Geoff Verrall Hamstring Injury Symposium presentation part 1
1. Hamstring Muscle Strain Injury
– Specific muscles with Specific
Injury Mechanisms
Griffith University HAMSTRING Symposium Gold Coast, QLD
Dr. Geoffrey Verrall
(MBBS, FACSEP)
Sports and Exercise Physician (ACSEP)
Full time clinical practice at SPARC (Sports and Arthritis Centre) (a new multidisciplinary
practice)
South Australian Sports Institute (SASI)
Australian and South Australian Cricket Team Doctor
Adelaide, South AUSTRALIA
3. Presentation Outline
1. Mechanism of all Musculoskeletal Injuries
2. Hamstring Injuries – Biomechanics and Gait Cycle
3. Specific Hamstring Muscles Specific Injuries
4. Implications for Rehab and Prevention
5. Is there a role for specific exercises
5. Mechanism of all Musculoskeletal
Injuries
MLTJ Open access
Verrall, Dolman (Muscles, Ligaments and Tendons Journal 174 2016;6
(2):174-182)
6. Elasticity
• Defined as the ability of a solid material to return to
its original shape following deformation
• All MSK structures have elasticity including bone
7. Normal Movement
• Crimp (tendon and muscle fibres)
• Tendon and Muscle fibre elongation – energy efficient
• Active lengthening of muscle fibres – metabolic
energy cost
• EFFICIENCY is to try and minimize active lengthening
• “Contraction” is Force Dependent (walking vs running)
8. Lengthening Shortening
• Lengthening occurs as a result of applied force. This applied force is
external to the MTU (Muscle Tendon Unit) attachments
• Shortening of the MTU applies force to the attachment points. This
enables movement.
• Shortening occurs over a shorter time period than lengthening =
more powerful. Not more force. But force applied over a shorter time
period
• More reading Lappin 2006 J Exp Biol, Monroy 2006 Inter Comp Biol,
Roberts 2011 J Exp Biol
9. Energy
• During lengthening Muscle Tendon Units have the ability to store
potential energy.
• Tendon and Muscle fibre structures have good ability to store
potential energy
• This potential energy is returned to the MTU during shortening as
kinetic energy.
• Ligaments and other non MTU MSK structures (eg bone) have less
ability to store energy but still undergo a lengthening shortening cycle
10. Non idealized Hookean Spring
• Arguments in Verrall, Dolman (Muscles, Ligaments and Tendons Journal
174 2016;6 (2):174-182)
• Hookes Law F=kx
• k is the spring (proportionality constant)
• x is the length change
• k alters with lengthening and shortening
• k increases with lengthening (Lappin 06) and decrease with shortening
(Lappin06, Monroy 2007 Exer Sports Sci Reviews)
• Relationship between Force and Length is non-linear but is predictable
(Monroy 2006). There is a formula for this
•So MTU as a SPRING applies
11. So where does this lead
• Elasticity
• Lengthening / Shortening cycle
• Non idealized Hookean spring
• Therefore MTU act as a “spring”
• DO elastic motion laws apply
•A spring will have a resting length
12. Resting Length
• When an elastic structure is at its resting length, it is neither
compressed or stretched, and experiences no force
• If it is lengthened it will restore to its resting length
• If it is shortened it will restore to its resting length
13. Strength (Tensile / Compressive)
• When Lengthening beyond resting length the elastic structure will
need tensile strength (the ability to match tensile force)
• When Shortening beyond resting length the elastic structure will need
compressive strength (the ability to match compressive force)
14. Skeleton is a Constrained unit
• During normal operation the attachment points of the Muscle Tendon
Unit (and the Ligament Bone Unit) will have a minimum and
maximum distance from each other
• TO disrupt these attachment points is a catastrophic (in terms of
movement) injury
15. Resting length of MTU
• Same as a spring = The position where the structure has minimal or
no force on it
• = There is minimal force when the tendon and muscle fibres return to
crimp
• At the minimum distance between attachment points WE WILL
DEFINE AS THE RESTING LENGTH OF THE MTU SPRING
• Please note: The minimum distance between structures is not always
at the anatomical at rest position
16. MAGIC TRICKS!! = DEDUCTIONS
• MTU is CONSTRAINED and has a minimum length between attachment points
• RESTING LENGTH is at the minimum distance between the attachment points
• SO (in normal (non-catastrophic) operation) the MTU cannot be shortened
beyond resting length
• From RESTING LENGTH to FULL LENGTH (The MTU will experience tensile force
and therefore will need tensile strength)
• From FULL LENGTH restoration to RESTING LENGTH (The MTU will experience
compressive force but only the restoration of the lengthening process so will
ALWAYS have sufficient compressive strength for this)
• Cannot get shortened beyond resting length
• SO
• CONSEQUENTLY the MTU will ALWAYS have adequate compressive strength
17. INJURIES
• If the MTU always has adequate compressive strength
• DEDUCTION Injuries will result from inadequate tensile strength
• Tensile forces are a consequence of lengthening
• Lengthening occurs as a consequence of externally applied force
• Movement related injuries for all musculoskeletal structures result
from an inability to counter applied forces whilst the structure is
lengthening (The MoMI theory)
Life is really simple, but we insist on making it complicated.
