Sports

Why and How Exercise is the Best Treatment for Tendinopathy

Tendinopathy (pathology and pain in a tendon) is a prevalent injury in athletes

and is very common in the competition season when loads are high. Treating
tendinopathy, especially in season, can be very frustrating due to typically poor
responses to intervention.

Mechanotransduction is an intervention model that refers to the process by which

the body converts mechanical loading into cellular responses. These cellular
responses, in turn, promote structural change in tendon, muscle, cartilage and
bone.

Understanding how tendinopathy develops, and how this affects clinical

assessment and treatment is critical to improving outcomes for the athlete. The
role of exercise is often underestimated despite evidence that supports its use in
tendinopathy. There is good physiological, research and clinical support for
physical therapists having a leading role in the management of tendinopathy.

The session will cover the pathoaetiology of tendinopathy, identifying stages of

tendinopathy and how mechanotransduction through exercise helps tendon
recovery.

Course Objectives: Upon completion of this course, course participants will be

able to:
a. Define mechanotransduction.
b. Define the stages of tendinopathy.
c. Describe how mechanotransduction through exercise helps tendon
recovery.
d. Describe the effect of load on various tendons, and the evidence for
“unloading” these tendons.

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Outline: time and content

I. Introduction

II. Introduction of Mechanotransduction, pathoaetiology of tendinopathy, and

identifying stages of tendinopathy

III. Description of how mechanotransduction through exercise helps tendon recovery

in various lower extremity tendons in the human body.

Discussion on the following topics:

1. How the various type and amount of load can influence tendon response

2. How to modify exercise to achieve the best outcome

3. How to amend load for the different pathoaetiology stages

Question and Answer

Jill Cook, PT, PhD

Professor
La Trobe University School of Allied Health

Karim Khan, MD, PhD, FACSM

Professor
Deputy Director, University of British Columbia (Centre for Hip Health and Mobility)

Michael P. Reiman, PT, DPT, OCS, SCS, ATC, FAAOMPT, CSCS.

Assistant Professor
Division of Physical Therapy
Duke University Medical Center, Durham, NC.

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Jill Cook, PT, PhD

Professor Jill Cook, physiotherapist, PhD, is a Professor in musculoskeletal health in the

La Trobe University School of Allied Health in Australia. Jill’s research areas include
sports medicine and tendon injury. After completing her PhD in 2000, she has
investigated tendon pathology, treatment options and risk factors for tendon injury. Jill
currently supplements her research by conducting a specialist tendon practice and by
lecturing and presenting workshops both in Australia and overseas.

Jill has been awarded numerous professional and research awards, including multiple
“best paper” of the conference awards at several prestigious national conferences. She
has over 175 peer reviewed publications, serves as deputy editor of the British Journal
of Sports Medicine, and is a member of the High Performance Commission for
Basketball Australia.

Karim Khan, MD, PhD, FACSM

Professor Karim Khan, MD, PhD, FACSM, is a Canadian sports physician and
academic who played a role in the paradigm shift that ‘tendinopathies’ are not
inflammatory conditions. Although that paradigm remains under scrutiny, the research
helped provide a strong rationale for physical therapy treatment of these conditions
rather than NSAIDs. His paper “Mechanotherapy: how physical therapists' prescription
of exercise promotes tissue repair” (2009) has been downloaded > 50,000 times and
cited > 100 times. It provides a rationale for physical therapy treatment across
conditions – tendon, muscle, ligament, bone and joint.

He is a founding investigator and Deputy Director of the $40 million research enterprise
at the University of British Columbia called the Centre for Hip Health and Mobility. In
2015 he is on leave from UBC to head up the Research & Education Department at
Aspetar, Qatar Orthopaedic and Sports Medicine Hospital, one of only 9 IOC research
centres world-wide.

Karim is in his 8th year as Editor-in-Chief of the British Journal of Sports Medicine which
has very strong Physical Therapy focus. He is also an author of Brukner & Khan’s
Clinical Sports Medicine (currently in 4th edition).

