Orthopaedic Biomechanics:

Muscles

Wednesday 6th March, 2024

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 Objectives
 Review the composition & structure of muscles
 Introduce the mechanism and types of muscle contraction
 Describe length-tension and velocity-tension non-linearities
of muscle contraction
 Learn about muscle architecture
 Discuss factors affecting biomechanics
 Explore methods of determining muscle forces

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 What makes muscle tissue unique?
 Extensibility

 Elasticity

 Contractility

 Irritability

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 What creates motion?
 CNS sends signal to motor unit
 Muscle shortens and applies force on bones
 Generates a moment around joint

origin = proximal attachment

insertion = distal attachment

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 Muscle structure
 Hierarchical structure
Sarcomere → Myofibril → Fibres → Fascicles → Muscles

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 Muscle structure: Sarcomeres
 Actin = thin filament
 Myosin = thick filament
 Titin = maintains structure

Actin

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 Actin
 Thin filament
◦ 5-8 nm in diameter

 Tropomyosin:
◦ Rod-shaped protein
 Troponin:
◦ Globular polypeptide
complex

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 Myosin
 Thick filament
◦ 12-18 nm diameter
 Each thick filament contains ~ 300 myosin molecules

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Image: Encyclopedia Britannica
 Muscle structure

Regular architecture of insect flight muscle:

Actin filaments are dashes and myosin filaments are circles
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Image: Ethier & Simmons, 2008; From Fawcett, 1986 and Prof. Hans Ris
 Muscle contraction: Sarcomere scale
1. Activation
2. Endplate potential propagated to the motor unit
3. Rise in intracellular calcium ion levels

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Image: Ethier and Simmons, 2008, Figure 8.7
 Muscle contraction: Sarcomere scale
4. Ca2+ binds to troponin
5. Tropomyosin exposes binding sites on actin

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Image: Ethier and Simmons, 2008, Figure 8.6
 Muscle contraction: Sarcomere scale
 Relative movement of actin & myosin filaments yields active
sarcomere shortening
 Tension generated by cross bridges on thin filaments
exceeds forces opposing shortening

Relaxed

Contracted

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 Muscle contraction: Sarcomere scale

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Image: Adapted from www.mrothery.co.uk
 Length-tension curve: Sarcomere scale
Maximum tension at resting length
(most overlap)

Mow & Huiskes, 2005

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 Muscle structure: Myofibrils
 Composed of sarcomeres
 Parallel to length of muscle fibres
 1-2 µm in diameter

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 Length-tension curve: Whole muscle scale

‘Ideal’
Shorter Longer
Tension

Active tension
Passive tension
Total tension

1.0
Relative Length

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 Application: Muscle ‘weakness’
 Try flexing your fingers with your wrist in flexion, neutral,
and extension
– Active insufficiency

– Passive insufficiency

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 Modelling muscle contraction
Hill muscle model
Contractile Elastic element Contractile
element in series element
Elastic element
Factive in series
Ftotal Ftotal
Fpassive
Elastic element Elastic element
in parallel in parallel
Contractile element = actin/myosin
Elastic element in series = tendon (and cross-bridges)
Elastic element in parallel = connective tissues
(epimysium, perimesium, endomesium)

Factive + Fpassive = Ftotal

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 What affects the force production?
 Tension depends on:
◦ Amount of stimulation
 Controlled by you or FES
 Measured by EMG
◦ Length of the muscle
◦ Velocity of muscle shortening

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 Muscles and motions
 Agonist – responsible for movement
 Antagonist – opposes the movement, adds control
◦ Antagonistic pairs: examples?

