334SPO Mechanics of the

Musculoskeletal System
 Animal tissues
 Structure
 Function
 Biomechanical properties
 Including failure

 Lectures from RJ & AP: 20 hours for 334SPO

and 239SPO, 12 hours for 333SPO/335SPO
 Tutorials/Labs/workshops RJ et al: 10
hours (often in vivo assessments)
 Reading list
 Marking criteria & CW proformas
 Timetable & corrections
 Notice board
 CUOnline
 Online quizzes (1 tutorial)
 What Happened 2007/8
Mean scores 232SPO?
5= excellent, 1 = very bad
 Module well organised: 3.75

 Module met aims and Objectives: 4.00

 Teaching methods effective: 3.75

 Assessment methods effective: 4.00

 Satisfied with this module: 4.50

 Effective lecturer RJ: 5.00

 Specific comments
 Liked the small group tutorials
 Liked the book of lecture notes at the start
 Wanted last lab earlier in the year (it is now)
 Wanted more information on handouts (there is
now)
 Lectures to be done on PowerPoint (they are
now)
 94% of students attended >60% of taught
classes
 64% of students passed 232SPO pre resit
 Attendance
 Significant relationship between
attendance and module mark

80
R2 = 0.205 P = 0.002
70
Module mark (%)

60
50
40
30
20
10
0
0 20 40 60 80 100 120
Lecture attendance (%)
 Resources
 module handbook:
 Books
 Videos

 CUOnline site
 Quiz

 Practice short answer quizzes for each book

chapter
 Module handbook
 Timetable
 Tutorial topics list
 Handouts
 Journal articles to download

 References stated on many handouts

 Some on CUOnline 334SPO site
 Some in library or via library portal
 Some via document supply service or ask Rob
 Module marks 2010/11
334SPO (BSc Sport and Ex Sci students)
50% for 1500 word CW essay (term 2)
50% for 2 hour Exam

333SPO/335SPO (BSc Sports Therapy students)

50% for 2000 word CW essay (term 2)
50% for Critical appraisal of physiological
scenario. Maximum 1500 words (Mike Price
will set this)

239SPO (BSc Rehab Eng; BSc Assist Tech)

50% for 2000 word CW essay (term 2)
50% for 30 minute phase test (term 1)

Turnitin: submit essay to Turnitin via

CUOnline site.
Can submit draft to check, pre real
essay submission
 Labs/Workshops
Whole body analysis
Kinematics: 2D low speed video
analysis

Usage of electromyography and

electrogoniometer

Tissue mechanics
Instrom bone mechanics and work
loop muscle mechanics
 Structure and
Properties of
Materials
 What is the material composed of?

 How do we test the biomechanical

properties of the material?

 What are the biomechanical properties?

 What should the material be used for?

 Muscle Structure
Muscle
Tendon Tendon

Blood supply

Muscle
fibres
Nerve supply
Muscle Sarcomere
Thin filaments

Thick filaments
Muscle filament structure
Thin filament
Helical arrangement

(i) Double strand of actin monomers

(grey and white circles)
(ii) Troponin complexes (black circles)
and Tropomyosin (black lines)
which regulate actinomyosin interactions

Thick filament

Bare zone

Myosin: heads, neck and body

 Myosin molecule
structure
Myosin light chains

Heads
Hinge

Neck
Body

Myosin heavy chains

Head (S1 region) has ATP and actin binding sites
Neck (S2 region) pivots on hinge
Body embedded in thick filament

Myosin light chains stabilise head and neck region

 Optical Trap Technique
 Isolated actin and myosin filaments

 Actin filament attached to plastic beads

 Laser beams hold the beads
 Lasers can move actin filament

 Lower actin filament towards free

myosin molecules
 Interaction causes beads to move
 Very low forces pico Newtons pN

Laser beam Laser beam

 How is force produced?
 ATP bound to Myosin head (S1 region)
 ATP broken down
 Myosin head binds to actin
 Myosin head rotates
 Rotationstretches neck (S2 region)
 This causes force to be produced

 ADP & Pi & energy released

 ATPADP + Pi + energy

Heads (S1)
Hinge

Neck (S2)
Body
ATP Binding and hydrolysis
Myosin molecule S2 neck
S1 head
Body Actin
binding
sites
‘rigor’
ATP
NB. 2 sites for
2 heads!

ATP

Dissociation
ATP

Pi
Hydrolysis ADP
 Force Production
During isometric activity = constant length and active
Iso = constant metric = length
While isometric there is no movement of the thick and
thin filaments with respect to each other
B
neck
Head S2 stretches
Pi Pi + energy
ADP
B=body
Actin binding site
B

ADP

ADP ADP

Force

More stretch of neck (S2 region) = more force

Force-velocity Relationship
During concentric actions (muscle shortening and active)

A) Filament sliding Velocity

Thick
filament

Thin
filament Force

B) S2 head rotation

S2 stretch
B

ADP

Faster velocity of shortening = less myosin heads bind

and neck stretches less
increased shortening velocity = decreased force
Full Cross-bridge Cycle
(Diagramme)
Pi + energy
Pi Pi
ADP ADP Force
produced

ATP ADP

ATP ADP

ATP ADP
‘rigor’
 Full Cross-bridge cycle
 Myosin is bound to actin (rigor state)

 ATP binds to myosin

 Myosin dissociates from actin

 ATP is hydrolyzed and myosin head

rotates

 Myosin binds to actin

 Phosphate and energy release

 Rotation of head causes force

production
 The Muscle Switch:
activation
Depolarization of nerve
ACh Neuromuscular junction
Depolarization of muscle membrane

Depolarization of T-tubules

Calcium release from SR

Nerve

ACh Surface membrane

T tubule
receptor
Sarcoplasmic
reticulum
 The Muscle Switch:

Nerve Muscle
Ca2+ Force
Level of response

AP AP

Time

•Calcium in cytoplasm binds to troponin C

•Change in shape of troponin T
•Troponin I no longer physically blocking actin
binding site
•Strong binding of myosin head with actin binding site
•Force production
 Calcium Binding
Cross-section through thin filament
Troponin complex = TnC, TnT, TnI

Tn-T
Tn-C
Relaxed TM (Tropomyosin)
Weak AM Tn-I
binding
Actin
Actin

Binding site
Calcium concentration
increases

Tn-C Tn-T
Active
Tn-I
TM
Strong AM
binding Actin

Tn-I inhibits Myosin ATPase

 Muscle Relaxation
 Cessation of neural stimulus
 Decreased Calcium release
 Decreased calcium
concentration decreases
chance of calcium binding to
TnC
 Decreased muscle force
 Calcium binding in cytoplasm by
parvalbumin
 Further decreased Calcium
concentration
 Decrease in calcium binding by
Tn-C
 Calcium pumped from
cytoplasm to sarcoplasmic
reticulum (requires ATP)
 Whose muscle is it anyway?
 Muscle mechanics similar between
vertebrate species
 Frog muscle main one used as easy to
use!
 Why little human data?
 Ethicsproblems of invasive experiments
 Experimental rigor of non-invasive…

