to read more of this topic, I highly recommend reading the following OPEN ACCESS paper:

The training-injury prevention paradox: should athletes be training smarter and harder? (Gabbett, 2016) Br J Sports Med doi:10.1136/bjsports-2015-095788

 

Rehabilitation

There is plenty of application to this approach in the training environment however; it is just as important in the rehabilitation setting as highlighted in the following paper:

Has the athlete trained enough to return to play safely? The acute:chronic workload ratio permits clinicians to quantify a player’s risk of subsequent injury (Blanch and Gabbett, 2015).

Rehabilitation is without doubt a very complex continuum in which medical staff assist the athlete through early stage rehabilitation to the multifaceted return to train, play and performance decisions, which I have tried to tackle previously (here)  and specifically for hamstring injuries (here). Previous to the paper by Peter Blanch and Tim Gabbett much of the literature on Return to Play failed to acknowledge the consideration of the progression of load in the RTP decision.

Often the evaluation of health status that directly influences the Return To Play decision may incorporate instantaneous physical testing results such as isokinetics or force plate assessment, as well as functional on pitch activity profile targets such as peak speeds, distances, high intensity running and velocity changes. Whilst there is no doubt these have their place, there also needs to be consideration for the loading achieved throughout the rehabilitation continuum in preparation for the acute and chronic loading demands of training and matchplay.

Blanch and Gabbett present a real world example from rugby league (Figure 3) in which a player suffered a hamstring injury after an acute:chronic workload ratio of 1.6 in training week 15. After two low-minimal weeks of high speed running due to the injury, the acute:chronic workload three weeks later spiked to 1.9 (presumably as high speed running was reincorporated into the rehabilitation phase in week 18) and then suffered a reinjury. This example also reminds us to consider which measure(s) of load is most relevant to each sport, injury and individual. High speed running is no doubt important to a hamstring injury but may be of less importance with other sports and injuries. The acute:chronic workload ratio can be applied to any of the variables you collect and may represent a different picture across different metrics.

fig 3

Figure 3: From Blanch and Gabbett (2015), p2.

Rod Whiteley recently gave an excellent presentation at the Aspire Monitoring Training Loads conference entitled “The conditioning-medical paradox: should service teams be working together or as enemies on the training load battlefield?” He applied Tim Gabbett’s work to rehabilitation workloads and related it to the “chronic rehabber”; s/he who never gets to build a consistently high base of chronic workload to prepare themselves for returning to the training environment, so suffers a spike in acute:chronic workload and then a reinjury (Figure 4). He called upon us to “fundamentally rethink how we’re reintroducing the athletes” as well as breaking down the traditional silo structure between medical staff and conditioning staff.

fig 4

Figure 4: Presented by Rod Whiteley, Aspire Monitoring Training Load Conference February 2016

Now we obviously cannot keep athletes away from the training environment forever and nor would we want to. However, it seems avoiding spikes in acute:chronic workloads with returning athletes may help the transition into return to training and competition, and to reduce reinjury risk. This may be achieved via further progressing the load achieved prior to RTP and/or reducing the load from reintegration by using modified training (or a mixture of both). In reality it may not be as simple as that – a major challenge for the Science and Medicine team is to manage expectations of both the athlete and the coaches. I’m sure if the athlete is looking good and undergoing a substantial training load there will be pressure to incorporate them into training.

I believe this paper highlights the need firstly to consider and plan (where possible) the progression of load throughout rehabilitation, end stage and continued into training and games. Whilst the athlete may be physically prepared for the demands of a one off training session, we must also pay attention to the demands in terms of acute and chronic load. It also highlights the need to consider the consequences of each decision relating to loading of the athlete; whether that is the decision to offload the athlete for a day (which may of course be truly necessary based on the clinical presentation) or the decision of how much load to put the athlete through day to day. In another example from the Blanch and Gabbett paper the authors put forward a representation of an injured player’s Return to Play and demonstrate how the variations in load in that week directly influence the likelihood of injury – i.e. 90% acute load would return an 11% likelihood of injury, compared to 120% which would be related to 15% risk.

Whilst injuries are undoubtedly complex, multifaceted and influenced by many factors, and statistical modelling of the risk has its own limitations, it seems the evidence is strong enough to suggest that the interaction of acute and chronic load through rehabilitation and RTP is another piece of the puzzle that is worthwhile considering.

Jo Clubb (@JoClubbSportSci)

 

References

Banister EW & Calvert TW. (1975) A systems model of training for athletic performance. Aust J Sports Med; 7: 57-61.