Michael P. Reiman, PT, DPT, OCS, SCS, ATC, FAAOMPT, CSCS (Moderator)
Mike is an assistant professor of physical therapy at Duke University Medical Center. As
a clinician Dr. Reiman has over 20 years of experience in assessing, rehabilitating, and
training clients at various levels of ability. He received his doctoral degree in physical
therapy from MGH Institute of Health Professions. In addition to his certifications as an
athletic trainer and strength and conditioning specialist, Dr. Reiman is a manual therapy
fellow through the American Academy of Orthopaedic and Manual Physical Therapists,
a USA Weightlifting level 1 coach, and a USA Track and Field level 1 coach. Dr.

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Reiman has co-written the only textbook on functional testing, Functional Testing in
Human Performance, written over 10 book chapters on orthopedic
examination/intervention and training. He has also written over 40 peer-reviewed
articles Dr. Reiman currently serves on the editorial board, and is a reviewer for,
multiple orthopedic and sports related journals. Dr. Reiman presents on and researches
various areas of assessment and treatment methods in orthopaedic and sports
medicine. He is the current Sports Section Hip SIG Chair for the APTA. He continues
to practice clinically on various sports and orthopedic-related injuries. He is a member of
the American Physical Therapy Association, National Athletic Trainers’ Association,
National Strength and Conditioning Association, USA Weightlifting Association, and
USA Track and Field Association.

Bibliographic References:

1) Cook JL, Purdam CR. The challenge of managing tendinopathy in competing

athletes. Br. J. Sports Med. May 10 2013.

2) Cook JL, Purdam CR. Is tendon pathology a continuum? A pathology model

to explain the clinical presentation of load-induced tendinopathy. Br. J. Sports
Med. Jun 2009;43(6):409-416.

3) Cook JL, Purdam C. Is compressive load a factor in the development of

tendinopathy? Br. J. Sports Med. Mar 2012;46(3):163-168.

4) Scott A, Docking S, Vicenzino B, et al. Sports and exercise-related

tendinopathies: a review of selected topical issues by participants of the
second International Scientific Tendinopathy Symposium (ISTS) Vancouver
2012. Br. J. Sports Med. Jun 2013;47(9):536-544.

5) Wearing SC, Smeathers JE, Hooper SL, Locke S, Purdam C, Cook JL. The
time course of in vivo recovery of transverse strain in high-stress tendons
following exercise. Br. J. Sports Med. Mar 2014;48(5):383-387.

6) Khan KM, Scott A. Mechanotherapy: how physical therapists' prescription of

exercise promotes tissue repair. Br. J. Sports Med. Apr 2009;43(4):247-252.

7) Scott A, Khan KM, Duronio V, Hart DA. Mechanotransduction in human bone:

in vitro cellular physiology that underpins bone changes with exercise. Sports
Med. 2008;38(2):139-160.

8) Scott A, Huisman E, Khan K. Conservative treatment of chronic Achilles

tendinopathy. CMAJ. Jul 12 2011;183(10):1159-1165.

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Disclosures
• No disclosures
Why and how exercise is the
best treatment for tendinopathy
J Cook
La Trobe University

Tendons
1. Patho-aetiology
2. Tendon load
3. Structure, function and pain
4. Management of tendinopathy
1. How does tendon pathology develop?

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Pathology of tendinopathy Sequence of pathological changes

• Normal tendon • Abnormal tendon

• Regular collagen fibres • Disorganised & altered

• Inconspicuous ground collagen
substance • Type III
• Spindle shaped • Abundant ground
tenocytes substance
• Minimal vascularity & • Activated cells &
nerves hypercellular
• Increased vessels &
nerves

Ultrasound imaging
Normal tendon

Cells activated and increased

Reactive tendinopathy proteoglycans increased

+
Matrix disruption by increased
Tendon dysrepair PGs, Opportunity for vascular
ingrowth

+
Cell death can occur, islands of
matrix degeneration,
Degenerative tendinopathy neovascularisation