 These lectures
 Will use any muscle data as typical of
vertebrate muscle
 Will try to highlight any relevant human
data where available
 Muscle Mechanics
Muscle fibres vs. whole
muscle vs. sarcomere
•in vivo = in life; in vitro = in glass; in situ = in
place
•Whole muscle simulates in vivo
•Easier to dissect
•Larger preparations have: O2
•Increased risk of anoxia (diffusion distance)
•Increase in passive structures
•Increased problems of diversity of fibre
orientation
•Muscle>muscle fibre bundle>muscle fibre>
sarcomere

Pennate fibred
Parallel fibred
 Sarcomere level
 Could use a muscle biopsy
 Chemical treat muscle (‘skinned’) to
remove membranes

 Clamp single fibre so only monitoring a

single sarcomere

 Use chemical solutions to:

 Activate (high calcium concentration)
 Relax (low calcium concentration)

 Measure force-length properties

Force

Length
 Fibre/muscle level
 Muscle removed from animal and test:
 Whole muscle
 Fibre bundle
 Single fibre

 Electrical stimulation (via nerve/direct)

 Activatesmuscle
 Force production

 Different types of studies

 Isometric = constant length
 Isotonic = constant force Force-
 Isovelocity = constant speed velocity
 Work loop (simulate in vivo)
 Muscle rig
Force transducer
Motor
Oxygenated
Ringer
/Krebs in Ringer out
(salt solution)

Muscle Platinum electrodes

Salt solution composition to mimic blood plasma

and includes an energetic substrate e.g. glucose

Temperature regulation of salt solution

35 to 37C for mammalian work
historically 0 to 20C for ease!
 Isometric Tests of Muscle
Twitch: used to optimise muscle length
and stimulation amplitude
Response

Force
Stimulation (V)

Time

Tetanus: used to optimise stimulation frequency

Stim. frequency =
fused # of stimuli per second

unfused Force

Stimulation
Multiple stimuli cause multiple releases of calcium
Leading to summation of twitches and greater force
 Isometric Times
Force (% maximum)

Rates of activation and relaxation

Twitch

THPT

Stimulus
Time
THPT = time to half peak twitch
TPHR = time from peak twitch to half relaxation
THPTet = time to half peak tetanus
TetPHR = time from peak tetanus to half relaxation

Tetanus

THPTet
Force-length Curve Sarcomere

Actin binding
1 sites covered

2
Only bare zone
uncovered on
3 thick filament

No
4 overlap
Force
2 3
Total
Passive
(collagen)
Active 4
Sarcomere
1 Length
 Titin filaments
Titin

Z line M line
•Titin (also sometimes referred to as
connectin)
•Runs from Z line to M line
•Two sections of titin with different
stiffnesses
•These correlate to the mechanical
models of muscle passive stiffness
•So titin has two functions
•Provides passive stiffness (protective)
•Stability of sarcomere structure
 Force-velocity
(Isovelocity version)
Time

Length

Force

Stimulation
Can compare muscles:
Velocity
Vmax = maximum
Faster Vmax shortening velocity
Fmax = maximum
Slower Vmax tetanic force

Force
Fmax
Eccentric vs Concentric
 What is the difference?
 Eccentric = lengthening and active
 Concentric = shortening and active

 When might eccentric force be important?

 large external force
 braking/controlling movement

Force

Concentric
Eccentric

0
Velocity
Isometric
Speed and direction of movement affects force
via stretch of myosin neck and # of cross-bridges
Power output-force/velocity
Curves
Power output (P.O.) = force  velocity

Power Peak P.O. at V/Vmax of

Output c. 0.3-0.4
V = velocity
Vmax = maximum
Velocity velocity

Velocity

Force

Peak P.O. at F/Fmax of

Power c. 0.3-0.4
Output
F = force
Fmax = maximum
force

Force
 Efficiency
 Work output  energetic cost
 energy cost in ATP
 work done = Force  distance
 Power output = work done  time taken
Efficiency

Maximum efficiency around 0.3 to 0.4 V/Vmax

 Muscle Pennation
Parallel fibred muscle

Longitudinal axis
Tendon Tendon

Increased length
E.g. Extensor digitorum longus

Pennate muscle e.g. Bipennate, multipennate

Tendon Tendon

Increased physiological cross-sectional area,

(measured perpendicular to fibre longitudinal axis)
increased force
E.g. gastrocnemius, soleus, quadriceps
Lower fibre length,
Angle of
 pennation
 Design of Muscle
 Imagine we have a muscle of constant volume
 We can alter the muscle length but this will also
change muscle cross-sectional area
 What effects would such changes have on muscle
mechanics?

 Muscles with higher cross-sectional area = high

force production, good for stabilizing limbs

Muscle length
Muscle cross-sectional area

A fictional muscle
one sarcomere long
but many sarcomeres wide
 Design of Muscle 2
 Each sarcomere generates force and pulls the
sarcomere next to it
 Along the length of a muscle some of the forces
will effectively cancel each other out
 Essentially we just need to count the number of
sarcomeres across the cross-sectional area (the
sarcomeres at the end) to determine the force
producing capacity of the muscle
Length
F F

width

Longer muscle: 4 sarcomeres wide

Wider muscle: 12 sarcomeres wide

So wider muscle would produce

3 times more force
 Design of Muscle 3
 Longer muscles = higher absolute speed,
acceleration and deceleration

Speed = distance moved  time taken for movement

Acceleration = change in speed  time taken for
change

Length
F F

width

Longer muscle: 3 sarcomeres long

Wider muscle: 1 sarcomere long

If we assume each sarcomere can

shorten at the same speed
The longer muscle would produce
3 times more shortening speed
 Wider muscle but same length
Isometric force-length curves
Same length = same range of motion
Force Larger PCSA:
Higher force at all
lengths
Smaller PCSA

Length
Isovelocity force-velocity curves
Same length = same maximum shortening velocity
Force

Larger PCSA: Higher force at all

velocities

Velocity
0 Smaller PCSA
 For review see Lieber, R. & Friden, J. (2000) Muscle & Nerve
23 1647-1666 (not in library: ask Rob)
 Longer muscle but same PCSA
Isometric force-length curves
Same cross-sectional area = same maximum force
Force
Longer muscle has
larger ROM

Shorter Longer fibres

fibres
Length
Isovelocity force-velocity curves
Same length = same maximum shortening velocity
Longer muscle has
Force higher Vmax, so lower V/Vmax
at each V, so higher force
Longer fibres

Shorter
fibres Velocity
 For review see Lieber, R. & Friden, J. (2000) Muscle & Nerve
23 1647-1666 (not in library: ask Rob)
 Human Muscle
Pennation Effects
more pennate
soleus
PCSA

Less pennate
EDL Semitendinosus
FDL
Fibre Length

 Pennation angle 0-30°

 Fibre length  ROM (range of motion)
 Fibre physiological csa  F maximum
Increased pennation tends to cause
decreased fibre length

 For review see Lieber, R. & Friden, J. (2000) Muscle & Nerve
23 1647-1666 (not in library: ask Rob)
 Muscle Pennation
 Assume muscle of fixed volume

 If used lower pennation angle (more

parallel fibred)
 longer fibred and longer muscle
 Faster shortening velocity
 Greater range of motion

 But pennate muscle fibres do not need

to shorten as fast as the muscle!
 pennate muscle = higher PCSA = higher
force
 So produce more force at same velocity

 Pennation changes during activation!