Blanch P & Gabbett TJ. (2015) Has the athlete trained enough to return to play safely? The acute:chronic workload ratio permits clinicians to quantify a player’s risk of subsequent injury. Br J Sports Med;0:1–5. doi:10.1136/bjsports-2015-095445

Busso T, Hakkinen K, Pakarinen A, et al. (1990) A systems model of training responses and its relationship to hormonal responses in elite weight-lifters. Eur J Appl Physiol; 61: 48-54.

Colby MJ, Dawson B, Heasman J, et al. (2014) Accelerometer and GPS-dervied running loads and injury risk in elite Australian footballers. J Strength Cond Res; 28: 2244-52.

Fleisig GS, Andrews JR, Cutter GR, et al. (2011) Risk of serious injury for young baseball pitchers: a 10-year prospective study. Am J Sports Med; 39: 253-7.

Gabbett, TJ. (2016) The training-injury prevention paradox: should athletes be training smarter and harder? Br J Sports Med doi:10.1136/bjsports-2015-095788

Gabbett TJ & Ullah S. (2012) Relationship between running loads and soft-tissue injury in elite team sport athletes. J Strength Cond Res; 26:953-60.

Hulin BT, Gabbett TJ, Blanch P, et al. (2014) Spikes in acute workload are associated with increased injury risk in elite cricket fast bowlers. Br J Sports Med; 48: 708-12.

Hulin BT, Gabbett TJ, Lawson DW, et al. (2015) The acute:chronic workload ratio predicts injury: high chronic workload may decrease injury risk in elite rugby league players. Br J Sports Med; Published Online First: 28 Oct 2015. doi:10.1136/bjsports-2015-094817doi:10.1136/bjsports-2015-094817

Rogalski B, Dawson B, Heasman J, et al. (2013) Training and game loads and injury risk in elite Australian footballers. J Sci Med Sport; 16: 499-503.

 

Taking your time with acute injuries

One of the benefits of working in sport is that you usually get to see injuries first hand, the mechanism, the severity, even the initial management. We have discussed pitch sidee management before (here) but what about the day, or days, following? Are we doing enough to aid the healing processes in the early stages, or perhaps too much? With our best intentions of helping an injured athlete, are we over looking the importance of “protection”?

This blog discusses the assessment of those more serious injuries – the ones that require athletes to stop in their tracks, cease the game / training. Not those little niggles that walk in at the end of the day.

Reasoning with the history:

Knowledge of the mechanism of injury can greatly aid your management throughout the later stages of your treatment. Muscular injuries for example, can be simply divided into two traumatic categories; direct (laceration and contusion) and indirect (strains) (Huard et al 2002 (here); Petersen & Holmlich 2005 (here)). Appreciating the differences in these mechanisms will certainly influence your return to train criteria later on, but what about in the acute settings? Would your treatment change on day 1 or 2 with these different mechanisms? Skeletal muscles are built of basic structural elements, myofibers. Individual myofibrils are surrounded by the endomysium and bundles of myofibrils are surrounded by the perimysium (Haurd et al 2002). Lower grade injuries such as exercise induced muscle fatigue, will only affect the myofibrils, resulting in raised creatine kinease levels (Ahmad et al 2013 here). Regardless of the mechanism, damage to the fascia and extracellular matrix would be consistent with a higher grade injury and would see the release of muscle enzymes, destruction of collagen and proteoglycans as well as the presence of inflammation (Huard et al 2002; Ahmad et al 2013). The formation of haematomas in combination with inflammation can create an ischaemic environment, increasing the risk of further muscle damage (Ahmad et al 2013).

There seems to be an false sense of urgency created in these acute situations, especially at the elite level where time lost to injury means big money and with that brings an extra level of stress and pressure to the therapist, the athlete & the coach. But the injury has happened.. we can’t change that! We can certainly make it worse though. What are we expecting to find and see with our immediate objective tests? Lets say we have just seen someone recoil, fall to the floor clutching their hamstring, unable to walk off the field of play.. is a straight leg raise or resisted knee flexion test going to tell us something we didn’t already know? OK, so maybe we want to give all parties an idea of how bad this is.

“Do you think its grade one or two?” 

“Yes?”

There are numerous injury classification systems currently used in practice, although traditional classifications can be confusing. Ahmad et al (2013) describe 3 grades of injury from mild to severe, with one set of definitions relating to clinical presentation but with differing definitions depending on the influence of Magnetic Resonance Imaging (MRI). When I was training, we used the Gr I, II & III system that was disseminated by Peetrons in 2002 (here). In 2012, the Munich consensus group (paper here) sought to clarify the term “strain” and provide a structured classification system for clinicians. Table 1 is an overview of the existing classification systems pre-2012 that are widely used in the literature as well as clinical practice.