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Mechanically compromised
tendon
Optimised
Unloaded Optimised
load
Load
Normal
or excessive Normal tendon Adaptation
load +/- individual Excessive
factors Appropriate Strengthen
load + individual
modified
factors
load

Reactive tendinopathy

Tendon dysrepair

Degenerative tendinopathy Degenerative tendinopathy

Reactive on degenerative tendinopathy Reactive on degenerative tendinopathy

Is there evidence of transition along the continuum? Clinical classification of pathology

• 2 stages are clinically relevant
Normal Reactive Degenerative • 1. Reactive, early dysrepair where the pathology is reversible
• Late dysrepair/ degenerative where the pathology is not reversible

Normal 226 58 5
• Remember that not ALL the tendon has pathology
.78 .2 .02
Start of • Can have islands of pathology amongst normal tendon
season
Reactive 35 72 26
.26 .54 .2 But these stages do not fully explain all presentations
Degenerative 4 25 129
.02 .16 .82

End of season
Malliaras et al 2009

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What about the commonest clinical What is the second commonest clinical
presentation?
•A person presenting with increase in pain is most likely to be
presentation?
Your best player
a degenerative who
lesion with some has occasional
reactive aspects
• Reactive after unloading Mechanically weaker

•What causes • Unloading decreases tendon

patellar tendon pain trains
a degenerative tendonmuch harder
to become reactive?
tendon mechanical
•Mismatch between load tolerance and capacity of the
than normal properties and tendon
tendon andand then
the load hobbles
placed on it in for capacity to tolerate load
Normal
or excessive
•Degenerative
treatment a coupletendonof hasdays later
poor load tolerance • Present after a period of
load +/-
individual
factors
time off
• Injury, off-season
• Return to loading at Reactive tendinopathy
Normal tendon Reactive tendon previous levels
• Tendon reacts to load
Degenerative area
Degenerative area

Clinical presentation Treatment based on the continuum

• Reactive • Reactive on • Degenerative
• Younger (15-25yrs) degenerative • Older (30-60yrs)
• Reactive tendons
• Rapid onset generally – Older adult (40- • Long history of • Reactive and reactive on degenerative
related to load 60+yrs) minimal • Leave them alone
• Load substantially – Past history with symptoms
exceeds tendon’s • Take away abusive load
previous exposure load related • Variable swelling • Use loads that are tolerable or helpful
exacerbations and lumps/bumps
• Fusiform swelling of • Nothing to further irritate the tendon
tendon 3-4cm – Onset after • Often exhibit
overload unloading • Frictions, eccentrics, injections, needling
• Easily aggravated by
exercise, slow to – Variable swelling strategies or • Degenerative tendons
settle – Less irritable atrophy
• Strengthen the normal part of the tendon
NOT PAINFUL
• Strengthen the kinetic chain
PAINFUL PAINFUL COMMON • Tendon, muscle and brain
UNCOMMON VERY COMMON NOT SEEN
CLINICALLY

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Questions

2. How do tendons
respond to load?

What sort of loads are placed on tendons?
• Depends on what sort of load
• Tensile
• Maintains fibrous tissue
• Compressive
• Forms/maintains cartilage
What sort of loads are placed on tendons?
• The type of load depends on where in the tendon
• Mid tendon
• Achilles is the only tendon to fail in the midsubstance
• Not hypovascular
• Tensile load
• Insertion
• Not commonly where tendon inserts, but just proximal to it

• Friction/shear • Compressive load

• Peritendon
• Posterior gliding membranes and anterior fat structures
• Combination • Complex and multifunctional
• Mechanoreceptive, nociceptive structures and macrophages Shaw et al 07
• Forms maintain bone • Friction

Ingber

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What is the highest tensile load for tendon? Combination loads induce tendinopathy
• Rat model - three groups
• Tensile overload, compression only,
• Eccentrics compression and tensile overload
• Injury worst in the tensile and
• Heavy weights compression rats
• Stretching • Next tensile overload
• Energy storage and release • Compression minimal effect by
itself
• Soslowsky et al 2002