 Increased pennation angle as shorten

 For review see Lieber, R. & Friden, J. (2000) Muscle & Nerve
23 1647-1666 (not in library: ask Rob)
 Muscle roles
 Power (FV)
 e.g.for jumping
 long muscle for high speed
 high csa for high force

 Acceleration
 to rapidly increase speed
 long fibres and muscle

 Brakes
 stabilisation
 high force
 high pcsa, high pennation

 Endurance/efficiency
 reduce energetic cost?
 slower fibre type
 minimise muscle size
 Fatigue resistance
(endurance)
Fatigue tests (performance over time)
•Test muscle properties
•Fatigue muscle
•Test muscle properties

Effects of Muscular Fatigue

•Decreased force production at any speed
•Slower activation and relaxation rates
•Decreased maximum shortening
velocity
Isometric Isovelocity
Force Fresh Force
Fresh
Fatigued
Fatigued

Time Velocity
 Why use work loops?
 Isometrics measure at constant length
 Isovelocity at constant velocity
 Isotonic at constant force

 In vivo all these conditions are likely to vary

I.e. dynamic

 Work loop technique (also called oscillatory

work technique) to simulate/approximate in
vivo

 Isotonic/isovelocity overestimate power output

 Isometric underestimate rate of force
activation and relaxation
 All these ignore passive properties of muscle
due to collagen etc

 James, R.S., Young, I.S., Cox, V.M., Goldspink, D.F.,

and Altringham, J.D. (1996) Pflugers Archive 432 767-
774.
 Work loops
This example uses a sinusoidal length change waveform

Time
1 length change
cycle
Length

strain
e.g. 0.10 (5%)
Activity

Force

stress
Plot force against length
to create work loop

The area of the loop

= net work done
strain
e.g. James, R.S., Altringham, J.D., and Goldspink, D.F.
(1995) J Exp Biol. 198 491-502
Why use stress and strain?
Measurements normalised (realtive) to muscle size
Stress (N.m-2) = force (N)  cross-sectional area (m2)

Force

Strain = length change  initial length

= L  L0
e.g. 0.1m  1m = 0.10 (i.e. 10% length change)
Strain has no units
L0
L
 Passive Stress-strain curves

Stress (force  csa)

y

x

Strain
(length change  initial length

Modulus of elasticity/stiffness/Young’s modulus

= stress  strain = the slope of the line = y   x

Stiff = lots of force required to cause a small strain

e.g. bone more stiff than muscle
 Elasticity 1
We are now considering passive properties
Elasticity = ‘wish’ to return to original shape
e.g. length
Perfectly elastic material (doesn’t exist)
Stress-strain relationship is linear and identical
in extension and compression of material

Energy required to stretch the material =

energy released during shortening

No net energy cost to undergo length change

cycle

Stress

Strain
 Elasticity 2
Perfectly viscous material
Deforms when force is applied
When force stops the material does
not return to it’s original shape.
i.e. no elastic recoil

Blue tac is fairly viscous!

Stress

Strain
 Elasticity 3
Visco-elastic material
Biological materials (e.g. muscles and tendons)
require energy input during stretch which is
not fully returned during recoil

Stress

Strain

Area within work loop = net energy required to

undertake length change cycle

Work (energy) = force  distance

Muscle stress-strain curves 1
Passive

Stress
During stretch:
Work (energy) input

Strain

Stress
During shortening
Work (energy) output

Strain

Stress Net work done on the material

during the length change cycle
(energy cost)

Strain
 Muscle Stress-Strain curves 2
Active when shortening
(concentric exercise)
Stress Work input to stretch
work done on the muscle
by antagonist or other external force

Strain

Stress During
shortening
work is done
Work output by the muscle
Strain

Stress

Net work

Strain
Net work done by muscle during length change cycle
 Ultimate Properties of
Tissue
• The maximal performance of a tissue
before it breaks (total failure occurs)
• Strength
• Extensibility
• Toughness

 Vary between tissues

 Vary between parts of body

 Depends on cost of failure!

 Strength
The maximal stress (force  csa) a material can
withstand before it breaks

e.g. bone stress-strain curve:

Ultimate strength
(maximal stress)

Stress Failure strength

stress at failure

Yield strength
(damage begins)
i.e.. micro damage

Elastic Strain
Deformation
Plastic
so no damage
Deformation (damage)
(Hookes law)
 Extensibility

The maximal strain a material can be subjected

to before it breaks

Stress
Maximal stress

Strength Breaking point

Extensibility

Strain

Maximal strain

Tendon extensibility > bone

Bone strength > tendon
 Toughness

The energy required to break a material

= the area under the stress-strain curve

Energy (work) = Force  distance

Stress
Less tough

More tough
(but less strong
and more extensible)

Large area

Strain
Typical Mechanical Properties of
Mammalian Tissue
Muscle Tendon Cortical Mild Steel
Bone
Maximal 0.25 0.09 0.02 0.1
extensibility
(strain)
Ultimate 0.4 90 150 400
tensile
strength
(MPa)
Ultimate ? 5.6 25 Higher
Toughness low than bone
(KJ kg-1)
Modulus of Low or 1.5 20 200
elasticity high cf.
(GPa) tendon

1Pa = 1N m-2
1000 Pa = 1 KPa 1000 KPa = 1MPa
1000 MPa = 1GPa

Compact bone = cortical bone

Tensile = during stretch (under tension)
Modulus of elasticity = slope of stress-strain curve
= stiffness
Stiffness higher in active than passive muscle
 Shear vs. Tension
Material in tension
Forces applied are directly opposite to each other

Force Force

Fracture

Material in shear
Forces applied are parallel but not directly opposite to
each other
Force

Force

Fracture
Compression vs. Bending
Material in compression
Forces applied are directly opposite to each other

Force Force

Fracture

Material in bending
Force Tension Force

Compression

Fracture
 Safety Factors
 If we could ‘design’ a person:
 How would you decide how strong
to make the long bones in your leg?