O’Donoghue 1962 Ryan 1969 (initially for quadriceps) Takebayashi 1995, Peetrons 2002 (Ultrasound-based) Stoller 2007 (MRI-based)
Grade I No appreciable tissue tearing, no loss of function or strength, only a low-grade inflammatory response Tear of a few muscle fibres, fascia remaining intact No abnormalities or diffuse bleeding with/without focal fibre rupture less than 5% of the muscle involved MRI-negative=0% structural damage. Hyperintense oedema with or without hemorrhage
Grade II Tissue damage, strength of the musculotendinous unit reduced, some residual function Tear of a moderate number of fibres, fascia remaining intact Partial rupture: focal fibre rupture more than 5% of the muscle involved with/without fascial injury MRI-positive with tearing up to 50% of the muscle fibres. Possible hyperintense focal defect and partial retraction of muscle fibres
Grade III Complete tear of musculotendinous unit, complete loss of function Tear of many fibres with partial tearing of the fascia Complete muscle rupture with retraction, fascial injury Muscle rupture=100% structural damage. Complete tearing with or without muscle retraction
Grade IV X Complete tear of the muscle and fascia of the muscle–tendon unit X X
Table 1: Descriptions of muscle classification systems used clinically From Mueller-Wohlfahrt et al (2012)

The Munich consensus established that there was disparaging definitions amongst clinicians regarding the term “strain” and also the classification of injury. The rise of imaging to support clinical findings further added to the confusion of defining a Grade I injury that may not be present on MRI. Amongst many irregularities with the classification systems in Table 1, there was the vague nature of defining when one grade becomes another. As a result, Mueller-Wohlfahrt et al (2012) produced a new classification system that included delayed onset muscle soreness (DOMS) & contusions and allowed clinicians greater manoeuvrability in diagnosing muscle injuries. In 2014, this was taken a step further by Noel Pollock and colleagues at  British Athletics (paper here) (he explains why much better than I could, here on this BJSM podcast).

“If you can’t help them, at least don’t hurt them” – Dalai Lama

dalai4601
I’m pretty sure he just referenced the Dalai Lama…

So with all this confusion regarding classification ,what are we supposed to say to the athlete and what are we to do? Things always look bad in the initial stages. Generally if there is pain on the way to the treatment room (if they have stopped playing, then there almost certainly will be) how much more do you need to know? This is where the mechanism & history is key. It may be required to rule out any bony injury at this stage, but again, if you have seen them pull up and clutch a muscle belly then that may not be essential – a bonus of being pitch side to observe such things. What about ligamentous injuries? Well do we need to assess instability today? Is there a chance that we could make something that is stable unstable by repeatedly testing it in the early stages? Even if we think its severe, like a complete ACL, most surgeons won’t operate while there is active swelling anyway. Some specific injuries DO require this, hand injuries for example may require more immediate attention from an orthopedic surgeon. Or total syndesmosis ruptures that usually require an operation within 2 weeks. (A good discussion on this injury was had recently by the PT Inquest guys here)

In the very acute stages (I’m talking first day or two) our role is to help reduce and minimize pain, reduce risk of secondary injury and ensure the athlete is safe to mobilize at home independently. What do we gain by giving them a classification of injury there and then?

“Lets let the swelling and pain settle down, get you comfortable and in a day or two we will be able to be more accurate with our assessment and diagnosis” – I think thats a pretty reasonable thing to say on the day of an injury and I’m yet to have any complaints from athletes, providing you explain why you are doing this. I’m not going to expose myself to sensitivity and specificity of tests because I will undoubtedly get it wrong, but in the heat of the moment, when everything hurts, you will almost certainly find false positives in tests – resulting in inaccurate diagnosis.

32619_sponge_bob_todo_list_nothing

I’ll admit, this takes a bit of confidence. When the treatment room is full of staff, other athletes, the injured athlete themselves. To stand there and hardly do anything seems counter intuitive. But take a breath and ask yourself, “what do I NEED to know at this very moment?” It shouldn’t be, “What tests do I know that I could use here” – these two questions are very subtly different but the actions that follow them are huge. You aren’t there to show the room what assessment skills you have, not on day one. Respect the injury.