What tendons does compressive load have a

Where is compression a problem? role in tendinopathy?
• At the bony fulcrum prior to the Most of the problem ones!
insertion • Achilles insertion
• Tendon inserts over a bony prominence
• Gluteus medius/minimus
• Reduces stress on the insertions
• Confers mechanical advantage • Supraspinatus
• Adductor longus
• This is where the compression and • Hamstring (upper)
pathology occurs
• Tibialis posterior
• Remember that this will really be a • At malleolus
combination load • Peroneals
• Compression and tensile load • Quadriceps
• =shear loads • Femoral condyle in deep knee
• Stretching not good for tendon insertions flexion

Rufai et al 95

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What about compression in other areas?

What affects the peri-tendinous tissues?
• Plantaris may be invaginated within
Achilles or separate
• Stiffer than TA • Excess movement between
• Well-localised medial achilles pain on the tendon and surrounding
load structures
• Tendons that don’t have
much movement don’t have
• Posterior retinaculum complex peritendon tissue
• Pain on plantar flexion • Peroneals compared with
patellar tendon

What about rest? Questions

• Catabolic to tendon • The strength of any tissue will
• Tendon tissue turns to mush only be as great as the load
• Becomes pathological placed on it
• Musculotendinous strength drops • Decrease the load=decrease the
• Mechanical strength of tendon tissue capacity
decreases in 2 weeks
• Return to high load after rest
• Kinetic chain function deteriorates • Tissue failure
• Anti-gravity muscles
• Motor drive changes
• Luckily our brains don’t turn to mush
as well

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3. What is the relationship between structure,

Structure, function and pain
function and pain?
• Is structure important?
• Is pain important?
• Is function important?
Poor Pathology/ • Does importance differ between clinicians and patients?
Pain
function poor structure • Patients want no pain but they are surprisingly interested in structure
• Clinicians want good structure and of course pain
• So who cares about function?

Structure is complex Tendons are smart

• Degenerative tendon is highly

viable tissue
• It is HYPER-cellular
• It is HYPER-metabolic because it is
hyper-cellular
• It makes and degrades proteins at a
hysterical rate
• 25x higher turnover
• Leaves the debris in the matrix
• Type II and III collagen
• Large PGs

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So what do we do about degenerative

pathology?
Tendons are smart Nothing!
• Degenerative tendon is highly viable tissue - Normal tendon
Normal Pathological
Just not functional
• It is mechanically indolent Achilles tendon

• Cannot respond or transmit load AP diameter (mm) 6.5 ± 0.5 8.4 ± 1.5
• Therefore cannot change mCSA of poor structure( mm2) 1.4 ± 1.4 4.7 ± 8.3

• No collagen structure mCSA of good structure (mm2) 80.8 ± 15.8 94.8 ± 26.5
Pathological tendon
• Limited type 1 collagen
Patellar tendon
• No cell-cell communication AP diameter (mm) 6.0 ± 0.6 7.8 ± 2.6
• Therefore not able to respond to load mCSA of poor structure (mm2) 4.5 ± 3.4 17.1 ± 22.3

mCSA of good structure (mm2) 125.9 ± 11.7 139.9 ± 23.1

Docking and Cook 15

What do we do about degenerative Function is what we do

pathology?
• Restoration of full painfree • Restoration of painfree capacity in
function the tendon
• Regenerative therapies for • Able to tolerate the highest load on • No evidence that tendon adapts
tendon pathology are not the tendon structurally after early adulthood
necessary • Energy storage and release • Adapts mechanically
• Identify (the very few) • Able to tolerate loads other than • Where is unknown
tendons that may need tensile
adjuncts • Compression

• Docking and Cook 15

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What does pain do to function? Structure, pain, function interaction

Unloaded tendon with low
capacity (older person, post-
• Completely destroys the kinetic chain injury), susceptible to overload
Pathology and pain with loss of
function
• Athletes will say “ I can play with back pain, a sprained ankle or a fractured and pathology and pain
finger but I cannot play with this”
• Tendon pain takes away everything that makes the athlete good at their sport
• They are usually power athletes Poor function
Pain Pathology
• Ask them what they are good at and they will tell you that they can jump and change
direction well