 Consider:
 function of structure
 direction and magnitude of loading
 cost of production of structure
 cost of repair
 Safety Factors
 How safe is the structure?
Safety factor = Failure stress functional stress
 e.g. failure stress (strength) = 4 MPa
functional (everyday) stress = 2 MPa
Safety factor = 4 MPa  2 MPa = 2
 Cost of failure Vs. cost of structure
e.g. broken leg bone c.f. broken finger
 Increased material = increased cost
synthesis and maintenance
(replacement & repair) costs
 material and locomotory costs
(including overcoming inertia)
internal space cost
weight = locomotory cost (muscle
activation; higher in lower limbs)
 Complications in
Safety Factors
 Variation in expected load
depend on direction of impact
e.g. in long bones usually loaded in
compression and tension, weaker in
shear weight

 Deterioration in material
previous damage
ageing

 Unpredictable strength of material

 Increased strength if loads less

predictable and tissue more

important for survival Ground reaction
force
 Safety Factors in Bone
 1.4 - 4 for bone (i.e. failure stress 
functional stress)
 e.g. Weightlifter: backbone safety factor 1.0-1.7

 Bone remodeling in shape, elasticity,

density and mass
 density = mass  volume

 Load dependent tissue growth and atrophy

 Atrophy: astronauts in microgravity (lower
loading so decreased osteoblast activity )
 Growth (hypertrophy): exercise (weightlifters,
tennis players)
 Load generates strain
 Strain causes micro damage

 damage induces remodeling (overcompensation)

 OR strain detected by nerves in periosteum (bone

sheath)?
Hall, S.J. (2007) Basic Biomechanics. Boston: McGraw-Hill
 Leg Bone Stresses

weight

Ground reaction force

•Stress on long bone at impact depends on angle 

•unpredictable
•curved bones bend focussing peak force
(predictable)
•Higher strength at focus (minimise bone weight
and minimise locomotory cost)
•High strength and safety factor along bone length
•for compression and tension
•Lower strength for side impact (shear)
•Use force platform to measure forces
•inverse dynamics to calculate bone stresses
 Bending
Force Tension Force

Compression

predictable focus of forces

strengthen here

Fracture

Force
Shear forces:

Force
 Measurement of in vivo action

Muscle
Tendon Tendon

Muscle activity: Electromyography

 surface (external) EMG electrode cuffs
 problems of cross-talk (interference from
other muscles): so better on larger muscles
 conductance of skin changes between
people, with exercise: affects signal
 internal EMG electrode wires
 ethical issues
 signal is definitely from the muscle of
interest
 Measurement of in vivo action 2
Amplitude
IEMG
Raw EMG
Time
EMG signals
 Raw EMG indicates motor unit action

potentials
 indicates duration of action potential
 doesn’t indicate muscle force or timing
of force production
 force rise and relaxation delayed with
respect to EMG onset and finish
 Integrated EMG (IEMG)
 calculation of amplitude of action
potential
 affected by subcutaneous tissue, firing
rate, # active muscle fibres
 Measurement of in vivo action 3
emitter receiver
Muscle length
 Direct measurement: Sonomicrometry

 crystalsimplanted into muscle

 measure time taken between crystals

 calculate distance

 Calculation from joint angles

 1: use external markers on joints
 use motion analysis to track movement of
markers to calculate changes in joint angle
 assumptions of tendon vs. muscle strain

 E.g. James, R.S., Altringham, J.D., and

Goldspink, D.F. (1995) J Exp Biol. 198 491-502: on
CUOnline

• Mouse ankle angle for EDL and soleus muscle

lengths
 2: use X-ray video or cine to track bone movement
 could use markers on tendon ends

 Direct measurement via ultrasound

 Strain from joint angles
Strain = change in length  initial length
Velocity = length change  time
SARCOMERE LENGTH (m)

3.0 EDL
Soleus
2.6

strain 2.8

2.4
2.6
2.2 EMG
2.4 EMG
0 150 300 450 600 0 150 300 450 600

LIMB CYCLE PHASE (0)

 Mouse muscle strains calculated from ankle
joint angles (measured from high speed video)
 See James et al. (1995) J. Exp. Biol. 198 491-
502. [Figure 7]: On 232SPO CUOnline site
 But when are the muscles active?
 NB. EMG from rat Nicolopoulos-Stournaras &
Iles (1984) J. Zool. Lond. 203 427-440.
 Muscle functioning as? power producer =
active and shortening; stabiliser if active and
near constant length
 In vivo (in life) V/Vmax
Force

 V/Vmax
Velocity
V = in vivo shortening velocity
 Vmax = maximum shortening velocity
 Mouse soleus trot 0.20 – 0.31
 Mouse soleus gallop 0.34 – 0.48
 Mouse EDL trot 0.24 – 0.39
 Mouse EDL gallop 0.37 – 0.52

 Remember peak power produced at

V/Vmax c. 0.3 – 0.4
 So peak muscle power at trot?

 See James et al. (1995) J. Exp. Biol.

198 491-502. [Table 2].
 In vivo (in life) SL
 Sarcomere length-force curve based on rat
filament lengths and isometric (constant
length)
 Calculated range of sarcomere lengths used in
vivo
 Calculated sarcomere length at L0 (length for
maximal in vitro force)
 In vivo length ranges close to maximal force
 Descending limb usage…
 See James et al (1995) J. Exp. Biol. 198 491-502.
[Figure 6]. EDL L 0
EDL in vivo
soleus L0
100 soleus in vivo
Force (% maximum)

80

60 active passive
40
20

0
1.0 1.5 2.0 2.5 3.0 3.5 4.0
Sarcomere Length m
 Real work loops
 Active = anticlockwise
 Passive = clockwise
 Loop represents net work performed (Work =
F  d)
 Passive usually low (collagen) and represents
the work required to cycle the muscle through
one ‘stride’
 stress falls during shortening due to Force-
velocity relationship and shortening
deactivation
Time
Length
stress active

Concentric activity

passive
strain
 Real work loops 2
Mouse EDL at 8Hz cycle frequency
James et al. (1995) J. Exp. Biol. 198 491-

502 [Figure 5]
Increased muscle starting length =

increased passive work

Increased strain = increased passive work

Increased velocity = increased passive

work
Passive due to: collagen & other
L0
connective proteins

10% strain at each length

+ 10% L0
+ 10% L0

L0 + 20% L0
Force

Passive
(collagen)
Active
Sarcomere length
 Mouse soleus work – cycle
frequency
Work measured in Joules (J); power in Watts (W)
14 Frequency = # per second
Work decreases with cycle 
Net work/cycle (J kg-1)

12
10 (velocity increases causing
8 force to decrease & work to
decrease)
6
4
2
0 Same strain
0 2 4 6 8 10 different stress
Cycle frequency (Hz)