The next couple of days can also tell you a lot of information without you needing to pull and prod on the table. Whats the 24 hour pattern of pain? Any sign of inflammation? Yes? Then whats a prolonged assessment going to do other than promote more inflammation. Check Aggravating / easing factors or limiting ADLs – getting on and off the toilet seat without excruciating pain may be enough info that you don’t need to assess a squat today. Again, be comfortable treating what you do know, treat the inflammation and the pain. When that settles, we can begin to explore a bit more specifically. Will a positive test today get them back to training quicker? No.

What about treatments?

The classic PRICE guidelines have now been superseded by the POLICE (Protect, Optimal Loading, Ice, Compression, Elevation) guidelines (here). I’ve previously debated the clinical relevance of ice here and regular readers of this blog (mum and my mate Conor) are probably familiar with my interest in Optimal Loading. Regardless of if you use PRICE or POLICE, one thing we seem to overlook is the very first letter. Protect. Protect the injury from secondary damage and unnecessary pain. This may mean not doing very much at all. Consider the nociceptive input of us repeatedly prodding the injury, whether its part of assessment or treatment. Again, we go back to the pressures of sport – to have an athlete sat there doing nothing can be uncomfortable for the staff and boring for the athlete. This is where the creativity of “optimal loading” comes in handy. Protect the injury, keep the rest of the athlete busy.

Summary

I’m not suggesting we just sit and wait for weeks hoping they get better on their own, but just try and think about why you want to assess something and how is that answer going to influence your management on this day. I appreciate that objective measures are going to be beneficial, but just take the ones you need. Now obviously, if symptoms drastically improve over night, we can be a bit more direct with our assessment. It’s here we can start to expand our objective measures.

  • Don’t rush to a diagnosis or classification (have the differentials in the back of your mind or discuss them with colleagues / club doctors)
  • Don’t over assess for the sake of it (do enough to keep the athlete safe but minimize effects of injury)
  • Don’t over treat (sometimes, less is more!)

 

Remember, this isn’t aimed at those little niggly injuries that DO warrant further assessment – in these cases a thorough assessment may actually help reduce the risk of a full blown injury. Instead, this is for those injuries that you know in the back of your mind are out for a few days / weeks. If anything, the more severe (duration) the injury, the less acute assessment required perhaps? Just remember to exclude all those nasties!!

I appreciate I’ve probably given more questions than answers in this blog, but that was the aim. This wasn’t supposed to be a recipe but has hopefully sparked some questions about your clinical reasoning.

 

Yours in sport,

Sam

 

 

 

Laboring through a Labral Tear

One skill when working in sport is learning to compromise between your clinical brain (the one that tells you that pathology and injury needs to be managed a certain way) and your performance brain (which tells you that your job is to get athletes back over the “white line” in order to do their job). In an ideal world, we try and appease both of these brains where tissues heal well and performance is optimised with the lowest risk of re-injury. But there are some pathologies that cause these two brains to clash. Ones that can be “managed” until the off season where proper interventions can take place. One such injury that I’ve been trying to learn more about is the mid-season hip labral tear.

labral-tear-img

The purpose of these blogs is to encourage me to read more around certain topics, so in order to help with this I have to say thanks to a few people that have provided me with papers and words of wisdom (Erik Meira, Nigel Tilley & Joe Collins). And thanks to whoever invented Twitter because I probably wouldn’t have this access to knowledge otherwise.

The Problem..

Typically, hip instability injuries are seen in sports with high repetitions of rotational and axial load – football, gymnastics, hockey, tennis, martial arts.. and so on. The hip is widely accepted as being one of the most structurally stable joints in the body, with a deep acetabular socket lined by the labrum, which creates negative pressure within the joint to increase congruency of the femoral head. But what happens when this environment is disrupted? A recent review by Kalisvaart & Safran (here) explain that it takes 60% less force to distract the femoral head from the acetabulum in presence of a labral tear. (This review is great for explaining multiple causes of hip instability, not just labral tears, and also assessment techniques.)

Typically, a lack of stability is replaced by rigidity, where the surrounding soft tissues try to compensate for this increased translation (Shu & safran 2011 here and Boykin et al 2011 here). On assessment of an ongoing labral tear, its quite common to find increased tone or reduced range around adductors and hip flexors. Iliopsoas in particular plays a role to help increase congruency in the hip. (For tips on how to release iliopsoas, please tweet @Adammeakins) – one key thing when managing this condition is not to confuse high tone / over activity with being “too strong”. Chances are its the opposite, it more likely indicates a lack of control. Its not uncommon to see adductor tendinopathies secondary to labral tears as the the load around the joint increases – especially in sports like ice hockey where there is high eccentric load on the adductors (Delmore et al 2014 here).