Degenerative non painful tendon, can

Imaging normal painful tendon, rare, rupture
differential diagnosis

So how do we change pain? My take on it

• If you hop like a duck it does
• Changing structure is not the answer not matter what intervention
• Resting will give short term improvement you do to structure and pain
• Issue is that it decreases MSK capacity especially muscle AND tendon capacity you still hop like a duck
• Whole unit and kinetic chain becomes less load tolerant
• Fine until they return to load and then they are usually worse
• AND
• If you hop like a duck the
capacity of your tendon and
• An athlete with poor function will always have pain kinetic chain is poor
• An athlete with good function is protected from pain • THEN
Therefore
• You will always have tendon
• Improvement in function will nearly always improve pain pain unless you change it

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Tendon pain - the tendon Criteria for Classification of Central Sensitisation Pain
• Review by 18 pain experts across 7 countries
• Tendon pain is • Centrally driven pain entails:
• Aggravated by load • Exclusion of neuropathic pain
• Eased by unloading • No history of C/PNS disease, No evidence of C/PNS damage
• Therefore there is an unknown but existant nociceptive driver • No medical cause for the pain established

• Continuum model will say the cell • Disproportionate pain/disability to the pathology
• Presence of diffuse pain distribution, allodynia, hyperalgesia
• Separation of cell from peripheral nerves makes pain more variable
• Nerves are mostly peritendon and at junctions • Hypersensitivity of unrelated senses
• Cold, heat, stress, emotions, environment (light, sound, smell, food/chemical substances
• But what about the brain?
• Additional signs
• Motor and sensory change consistent with nociception • Phantom swelling or stiffness, altered perception of body part, cognitive deficits…
• No evidence of centrally driven pain

Nijs J et al Pain Physician 2014

Tendon pain – motor drive Tendon pain - Motor inhibition

• Recruitment curves for those
with tendinopathy were C o n tro l
• People with PT have HUGE
M E P a m p litu d e ( % o f M M A X )

completely different
60 † amounts of motor inhibition
*
• Changes in tendon pain are
PT
• Slope of the curve related to 40

the length of time of similar to...

symptoms 20
Stroke!
• Those with patellofemoral • Increased excitability and
pain had a normal curve drive and corresponding
-2 0 0 20 40
% S tim u la to r O u tp u t hypo-excitability and
inhibition other side
• RIO ET AL
• RIO ET AL
44

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So what does this mean for our athletes with

Questions?
tendinopathy?
• People with PT are like learner
drivers
• Increased excitability
• Huge amounts of inhibition!!!
• That they have all their motor
cortex on
• They moderate output by
subsequent inhibition
• Likely to be less effective, less
precise, harder work

4. Management Management and rehabilitation

• Unload the tendon (from high tendon load)
• Manage training loads
• Kinetic chain interventions
• Medical management as required
• Exercises to reduce pain
• Loaded isometrics
• Address co-morbidities
• Progress loading back to functional requirements
• Power, elastic function
• Graduated RTS
• Maintenance

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Dependent on the tendon,

How do we improve function? the activity and the person

• Determine the start point

• Determine the end point
• Work from the start to the end
• In VERY small steps because tendons are sensitive to change
• Work from strength through power to energy storage
• Build in endurance and compression

• We nearly always need good energy storage capacity

• Exception older people with low level function
• Those who play golf or walk for exercise
• Remember that the Achilles is still energy storing at these low levels of function
• Nearly always need to be rehabilitated back to this level

Phase one: Isometrics to reduce pain

Indications Implementation
Pain Build up
Play football 45 seconds X 5
Needs endurance • Reactive
2-3 x a day
Speed • Reactive on degen
Repeated loading Think “panadol”
High energy storage 2 mins rest between is important

Poor strength Achilles tendon

Muscle wasting
Poor endurance
Pain with energy storage
loads

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How we use it in tendons Isometrics