Confucius
18. DEDUCTIONS
• Movement related Muscle strain injuries result from an inability to
counter applied forces whilst the muscle tendon unit is lengthening
(The MoMI theory)
• SO ALL WE NEED TO KNOW ABOUT MUSCLE
INJURIES IS TO KNOW WHEN THE STRUCTURE IS
LENGTHENING
19. ARGUMENTS (MoMI)
• Non-idealized Hookean spring
• Resting Length
• Timing of Injury
• About proof / experimentation
• Viscoelasticity (Non linear force displacement (variable k), Hystersis (variable k),
Velocity-Dependent stiffness (variable k), Creep, Load relaxation,
• Think of viscoelasticity in the human movement cycle as the MTU still gets out to
length and then shortens but takes a different time to do either. BUT it still gets to
length and still gets to minimum
Arguments in Verrall, Dolman (Muscles, Ligaments and Tendons Journal 174
2016;6 (2):174-182)
20. SPECIFIC STRUCTURE LENGTHENING
• Muscles, Ligaments and Tendons have a well understood (or
reasonably well understood) Lengthening/Shortening cycle.
• IT and Bone need some help (No compression – at odds with the
herd!)
21. TREATMENT / PREVENTION
2 CHOICES
• Treatment is to increase the tensile strength of the injured MSK
structure (so it can match the applied forces during lengthening)
• OR Alternatively
• Decrease the Force Applied to the MSK Structure (so the structure
has adequate tensile strength during lengthening)
• This is the same for treatment and Prevention. So for the rest of this
presentation
• TREATMENT = PREVENTION
24. Hamstring Injuries - Biomech
Sprinting cycle
Force Application in the stance phase
Anatomical Considerations of the Hamstring Muscles
25. Newtons 3rd Law and Movement
• NEWTONS 3rd Law = equal and opposite force
• To move we need to construct a force differential with the ground –
as we said we lengthen as a response to applied force and we shorten
to enable movement
• So in effect we shorten our MTU’s when we are on the ground.
• We work in identical pairs
• Stance and Non-stance accelerators (shorten) and for the rest of the
time we lengthen
26. Force Application in Stance Phase
• 1. Ground contact (prepare for shortening)
We do this using our anterior momentum
• 2. Non-stance Quadriceps swing into hip flexion THEN
• 3. Stance hamstring and posterior leg/foot muscles shorten THEN
• 4. Non stance knee extends (after left the ground from the force of
the quadriceps pull on the patella) and stance knee flexes THEN
• Ground Contact again
29. Don’t worry about the
arrows
Quads / Hip flexors are nearly done
Posterior leg Hamstring Stance are
shortening
Non stance swing
Stance GC
30.
31. To get a Hamstring Strain you need
• MUST HAVES
• 1. A lengthening hamstring (must be activated) – if not you will tear a
free tendon
• 2. A tug of war between the two ends of the lengthening hamstring
• OTHER FACTORS
32. To get a Hamstring Strain you need
• MUST HAVES
• 1. A lengthening hamstring (must be activated) – if not you will tear a
free tendon
• 2. A tug of war between the two ends of the lengthening hamstring
• OTHER FACTORS
33. Proximal part of the Proximal tendon of LH BF
• A lengthening hamstring – non-stance hip flexion rotating about
stance axis
• A tug of war (force)
Hip flexors PLUS Q = Knee elevation (Hip flexion)
Stance HS and posterior chain muscles = Pelvic SPLIT.