Power = work  cycle frequency

POWER OUTPUT (W kg-1 )

35
30 = work done  time taken
25
20
15 NB mice tend to trot
10 trot c. 5 to 6 Hz
5
0
0 2 4 6 8
CYCLE FREQUENCY (Hz)
 Strain complications
 Sonomicrometry on Bufo americanus
semimembranosus (SM) muscle (hip
extensor)
 Differential strain along muscle length in
vivo and in vitro
 muscle architecture caused this
 Ahn et al (2003) J. Physiol. 549 877-888. in library

Sonomicrometry
implants

Proximal tendon
Distal tendon
(towards toes)

Pennation changes during activity

strain = change in length  initial length
 Strain from sonomicrometry
 Bufo americanus SM
 Ahn et al (2003) J. Physiol. 549 877-888. in
library

 strain differs between regions

 velocity differs
 different regions of muscle acting on
different part of force-length and force-
velocity curves

Distal segment
Strain

Central segment

Time

Central segment = increased strain and increased

velocity
 Complications in muscle
activity

 How active is a muscle?

 EMG vs. in vitro
 cannot determine % activity from in
vivo to relate to stimulation to apply in
vitro
 best approximations during maximal
activity e.g. sprinting and jumping
 assume all of muscle active

 Compartmentalisation of muscle
activity
 Cycling of fibres?
 increase fatigue resistance

active inactive active

 Fibre types
Type I Type IIA Type IIB
SO FOG FG
Red (s) Red (f) White
Slow FR FF
Contraction long short short
time
Mitochondria high high Low
and SDH
ATPase at low high high
pH 10.0
Glycogen low high High
content
Fatigue high high Low
resistance
‘contraction’ times = activation, relaxation
FOG = fast oxidative glycolytic
FR = fast & more fatigue resistant; FF = fast and more
fatigueable
SDH = succinate dehydrogenase (a marker enzyme for
oxidative metabolism)
ATPase = myosin ATPase staining (commonly used
to determine fibre type)
Glycogen stores especially important to fuel glycolysis
Different fibre types for different jobs
Mixed muscle fibre types in muscles
 Isoforms of Muscle
Proteins
•Overall phenotype of muscle fibre depends on
which muscle protein isoforms are expressed
•Slow and fast isoforms exist of:
•Thick filament proteins
•Myosin heavy chain (many)
•Myosin light chains
•Most thin filament proteins
•Tropomyosin
•Troponin-C
•Tn-T (many)
•Tn-I

•No known isoforms of actin in skeletal muscle

 Detecting Muscle
Protein Isoforms
 Determine composition by gel
electrophoresis
 e.g. Sodium Dodecyl Sulphate
polyacrylamide gel electrophoresis
(SDS-PAGE)
 isoforms move in gels according to
size, mass or electrical charge
 In humans: co-expression of MHC
isoforms within a fibre:
 I +I
 I + IIA contractile
 IIA + IIA speed
 IIA + IIB
 IIB + IIB

 IIX
  Many possible combinations of isoform
combinations
 Detecting Muscle
Protein Isoforms 2

contractile
speed

An example gel
 Myosin Heavy
Chain Isoforms

Vmax

% MHCIIB

Myosin heavy chain type IIB (fast glycolytic)

In human soleus and quadriceps muscle fibres

Larsson and Moss (1993) J Physiol 472 595-614.

in library
 Myosin Light
chain (MLC) Isoforms
Vmax = maximum muscle shortening velocity

Vmax

Ratio of myosin light chain 3 to myosin light chain 2

In rat muscle fibres with same MHC content

Ratio of alkali MLC’s : no effect on force

General finding that fibre type has little effect on force
faster muscles produce a little bit higher stress

Bottineli and Reggiani (1995) Eur J Physiol 429 592-

594. Not in library
Histochemical fibre typing 1
 Freeze muscle in liquid nitrogen
 Cut thin sections (um)
 Chemicals used to stain muscle
according to enzyme activities
 SDHase (succinate dehydrogenase)
staining (Krebs/TCA cycle) so indicate
how oxidative the muscle is
 Myosin ATPase staining indicates
contractile rate
 Assess ratios of I : IIA : IIB
 Semi-quantitative (indicative)
 Biochemical activity measurements
are better
 e.g. SDHase quantification of enzyme
activity IIB
IIA
I
Histochemical fibre typing 1
SDHase Myosin ATPase

darker blue = more oxidative dark = fastest

Fibre type I IIA IIB

SDHase activity high high low

ATPase activity low high high
 Isometric Properties of
Fast and Slow Muscle
Faster muscle = faster activation rate (as faster
calcium release from SR) and faster relaxation rate (as
faster calcium binding [parvalbumin] and reuptake to
SR [sarcoplasmic reticulum] via calcium pumps)

Twitch
Fast
Slow

Force

Stimulation
Time
Tetanus
Slow
Fast

Force

Stimulation
 Fast vs. slow muscle PO
Endurance
Sprint
Power output (W/kg)

(% of first loop)
slow

Power output
fast

fast
slow

Duration of activity (s)

Cycle Frequency (Hz)

Power = force  velocity

relative power in Watts per kilogramme of muscle

 faster muscles produce more force at any

shortening velocity, therefore more power
 Theoretical relationships between fast and
slow muscle for power output and fatigue
resistance
 Trade-offs….. between sprint and endurance
type activities
 Fast vs. slow muscle PO 2
 Mouse muscle power output-cycle frequency
curves
 Extensor digitorum longus extends the toes
and is a faster muscle (higher Vmax) producing
3 times as much power (power to flick toes
forward during swing phase)
 soleus is an ankle extensor (stabilisation role
during stance)
stride  trotting
stride  (normal speed)
slowest stride 
walk maximal
150 gallop
POWER OUTPUT (W / kg)

EDL faster
Right: Data from 100
James et al. (1995)
J. Exp. Biol. 198 491-502
Mouse EDL & soleus 50
soleus
slower
0
0 4 8 12 16 20 24
CYCLE FREQUENCY (Hz)
 Muscular Fatigue
Faster fibres fatigue here IIB
Force Slower fibres
fatiguing here
IIA

Time
•Above: Theoretical pattern of fatigue
•NB effect of fibre type
•Below: Pattern of fatigue measured in Xenopus
laevis gastrocnemius. all fibres maximally activated
all the time
140
A IIB fibres fatiguing
120
100
IIA fibres fatiguing
Force (mN)

80
60 slowest fibres
40
20
0
0 5 10 15 20 25 30
On 232SPO CUOnline: Cycle Number
Wilson, James & Van Damme (2002) J. Exp. Biol. 205 1145-1152.
Fatigue effects on work loops
 Mouse EDL muscle (a faster muscle)
 Wilson and James (2004) Proc. Roy. Soc. Lond. B.
(Suppl.) 271 S222-S225. On 232SPO CUOnline
 Stress (force per musclecross-sectional
area) decreases with fatigue
force
A
decreased
150
Stress (kNm-2)