• Sustained contraction
• Away from compression • Isometric exercise
• Short tendon length
• Often have no or little pain immediately and persistently
• Heavy loads relieves tendon pain
• Needs to be machine based is possible
• Don’t be shy with load
• Reduces stronger cortical
• Avoid exercise that requires postural inhibition and therefore Figure 2 Pain reduction on the single leg decline squat
control makes athletes 19%! with isometric and isotonic exercise for patellar
tendon
• Seated or lying
• If standing, good support
• Do 3-4 times a day if needed
• 40-60 sec holds, 4-5 times
• Immediate and sustained pain relief
• Suggests a cortical response rather than a
tissue-based one

Can we justify the use of isometrics at a tissue

level? Phase two: strength (isotonic)
Indications Implementation Considerations
• On the background of reactive tendon Pain is stable on 4 X 6-8 • Avoid compressive loads
• Cells are activated and producing excess proteins morning test Slow • Avoid speed
• Mechanotransduction is real!
• Complex mechano electrochemical sensory system
Pain is settled from Heavy • Encourage evening to
• Cells are integrally connected to the matrix peak Single leg avoid calf fatigue during
• Connections through proteoglycans and integrins with connection through to the cell nucleus day
• Alter gene expression in response to mechanical load
• Cells can detect and respond to movement
• Through cilia and integrins
Examples - weighted calf raises (conc / ecc), seated calf raise
• Lavorgnino 10, 11 • Kinetic chain
• So attempt to load the tendon without stimulating cell through matrix • Address deficits
• Add functional exercises
movement • Once weights are good
• Add endurance

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Phase three: energy storage Patellar tendon tensile load and loading rate
in typical activities.
Indications Implementation Considerations
100
Pain is stable on morning Every 2-3 days & assess Add / change one thing at a
test (may not be zero) response time 80

Symmetry in mm bulk? Must keep strength Break up absorption and 60

Loading rate Bwsec-1
This may takes a long time going propulsion phase early, add Tensile load BW
40
these together later in Phase
Good strength eg 25 raises Consider as much a 3. 20

single leg, 1.5 X BW on leg neural reprogramming as

press, addressed deficits muscle/tendon function 0

leg press 3times BW

land from jump

land in a stop jump sequence

• Faster stairs, split squats, skipping

Reeves 2003, Janssen 2013, Edwards 2012

Phase four: sports specific/elastic function

Indications
Pain stable on morning
test (may not be zero)
Good strength eg 25
raises single leg, 1.5 X
BW on leg press,
addressed deficits
Dealing with power
• Duration, frequency, change direction, speed
Weekly planning
Implementation Considerations
Every 2-3 days & Add / change one thing at a • Stage 1
assess response time • 2X daily sessions of isometrics
• Stage 2
Must keep strength Don’t add load & speed • Alternate strength and endurance
going together • Do isometrics before strength
• Add functional strength exercises
May mix Phase 3 and 4 exs
• Stages 3 and 4
• Only 2-3 days a week high tendon load
Consider tendon capacity • 2-3 days a week maintain strength (and isometrics) and endurance

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The wheel of tendons

Pain monitoring
• 24 hour behaviour is guide Injections
to tendon load and Pain XXXXX 5% Medications
overload on a day to day Load 10%
basis Guru juice
3%
• How it feels today reflects Load capacity/load
the response to the load Pain √ tolerance Massage
yesterday 5%
70% of short and
• As load increases over a long term recovery
program pain should Pain √√ Electrotherapy
decrease 1%
• Addition of speed and
Ice
energy storage and Taping, bracing 1%
compression can increase 5%
symptoms
• Monitor closely

What doesn’t help? Summary

• High load exercises 1. Patho-aetiology
• Too little recovery Critical to stage a tendon clinically

• Eccentric exercise 2. Tendon load

Understand and manage all loads affecting tendons positiverly and negatively
• Ultrasound
3. Structure, function and pain
• Frictions Complex interactions that must be understood clinically
• Any passive therapy
VISA score after 12 weeks

100
90
80
4. Management of tendinopathy
• ECSWT??
70
60
Patience and attention to detail
VISA

50
40
30
20
10
0

Pre Active (N=17)

Post
Placebo (N=20)

16
Declarations
 Declaration of
interest:

Thanks to 118
authors – key!!
Don’t buy this
edition!!