 Co-contraction – both contracting

 Synergist – assists the agonist in performing the movement

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 Concentric contraction
 Shortening of the muscle causes joint movement
◦ Muscle moment same direction as joint angle change

Quads
contract
M

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 Eccentric contraction
 Lengthening of muscle decelerates joint movement
◦ Muscle moment opposite direction to change in joint angle

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 Isometric contraction
 Contraction of muscle with no movement
◦ Muscle stays the same length

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 Which produces the greatest force?
 Eccentric > Isometric > Concentric

 Why?
1. Contraction time
2. Cross bridging
3. Tension in elastic components
4. Elastic energy stored in actin-myosin cross-bridges

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 Velocity-tension curve
 max(Teccentric) ≈ 1.25 x max(Tisometric)

Tension
Lengthening Shortening
(Eccentric) (Concentric)

Isometric

Vmax
Velocity
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 Velocity-tension curve

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 Pop quiz
 Which type of muscle contraction is being used by the
elbow flexors if you slowly lower your backpack to the
floor?

 To kick a football the quads experience what kind of

contraction?

 While straightening the elbow during a push-up do the

biceps function as agonists or antagonists?

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 Muscle architecture: Pennation angle
 Angle at which fibres are attached to tendon
Fmuscle = Ffiber x cos α
 Allows more fibres to be packed in = more force
 High α, shorter fibres, long tendons, static tasks
 Low α, long fibres, more shortening, motion tasks
pennation angle (a)

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 Muscle architecture: PCSA
 Physiological cross-sectional area
 Area perpendicular to fibre direction
 PCSA ≈ muscle volume / fibre length
PCSA

 Can use PCSA to estimate maximum muscle force

◦ Maximum muscle stress ≈ 20 N/cm2 for skeletal muscle1
◦ Fmax = PCSA x 20 N/cm2
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1. McMahon, 1984
 Effect of architecture

Volume = V Volume = V
Fibre length = L Fibre length = ¼ L
Pennation angle = 0o Pennation angle = 30o
Number of fibres = n Number of fibres = 4n

Which muscle produces more force?

PCSA = V/L PCSA = 4V/L
Fmax = PCSA * 20 Fmax = 4V/L * 20 * cos(30)

30 = 20 V/L = 69V/L
 Effect of architecture
Fusiform Very small pennation angle
Quick movement, easily fatigued
e.g. tibialis anterior

Unipennate Large pennation angle

Slower movement, powerful
e.g. gastrocnemius

Bipennate Multiple pennation angles

Static contraction, stability
e.g. erector spinae

Multipennate Short & long fibres, multiple angles

Stability plus movement
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e.g. rotator cuff
 Muscle excursion
 Change in length

 What affects this?

◦ Length of the fibres composing the muscles
 Muscle fibre can shorten by ~30% of its length
 Total shortening depends on number of sarcomeres in series
◦ Length of the muscle’s moment arm
 Larger moment arm = larger excursion for same change in
joint angle

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 Fibre length vs. pCSA – lower limb

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Image: Lieber and Bodine-Fowler, 1993
 Fibre length vs. pCSA – upper limb

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Image: Lieber and Bodine-Fowler, 1993
 Application: Tendon transfer
 If paralysed, muscles may be
replaced
 Need a replacement with similar
excursion generating capacity
 E.g. radial nerve palsy

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 Fibre types
 Type I: slow oxidative
◦ Recruited first
◦ Slow contraction
◦ Good blood supply
◦ Difficult to fatigue
◦ Small in diameter

Dorando Pietri, Olympic Games

36 Marathon, 1908
 Fibre types
 Type IIA: fast oxidative
◦ Moderately fast contraction
◦ Variable contractile force
◦ Long-term anaerobic
◦ Moderately good blood supply
◦ Intermediate fibres (between Type I and IIX)

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 Fibre types
 Type IIX or IIB: glycolytic
◦ Fast, powerful contraction
◦ Anaerobic
◦ Poor blood supply
◦ Rapidly fatigued

Jesse Owens,
38 Olympic Games, 1936
 Fibre types
 Human muscles contain a mixture of fibre types
 Muscle size and mechanical advantage have greater influence
on contractile force
 Allow muscle adaptation
 Effects of ageing:
Healthy juvenile Senile adult

Striped
dolphin

Type I fibres are blue; Type II fibres are red

39 Image: Sierra et al., (2013) Scientific Reports
 What happens with: Strength training?
 Strength training
◦ Hypertrophy of fibres
◦ Increase PCSA
◦ Improved innervation