The Intervention..

So, you’ve diagnosed the tear (clinically and / or radiographically) but other than being irritable, it isn’t affecting the athlete. (Note, not all tears can be managed conservatively, due to pain & some require mid-season surgical intervention – Philippon et al 2010 here). The key premise to your ongoing rehab should be to make the hip joint as robust as possible. Remember, “Stability – not rigidity”. Whats the difference? Can the athlete control the hip or pelvis while performing another task? Or do they lock into a position and rely on passive structures like ligaments and joints.

Consider the demands of the sport. Don’t just fall into the trap of working through what I’d call the “action man ranges” – true anatomical flexion, extension, abduction and adduction. Watch training and competitions of nearly all sports and you’ll rarely see these truly sagittal or coronal movements. They tend to be combinations accompanied by transverse movements of the body in relation to the limb. Make sure this is replicated in your rehab.

Using the three examples above, consider the role of the hip musculature throughout these movements. We don’t always have to replicate abduction in an open chain movement, sometimes its necessary for it to be closed chain and for the body to move relative to the limb. Note how none of these tasks fit the “action man ranges” but all involve some degree of traverse rotation, combined flexion and abduction or extension and adduction etc etc.

man4
No I can’t bench press, but my squats are awful.
Delmore et al (here) and Serner et al 2013 (here) describe some excellent exercise interventions for the adductors here. These include some good low-load isometrics for those early stage reactive tendons – with isometrics appearing to down-regulate pain associated with this acute pathology (Koltyn et al 2007 here; Rio et al 2015 here to name just two resources) . Moving forward through rehab, I’ve discussed exercise progression at length before (here), I’m not dismissing exercises that involve pure flexion, extension etc but as part of a progression, its important to combine these movements. For example, start with a single leg dead lift – can the athlete control their trunk through hip flexion and through extension back to neutral? No? Then here’s a range to work on, using regressions to help improve technique and control. Yes? Then add a rotational component at different ranges of flexion – rotation away from the standing leg will increase the demand on the adductors to control the pelvis in outer ranges. The leg itself hasn’t abducted, but relative to the trunk it is hip abduction.

Remember the bigger picture

Its important not to just focus on the affected structures. For those interested in groin pain, a summary of the 1st world conference on groin pain is here – one key message from that conference was that anatomical attachments are not as discrete as text books make them. Consider what else contributes to the hip and pelvis control. We have mentioned iliopsoas control, but also rectus abdominus. Its not just a beach muscle. Eccentric sit ups can help improve control of the hip flexors, along with some lower load exercises like dead bug regressions – a little imagination or some quick youtube research can turn this one concept into hundreds of different exercises.

We have addressed the issue of controlling abduction through range with the adductors, but also remember to maintain that abduction-adduction ratio with some external rotator & abductor muscle exercises (queue Clam rant here – clams to me are like psoas release to Meakins). Possibly the best piece of advice I was given when doing this research was from Joe Collins, who told me to consider hip joint pathologies like you would a rotator cuff injury in the shoulder. Don’t neglect those smaller, intrinsic muscles around the hip. The exercise below is an anti-rotation exercise working through ranges of hip abduction-adduction.

The athlete is tasked to resist the rotation of the femur into external rotation while slowly moving through hip abduction and back to adduction. (This example is done with a shorter lever to improve control and the bench provides feedback to keep the hips in neutral or extension, rather than the favored flexion). Anti-rotation exercises can also be incorporated into trunk / core control exercises (for any instagrammers – follow ETPI who post some great videos and snaps of golfers working on rotational control). Progress from anti-rotation into control through rotation. Some examples here:

anti-rotation plank with sagittal control

Anti-rotation plank with traverse control. Encourage the athlete to keep the pelvis still when moving the upper limb.

photo 4

Single leg bridge with arm fall outs. Can be regressed to a normal bridge if the athlete lacks lumbo-pelvic control.

Side plank with arm tucks – an example of controlled trunk rotation while isolating the lower body to stay stable. Can be combined with the adductor bridge mentioned in Serners paper to increase load through proximal adductors.

 

These are just some ideas of how to manage a labral tear mid-season; working on rotational control, analgesia via isometrics, improving congruency in the hip joint and overall hip stability via strengthening – Stability, not rigidity! The exercises mentioned here are by no means an exclusive list and I love learning about new drills and ideas, so please share any that you find useful.

 

Your in Sport,

Sam