1
100
15 force-velocity
50 relationship
35 changed:
0 decreased Vmax
0.00 0.05 0.10 0.15 0.20
Time (s)
So loop 35 indicates a problem in maintaining force
during shortening B 150
1
Stress (kNm-2)

100
15
Relaxation rate
35 50
has decreased so
slower to relax
-0.05 0.05
Strain (± L0)
 Sprint vs. endurance
Intuitive trade-off between sprint and endurance

Sprint
performance

Endurance performance
 But in whole animal locomotion normally:
 (problems of ‘athlete’ quality)
 Better athlete hypothesis genetics (setting range
of possible performances) + training and
environment (determining place in range)
sprint
 Human decathletes
 Decathletes of similar international
ranking
 Negative correlation between 100m sprint
(more anaerobic) and 1,500m run (more
aerobic)
 Positive correlations between more
anaerobic events: 100m sprint and: long
jump, 400m run, 110m hurdles
 Negative correlation between shot putt
and 1,500m run
 Van Damme, Wilson, Vanhooydonck & Aerts (2002)
Nature 415 755-756. in library

 Why?: fast vs. slow muscles?

negative positive
100m sprint

relationship relationship

100m
sprint

1500m race long jump

 Muscle trade-offs between
Sprint and Endurance capacity
i.e. how well can force be maintained
during prolonged exercise?
output (20th run/1st run)
index of power

0.6
R2 = -0.67
0.5
endurance
Endurance

0.4
0.3
0.2
Fatigue

0.1
0
30 35 40 45 50
Initial power output (W/kg)
sprint

 Bufo viridis gastrocnemius (ankle extensor)

muscle

 Wilson, James, Kohlsdorf & Cox (2004) J.

Comp. Physiol. 174 453-459. on CUOnline
 0.6
A
0.5

Fatigue Resistance
endurance
0.4

0.3

0.2
More Bufo viridis trade-offs
0.1

0.0
30 35 40 45 50
-1
Max. Power Output (W kg ) sprint
0.6

0.5
B
Fatigue Resistance
endurance

0.4

0.3

0.2

0.1

0.0
150 200 250 300

Max. Stress (kN m-2) sprint

Max. Power Output (W kg-1)

60
C
50
sprint

40

30

20

10

0
150 200 250 300

Max. Stress (kN m-2) sprint

 Mouse Trade-off Correlations

 Mouse EDL work loops & isometrics

(constant length)
 Work loop sprint and endurance

 +ve: Maximal isometric tetanic force &

Maximal work loop force
 +ve: Maximal work loop force and
power
 -ve: Maximum work loop power and
work fatigue resistance
 -ve: Maximum work loop force and work
loop fatigue resistance

 Wilson, R.S. and James, R.S. (2004) Proc. Roy. Soc.

Lond. B. (Suppl.) 271 S222-S225. On 232SPO
CUOnline
 Sprint and Endurance training
 Male rats trained on a treadmill for 10 weeks
 Tested passive stress-strain relationship
 Sprint or endurance training increased passive
muscle strength (maximal stress) and
toughness (maximal energy) and stiffness
(change in stress  change in strain) but not
extensibility (maximal strain)
 endurance: lots of lower speed and force
training compared with sprint training

endurance
Stress (force  csa)

sprint

control

Strain (length change  initial length)

Muñiz et al (2001) Acta Physiol Scand 173 207-212.

What causes muscle fatigue?
 Why do mammalian muscles fatigue during
high intensity activity?
 lactic acid build up – unlikely to be the cause
 at low temperatures lactic acid causes fatigue
 at physiological temperatures: minimal effect

 impaired calcium release – probable

 during fatigue less calcium released from SR
so incomplete muscle activation
 Mouse EDL work loops at 35C
 James et al (2004) J. Appl. Physiol. 96 545-552. On
232SPO CUOnline and in library
 Power output in fatigued muscle increased
with10mM caffeine treatment when
compared with controls
 Calcium is stored in SR when the muscle is
at rest
 during fatigue calcium phosphate precipitates
in SR?
 Caffeine enhancing opening of calcium
channels in sarcoplasmic reticulum
 Remember that Calcium binds to TnC during
activation (muscle switch)
 so increased force
 10mM Caffeine effects
pre fatigue 140 10mM caffeine
Power output relative to pre-
120
fatigue (%)
100
80
60
40 Control
fatigued 20 washout
0
-5 5 15 25 35 45 55
Time after fatigue run (min)

 What causes increase in power output?

180
Maximum work loop
stress (kN m )

130
-2

80

30

-20 -5 5 15 25 35 45 55
Time after fatigue run (min)

Other methylxanthines have similar effects

Effect of 70uM caffeine on PO
 So could caffeine improve an athletes
performance?
 70M caffeine in blood plasma in
humans (very high caffeine is fatal)
 No effect on fatigued muscle but affects
normal muscle
 Mouse EDL work loops
Power output (% of theoretical control)

106
Washout
104

102

100

98

96

94

92
-20 0 20 40 60 80 100
Time from start of caffeine incubation (min)
James, R.S., Kohlsdorf, T., Cox, V.M. and Navas, C.A. (2005)
Eur. J. Appl. Physiol. 95 74-82.
 What determines
muscle phenotype?
gene expression
Embryonic phenotype
determined by genotype

Birth

Innervation (EMG)
Volume of work
Peak forces
Plastic Phenotype Hormones
(e.g. testosterone)
Growth

I.e muscle phenotype alters to reflect changing

demands made upon the muscle
(‘environmental’ effects)
 Cross-innervation studies
1960’s cross-innervation experiments on mammals
FDL = flexor digitorum longus
nerves cut and rejoined to itself (sham operated) or
other muscle
Sham operated (rejoined to themselves)

FDL nerve soleus nerve

FDL soleus
FDL
soleus
Twitch force
Stimulation
Experimental
soleus nerve
FDL nerve

FDL soleus

soleus FDL
Twitch force
Stimulation
e.g. Buller et al. (1960) J Physiol 150 417-430. In library
Development and Growth
In humans
 During foetal development fibre

number increases (hyperplasia) i.e.

development of new fibres to increase
muscle size

 Once born muscle development

consists of repair to damaged cells
and growth by fibre hypertrophy (i.e.
increase in fibre size)

 Fibre hypertrophy: increased number

of myofibrils in muscle fibre =
increased fibre size (increased cross-
sectional area)