Donor to UBC & VGH

Hospital – Center for
Hip Health & Mobility
Orthopaedic Clinical Examination
 Editor in
Chief –
BJSM since
2008

Google
‘BJSM’
‘BJSM Blog’
‘Khan, mechanotherapy
podcast’
Free Jill Cook podcast…
Google BJSM…
 • Ann Cools

Karin
Silbernagel
Disclosures: Drug company &
implant influence in medicine
Disclosures: No sponsorship from
Arthrex (who make PRP)
Case: Jumper’s knee

Your 24-yr old patient has a 6

month history of jumper’s knee
- NSAIDs
- rest
- ice

provide only temporary relief.

Normal
tendon

Collagen
disarray
Puddu 1976;
Khan 96; 2002
Normal, inconspicuous
cell nuclei

Kraushaar, JBJS-A 1999

(ii)
Absent
cells &
prolific
cells
 Clinical
implication –
NOT THIS!!

• NSAIDs don’t cure

• Cortisone doesn’t cure
What really
happens!
Normal → AbnormalSummary
i. Collagen disarray
ii. Absent cells,
prolific cells
iii. Abnormal vessels
and nerves
iv. Abnormal
extracellular
matrix
v. Genetics
16th March 2002

One-line summary

an apoptotic

Khan, Cook, 2002

 Outline
• Karim
– I don’t have a mental image of how
exercise treatment works…
 Topic…
Mechanotransduction/
mechanotherapy
What the hell is it and
why should I care?
 Is this presentation for
you?
MPT / DPT student or
resident
Busy experienced clinician
Senior expert – you know all
this but might like some of the
slides for teaching
These 5 cases….
Case #1 – Achilles pain

• 34-yr old from

Florida with
midportion
Achilles
tendinopathy
because of
tennis
 Case #2 – Knee pain

• 52-yr old from

Indianapolis with
chronic knee
pain due to OA
of the lateral
femoral condyle;
keen golfer
 Case #3 – Hamstring strain

• 19-yr old league

player with a Grade III
biceps femoris strain
from sprint training
(Askling’s type 2).
 Case #4 – Sciatica

• 38-yr old former #1

golfer with sciatica
consistent with MR-
proven disc
herniation
Case #5 – Shin pain

• 23-yr old beach

volleyball player
coming back
after tibial
internal fixation;
fractured
playing
volleyball
What treatment is common?

• ‘What treatment (Rx) advice

is common to these 5
conditions?’
• (Feel free to write down an
answer)
 What I often hear…

• Exercises for rehabilitation

• Strength training
• Aligning tissue with
stretching
• Manual therapy
• NSAIDs, cortisone, PRP
What treatment works for all of them?
 From clinical experience…

1. Exercise is good treatment

What evidence is there for exercise R
 Level 1 evidence:
chronic tendon pain
responds better to load
than to rest…
Treatment study: soccer-
related groin pain
• Active exercise versus
passive electrotherapy and
rest
Prescribing active exercise is
high evidence-based (Level 1)

• Male soccer
players with
clinically
diagnosed
adductor
tendinopathy
Per Holmich,
1999 (Lancet)
Adductor exercises 13 times better
than rest and ultrasound
% Return to sport

80

70 67%
60

50 Exercise/loading
40 Rest & US
30

20 12%
10 23/34
0

Holmich, Lancet 1999

 You only had one job!

1.How does exercise work

to treat MSK conditions?
 How does the body
adapt to load?

‘Mechanotransduction’
• Cells convert mechanical signals into
biochemical responses,
= Turning movement
• Physiological - adjusts structure to
demand
into repair
• Non-neural communication (gap
junctions)
What ‘the
hell’ is
going
on?