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Images: Haun et al., 2019; Coletti et al., 2022
 What happens with: Endurance training?
 Endurance training
◦ Adapt by changing
energy supply
◦ Increase number of
capillaries in muscle
◦ Increase mitochondria

Gastrocnemius muscle fibres before

marathon training, after 13 weeks of
training, after 3 weeks of tapering

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Image: Trappe et al., 2006
 What happens with: Sore muscles?
 Tensile stress results in structural injury
◦ Diffusion of cell contents into interstitial fluid
◦ Macrophages come to clean up
◦ Elevated pressure, swollen fibres
 DOMS:
◦ Lactic acid?
◦ Muscle spasm?
◦ Connective tissue damage?
◦ Muscle damage?
◦ Inflammation?

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 What happens with: Disuse?
 Decrease in PCSA
 Muscle shortening
 Affects both type I and type II fibres
 Very muscle dependent:
◦ E.g. change in plantarflexion strength
without change in dorsiflexion
strength1
◦ E.g. 5 days of limb immobilization in
the elderly leads to a 1.5% loss of
quadriceps cross sectional area2

Image: afl.com.au
1. LeBlanc et al., 1988
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2. Wall et al., 2013
 Muscle disuse atrophy
 Time-course of human skeletal muscle atrophy is age
dependent (Suetta et al., 2012)

Image: Chrizz at sv.wikipedia

(24.4, range 21–27 yrs )

(67.3, range 61–74 yrs)

* Time effect, p<0.05 compared to pre

44 # Age effect, p<0.05 young compared to old within time point
 What affects muscle strength?
 Stretch of the muscle
 Contraction velocity
 Level of fibre recruitment
 Muscle size - pCSA
 Fibre type
 Muscle moment arm

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Image: OpenStax College
 Muscle moment arms

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Image: Lieber and Bodine-Fowler, 1993
 Determining strength
 Isokinetic dynamometer

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 Determining muscle forces: In vivo

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Image: AMJ Bull et al.
 Determining muscle forces: In vitro

Frog gastrocnemius muscle

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 Determining muscle forces: In silico
 Indeterminate (more unknowns than equations)
◦ For each joint:
3 force equation (Fx, Fy, Fz)
3 moment equations (Mx, My, Mz)
= 6 equations
◦ Usually more than 6 unknowns

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 Determining muscle forces: In silico
 Make the system determinate
◦ Reduce # of muscles considered
◦ Only consider agonist muscles
◦ No co-contraction
◦ Add equations
 Estimate muscle size
 Model muscle contraction to fit motions

 Use optimization algorithm (cost function)

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 Potential Pitfalls
 Muscle moment arms change over range of motion
 Muscle force depends on muscle length and velocity
 Pathological motions may not be optimised
 How can these be validated?

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 EMG
 Muscle activity
◦ Timing
◦ Magnitude
◦ NOT force

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 EMG during gait – hip

Below 20% max. voluntary contraction

Above 20% max. voluntary contraction

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Image: Modified from Nordin & Frankel, 2001
 EMG
 Surface EMG
◦ Summation of action potentials
◦ Good for superficial and large
muscles
◦ Non-invasive

 Fine wire EMG

◦ Specific motor units
◦ Good for small and deep muscles
◦ Invasive

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 Factors that affect EMG signal
 Cross-talk between muscles
 Changes in geometry between muscle and electrodes
 Impedance of the tissues
 External noise

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 EMG

𝐸𝑀𝐺𝑖 ×𝑃𝐶𝑆𝐴𝑖
 𝐹𝑖 ∝
𝐸𝑀𝐺𝑃𝑀 ×𝑃𝐶𝑆𝐴𝑃𝑀
where PM = prime mover

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Lenaerts et al., 2008
 Summary
 Considered the composition & structure of muscles
 Reviewed the mechanism and types of muscle contraction
 Discussed length-tension and velocity-tension non-linearities
of muscle contraction
 Examined muscle architecture
 Explored factors affecting biomechanics
 Proposed methods of determining muscle forces

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