 Although new fibres cannot be formed

fibre composition can change
 Growth & Development
 As animal gets older mechanics may
change
 Muscles and bones grow in length and
width
 Muscle stretch
 Body weight increase so greater forces
involved
 Minimal escape/prey capture
performance?
 Scaling relationships
 smaller animals have faster muscle
protein isoforms so faster stride
frequency
 larger animals higher stride length
 sprint speed dependent on stride
frequency and stride length
 Response to environment
 Respond to changes
 Muscle Adaptation
to new length
•If muscle under stretch
•e.g. growth of limb bones
L1 L2
Force L3

Length
•Response
•Addition of new sarcomeres to length
•Maximal active force at longer (L2)
resting length

•If muscle to slack at rest, atrophy and

shortening (L3)
•e.g. in plaster cast
 Scaling: Fish Body size effects
 Sculpin swimming
 James & Johnston (1998) J. Exp. Biol. 201 913-923. On
232SPO CUOnline
 As body size increases relative maximum
swimming velocity decreases (absolute
speed fairly constant)
 so smaller fish using higher stride frequency:
how?
Maximum velocity (body lengths s-1)

20

10

1
5 10 20 30
Total body length (cm)
 Fish mechanics
 Sculpin fast muscle: Isometrics & Isovelocity
James et al. (1998) J. Exp. Biol. 201 901-912.

Peak twitch to 50% relaxation (ms)

calcium
Time to peak twitch force (ms)

100 100
binding or
50 50 pumping?

20
20
10
10
5 10 20 30 5 10 20 30
Total body length (cm) Total body length (cm)
Last stimulus to 50% tetanus relaxation (ms)

100
V0 (muscle lengths s-1)

10

50
5

20 2

10 1
5 10 20 30 5 10 20 30
Total body length (cm) Total body length (cm)
 Explain fish mechanics?
 Sculpin study continued….

2
(umol released mg-1 min-1)
Myosin ATPase activity

Affects rate of ATP breakdown

0.5

0.2
5 10 20 30
Total body length (cm)

•Changes in TnI isoform

•faster isoform in smaller fish
•No changes in thick filament proteins MLC, MHC
•No changes in other thin filament proteins:
•TnC, TnT, actin or Tm
 Mammalian scaling of
muscle properties
 Vmax (maximum shortening velocity)
measurements in rat, cat and horse
soleus single muscle fibres
 Rome, Sosnicki & Goble (1990). J. Physiol. 431, 173-185. in
library

 Large decrease in Vmax of type I muscle

fibres with increased body size
 Smaller decrease in Vmax of type IIB
muscle fibres with increased body size

 Smaller animals tend to have

 Faster muscle fibres
 Higher stride frequencies (strides s-1)
 Lower stride length (shorter legs)

 Larger animals: slower more efficient

muscles (e.g. decreased calcium pump cost)
 Further Evidence on
scaling
 Xenopus laevis adductor magnus (slower) and
sartorius (faster) muscles from frogs of
different sizes
 Work loop experiments to look at cycle
frequency that yielded maximal power
 Altringham, Morris, James & Smith (1996) Experimental Biology
Online 1 (6): this is available online for free. You can search for the
journal name via Google

adductor magnus
Cycle frequency (Hz)

sartorius

Body Mass (g)

slower muscle, larger decrease
in cycle frequency for maximal power
 Why should temperature
affect locomotion?
 Temperature affects enzyme activity rates
 e.g. myosin ATPase
 therefore can affect rates of mechanics

• e.g. activation rate

 Range of muscle temperatures lower in ‘warm

blooded’ (endothermic) animals but basic
effects the same as in cold blooded
(ectothermic) animals
rate at which enzyme works
Enzyme activity

Temperature
so increase temperature causes increase rates.
eventually denaturation occurs
Human temperature effects
 Heating/cooling legs in water
 thigh muscle 39.3, 36.6, 31.9, 29.0°C
 Cycle ergometer
 Sargeant (1987) Eur J Appl Physiol. 56 693-698.

 Increased temperature caused

 Increased peak force
 Increased power
 Increased rate of fatigue

 Linane, Brooks, Cox and Ball (2004) Eur J Appl

Physiol. 93 159-166.
 Full immersion of human in 43C caused 1%
increase in muscle power output during subsequent
cycling

 Why?
 Sargeant (1987)

Maximum peak force (N)

Thigh muscle temperatures

39.3
36.6
31.9
29.0

Pedalling rate (rev./min)

Hotter muscles have higher maximal shortening V,
higher rates of activation and relaxation. so produce
more force at any velocity than colder muscles
Maximum peak power (W)

39.3
31.9

29.0

Pedalling rate (rev./min) i.e velocity

Human temperature effects 2
 Heating/cooling hands in water
 18, 25 or 39°C for 30 minutes or in
air at room temperature
 approximate muscle temperatures of
23.5, 28, 32.5 and 37°C
 Handgrip test: isometric force then
force-velocity relationship
 Binkhorst et al (1977) J Appl
Physiol. 42 471-475. in library

 Increased temperature caused

 Increased maximal shortening
velocity
 Increased power

 No change in maximal isometric

 Temperature Effects on Locomotion
Rana temporaria: Navas, James, Wakeling, Kemp and Johnston (1999)
J. Comp. Physiol. 169 588-596. see Rob for this

Jump take-off velocity (BL s-1)

40 A) 45 B)
Jump distance (BL)

35
40
30
25 35
20
30
15
10 25
5 10 15 20 5 10 15 20

power output per kg muscle mass

Mean swimming velocity (BL s-1)
Mean jump power output (W kg-1)

600 C) 12 D)

500
10
400
300 8

200 6
100
5 10 15 20 5 10 15 20

Temperature (degrees C)
More T. effects on locomotion
Xenopus laevis
Maximum Swimming Speed (m s-1)

1.6

1.2

0.8

0.4

0.0
0 5 10 15 20 25 30 35
Temperature (oC)

Wilson, James and Johnston (2000) J Comp. Physiol B 170 117-124.

On 232SPO CUOnline
Effects on Isometric Force
Xenopus laevis gastrocnemius fibre bundles
100
Twitch Force (% of max.)

90

80

70

60
0 5 10 15 20 25 30 35

100
Tetanic Force (% of max.)

90

80

70

60
0 5 10 15 20 25 30 35

Temperature (oC)

Wilson, James and Johnston (2000) J Comp. Physiol B 170 117-124.

Effects on Isometric Times
Xenopus laevis gastrocnemius fibre bundles
140 TPT PTHR
Time to Peak twitch (s)

120

100

80

60

40

20
0 5 10 15 20 25 30 35
400
TPT 1/2 Relax. (s)

300

200

100

0
0 5 10 15 20 25 30 35
Temperature (oC)
Wilson, James and Johnston (2000) J Comp. Physiol B 170 117-124.
Overall temperature effects
On work loops
 Increased temperature:
 More rapid force activation
 Increased maximal force output
 Increased maximal shortening velocity
 so can work at higher cycle frequency
 Better maintenance of force during
shortening
 More rapid force relaxation
 so larger area of work loop = more
work
 so more power output

higher temperature

lower temperature
 Comparison of species
 Increased optimal cycle
frequency for power output
with temperature
 Increased optimal cycle
frequency increases power
output
 ‘cold’ vs. ‘warm’ blooded….