Sir Astley Cooper

1768-1841
50 years as
a functional
joint

Scapula
becomes a
joint!!
Sir Astley Cooper
1768-1841
 4 steps to understand
mechanotransduction
1. Cellular anatomy
2. Mechanocoupling (initiation –
mechanical load turns into
biochemical signal)
3. Gene upregulation and
protein synthesis
4. Cell-cell communication
 1. Cellular anatomy
Cell-Cell Membranes
Communication • Ion Channels
• Surface
• Gap Junctions
• Cadherins Receptors
• Caveolae

Cytoskeleton
Nuclei • Microfilaments
• Ion Channels • Microtubules
• Gene • Intermediate
Expression Filaments
• Chromatin
• Nuclear Extracellular
Lamina Matrix
Cell-ECM • Collagen
Adhesions • Proteoglycans
• Integrins • Fibronectin
• Focal Adhesions • Basement
Membrane
 4 steps to understand
mechanotransduction
1. Cellular anatomy
2. Mechanocoupling (initiation –
mechanical load turns into
biochemical signal)
3. Gene upregulation and
protein synthesis
4. Cell-cell communication
 Mechanotransduction
1. Cellular anatomy
2. Mechanocoupling (initiation –
mechanical load turns into
biochemical signal)
3. Gene upregulation and
protein synthesis
4. Cell-cell communication
 Consider our
patient with
Achilles tendon
pain as just one
example
 Consider our
patient…
2.
Mechanocoupling

The loaded cell

responds to
tension, shear,
contraction
t = before
contraction
or heel
drop
Shear on
cell with
heel drop
 That was
shearing…
 4 steps to understand
mechanotransduction
1. Cellular anatomy
2. Mechanocoupling (initiation –
mechanical load turns into
biochemical signal)
3. Gene upregulation and
protein synthesis
4. Cell-cell communication
 The heel drop stimulates
integrins to flip and this triggers
signaling pathways
 The heel drop stimulates
integrins to flip and this triggers
signaling pathways
 The heel drop stimulates
integrins to flip and this triggers
signaling pathways
 The heel drop stimulates
integrins to flip and this triggers
signaling pathways
 The heel drop stimulates
integrins to flip and this triggers
signaling pathways
 The heel drop stimulates
integrins to flip and this triggers
signaling pathways
The nucleus is signaled to
create mRNA
The nucleus is signaled to
create mRNA
The nucleus is signaled to
create mRNA
The nucleus is signaled to
create mRNA
The nucleus is signaled to
create mRNA
The nucleus is signaled to
create mRNA
Ribosomes create protein

Ribosomes
Ribosomes create procollagen

Ribosomes
Procollagen extrudes from
matrix

Ribosomes
Collagen extrudes from matrix
Collagen is repaired
 4 steps to understand
mechanotransduction
1. Cellular anatomy
2. Mechanocoupling (initiation –
mechanical load turns into
biochemical signal)
3. Gene upregulation and
protein synthesis
4. Cell-cell communication
Communication
is biochemical
via Ca & IP3
Summarising Tendon cell-cell
communication…

Tendon cells

Behave more
like women
than men…

they love to
communicate!
 Summary of
mechanotransduction
1. Cellular anatomy
2. Mechanocoupling (initiation –
mechanical load turns into
biochemical signal)
3. Gene upregulation and
protein synthesis
4. Cell-cell communication
Process that works across tissues….
 Would you please
indulge me a one-slide
animation for bone’s
response to loading –
mechanotransduction?
 Marrow
cavity Anterior shin
(posterior)
 Mechanotransduction is
well-established in…
• Intervertebral disc (Setton, 05)
• Articular cartilage (Knobloch, 08)
• Tendon (Arnockzky, 02)
• Muscle (Durieux, 07)
• Bone (Turner, 1996)
• Vessels (endothelial cells)
 Mechanotherapy –
turning movement into repair!
 Google
‘mechanotherapy’
& ‘sport’
 Summary
• Karim
– I hope you have a strong mental image
of how exercise treatment works…
 Thank you for Broadly applicable
your attention !