• Too much strength in the MTU’s applying force
• “Balance” lost
• ?Fatigue role
• LOSS of specificity of training
34. Proximal part of the Proximal tendon of LH BF
EPIDEMIOLOGY / CLINICAL
• Sprinters 3:1 Prox:Distal (Askling)
• Recurrent Interval Sprinting 1:1 (using SH BF as mid point) (Slavotinek)
• Not associated generally with cramp (sudden tear) but painful
• Big Injuries
• High incidence of recurrence
• Sprinters (sprinting)
35. Proximal part of the Proximal tendon of LH BF
REHABILITATION
• Early motion, Stretch – the amount of F you are putting into the
system at reduced running speed is low. Day 2
• Sprint technique important
• (Stiffness is related to power) (So unstiffen) Emphasize Q stretching
(for Hip flexion) and distal SM HS stretches (tibial internal rotation)
(for Stance leg hamstring)
• RTS Unpredictable
36. Distal part of the Proximal tendon of LH BF and ST
• A lengthening hamstring – flight non-stance knee extension rotating
medially towards the previous stance axis
• Knee extension is balanced by hamstring deceleration in preparation
for alteration in direction. THAT IS THE TUG OF WAR
• Prone to fatigue and/or a sudden overstride/back flexion
• Fatigue causes a “cramp”
• Associates with ST (ST fibres come off the medial side of proximal LH
BF)
37. Distal part of the Proximal tendon of LH BF
CLINICAL
• Smaller injuries
• Recurrent Interval sprinters
• Associated with ST injuries
• Cramp
• Overstrider adapting to recurrent interval sprinting
• Errors in running programs (Length Strength imbalance)
38. Distal part of the Proximal tendon of LH BF
REHABILITATION
• Early motion, Stretch – the amount of F you are putting into the
system at reduced running speed is low. Day 2
• Sprint technique less important
• RTS Predictable
• Push hard on the rehab
• Work to length and strength
• Stiffness of medial hamstrings an advantage
39. Mechanism – Semimembranosus proximal
• Overstretch
• Post landing when you move from supination to pronation and internally rotate
femur and hyperextend your leg = prox SM
• Or your leg gets pulled when your knee is extended
• Rehab quickly
• Bad for certain sports
• Distal SM (never see this injury – WHY. I think biomechanically the lengthening
occurs after ground contact and knee flexion. The ant momentum pulls knee into
extension and rotates the tibia ER whereas the femur has gone IR. Hip flexion also
does it. If you overlengthen then you really have stuffed up your landing and take
off
• Shortest fibre length + Large muscle
40. Role of MRI
• Useful to plan rehabilitation
• Need to know type of injury as it is not always evident from the
history
• I think some have jumped the gun in saying MRI is prognostically not
useful (we don’t yet know)
• SO welcome back MRI
41. THANK YOU
• Nordic (analysis of RCT’s, How they are unlikely to be the vaccine)
• Muscle fascicle length alteration
• QUESTION TIME
42. Role of Nordic
• I think the RCT’s presented have significant methodological
weaknesses including commencing programs mid-season, failure to
use/report imaging (gold standard in Australian research), has a
definition of any time loss with posterior thigh injury as being a
hamstring injury (our imaging tells us this brings a 20% error), not
presenting findings in the paper with regards to imaging (they did use
ultrasound but didn’t report it, dividing subjects into elite and
amateur but not reporting results, no explanation re time loss
between the seasons, mean higher when matched for age, range for
control upper was 90 days, intervention 66 days, and having new
injuries to old injures at a ratio of 2-3:1 when in he AFL is it 1:5. (I
think this puts doubt on primary prevention to me)
43. Role of Nordic
• Specificity
• Repeat papers
• Herd mentality
• I have heard it called a vaccine
44. Role of Nordic
• Alignment is for distal > Proximal. Force is further from the distal muscle
than proximal
• Angle is central so preferentially activates medial hamstrings
• With strengthing of HS other than BF LH Prox has potential to improve
Force production (performance) but also to increase size of F generated at
the “pelvic split” so increase in size of Prox LH BF injuries
• I think we will see HS injuries in the weak Nordic HS tested group (ST and
distal LH BF) AND the strong Nordic HS tested group (prox LH BF) AND
• As we strengthen the group we will find an overall decrease in incidence of
the recurrent interval sprinter population but this will be countered by an
overall increase in prevalence (size of injury)
45. MUSCLE FASCICLE LENGTH
• Youngs Modulus
• E = Measure of Elasticity
• E= tensile stress/tensile strain
• E = F / CSA divided by Change in Length / Original length
• So adjusting the formula
• F= CSA * E * Change in length divided by the original length
46. F= CSA * E * Change in length divided by the
original length
• So if you want to Increase F
• You want increase CSA (the body decided how big this needs to be
and it is slow)
• Increase E (which is really stiffness)
• Change of Length (you can have an increase in Elasticity (stiffness)
and an increase in change of length (Elasticity is a property)
• Decrease original length (so to increase force production you actually
want to decrease fascicle length)
• But you cannot change fascicle length
• So what happens
47. F= CSA * E * Change in length divided by the
original length
• Activated lengthening (eccentric) exercises increase sarcomere number
• Activated lengthening (eccentric) exercises decrease pennation angle
• HAPPY WITH THAT
• If each sarcomere has a “E” number and these are in series well you have
effectively increase E
• If each sarcomere has potential for the same Change in length then we have
increased Change in length
• But we have sarcomeres (where have they gone – longer muscle -floppy –
increased original length bad for force production
• Pennation angle decrease is altering the tension of the MTU (how cytoskeleton,
better alignment of the head (titin) – Unknown
• Tension is a property (give example)
• By increasing tension we effectively decreasing original length (fulfills the criteria)
48. F= CSA * E * Change in length divided by the
original length
• So if you want to Increase F
• You want increase CSA (the body decided how big this needs to be
and it is slow)
• Increase E (which is really stiffness)
• Change of Length (you can have an increase in Elasticity (stiffness)
and an increase in change of length (Elasticity is a property)
• Decrease original length (so to increase force production you actually
want to decrease fascicle length)
• But you cannot change fascicle length
• So what happens