12
POWER OUTP

150 11

100 10
7
UT (W kg )

9
C)
(0

50 4
8
5
6
40
RE

3 30
TU

0 2 20
-1

RA

1
15 10
PE

CYC 10 0
5
M

LE F 0
REQ
TE

UEN
CY (H
z)
 Eccentric muscle activity
 Muscle active & being stretched
 Extra stretch of myosin neck region
(S2) causes:
 more rapid force rise
 enhanced force production
 E.g. quadriceps and gastrocnemius
when walking down stairs
 stabilise/brake the limb
 Eccentric activity before concentric
activity enhances force during
concentric as well!
Force 0 velocity =
isometric

Eccentric Concentric
(muscle lengthening) (muscle shortening)

Velocity
0
Eccentric Muscle Stress-Strain
curves
Active (eccentric exercise)

Stress energy required

to stretch
Work input

Strain

Stress
low energy output
during shortening
Work output as c. passive

Strain

net energy cost

Stress to cycle this muscle.
braking action
Net work

Strain
 Is long jumping
performance dependent on
tissue mechanics?
 Review long jumping performance in different
animals

 Review tissue mechanics in different animals

 Conclusions

 See James et al. (2007) Journal of Experimental Biology

review paper on CUOnline
 What does jumping depend upon?
v 2 sin 2
d
g
 d is distance jumped (e.g. m)
 v is take-off velocity (e.g. m s-1)
  is take-off angle
 g is the acceleration due to gravity
(approximately 9.8 m s-2)

  jump distance largely dependent on

take off velocity

 How increase velocity?

 Increase acceleration rate
 Increase distance over which accelerate

Centre of mass

 What else does jumping
depend on?
2
  3 Power = force × speed
 W  L  sin 2
d   
 Mb  g
 

 W is total average power required for

the jump
 L is the distance from the centre of
mass to the tip of the toes
 Mb is body mass of the animal

 So increase power
 Maybe: increase muscle mass, energy
storage, increase muscle speed and/or
force?
 Increase L by increased relative leg
length?
 Minimise body mass?
 How can muscle power
output be increased?
 Increased proportion of fast muscle
fibres in jumping muscles (leg
extensors)
 In jumping frogs:
 Jumping muscles 89% fastest fibres
 Non-jumping muscles 29%

 As % of fastest fibres increases from 0

to 100% there was a 57% increase in
power output and 22% increase in stress
and increased shortening velocity
 NB. Trade off in muscle function
 Increased temperature (mainly ectotherms)
 Endotherms regulate, ectotherms
behavioural thermoregulation
 Increased rates of activation and
relaxation
 Increased power output
 Energy storage and return
See James et al. (2007) Journal of Experimental Biology
review paper on CUOnline
 Energy storage
 In many animals including man
 Countermovement
 Active lengthening of extensor muscle
prior to shortening
Force enhancement
 OR rapid early shortening of muscle
without movement of body e.g. frogs
 Frog
muscle produce only c.30% of
power for the jump!
 OR catch mechanism (insects)

 Elastic potential energy storage

 Mainly in tendons of extensor muscles

 Amplifies power

 Virtually temperature independent

 Body Size affects muscle
performance
 As body size increases
 Muscle fibre type tends to become slower
(slight decrease in force)
 Rate of muscle activation and relaxation tends
to decrease
 Maximum relative muscle shortening velocity
decreases (in muscle lengths s-1)

 But larger animals have longer muscles

 Power output (W kg-1) and stress unaffected

 NB PO = F × V

 So larger animals can ‘afford’ to have slower

muscle fibre type and still achieve similar power
output
 But why are slower fibres useful?
 So why don’t smaller animals jump as far as
larger animals?
 Drag
 Shorter limbs so shorter time to accelerate over
so need greater peak power, so need faster
muscles
Body Size affects long jump
performance
 Long jump performance increases with
increased body size
 But muscle performance?
Long jump distance (m)

Line indicates 100 W.kg-1 BM

Compare with 100 W kg-1 muscle mass

Body length (m)

 Hindlimb length
 Hindlimb length increases with increasing
body size
 Jumping vs. non-jumping mammals

Jumping specialists (mammals)

Log hindlimb length (cm)

Log cubed root of body mass (g)

Emerson, S.B. (1985) In ‘Functional Vertebrate Morphology’

Cambridge: Harvard University Press.
 Morphology
 Leg length
 Frog and lizard species with relatively
longer legs tend to jump further

 Muscle mass
 Jumping c.f. non jumping frog &
mammal species increased leg extensor
muscle mass
 In frogs higher relative muscle mass =
longer jump distance (leg extensor
muscle mass as % of body mass)

 Muscle architecture
 Tend to be longer & less pennate in larger
animal species
 So increased maximum shortening velocity
 Muscle insertion more proximal
 Predicting jump performance
 Jump performance often assessed as
jump distance or jump take-off velocity
 One predicts the other

 Domestic cat jump take of velocity:

62%, lean body mass residuals of
hindlimb length and fat mass
 So fat cats with short legs don’t jump as far!
 Harris, M.A. and Steudel, K. (2002) JEB 205 3877-3889.

 Frog (Hyla multilineata) jump distance:

43%, body length residuals of hindlimb
muscle mass and pyruvate kinase
activity
 So frogs with more extensor muscle mass
and more glycolytic muscle jump further
 James, R.S., Wilson, R.S., Carvalho, J.E., Kohlsdorf, T.,
Gomes, F.R., Navas, C.A. (2005) PBZ 78 857-867.

 Jumping performance linked to fitness

in some species
 Accelerated development
All individuals (dashed line)
Mb0.37 r2=0.83 P<0.001

Adults (post-metamorph)
r2=0.01 P>0.05

Juveniles (metamorph)
Mb0.53 r2=0.67 P<0.001

So selected rapid development of tissues

Important for jump performance

Wilson, R.S., Franklin, C.E., James, R.S. (2000) JEB 203 1937-
1946. On CUOnline
 Modelling jump
performance
 In a human like animal: countermovement and
catapult jumps yield similar jump distances >
squat jump
 Squat jump = no or limited energy storage

 In bush baby and insect like animals catapult

jump>countermovement jump

 Increased muscle shortening velocity

increased jump distance in all animals (more
important in human)

 Decreased tendon stiffness increased jump

distance in all animals (more important in
insect)

 Increased leg length increased jump distance

in all animals (more important in human)

 Alexander, R. McN. (1995) Philos. Trans. R. Soc. Lond. B.

Biol. Sci. 347, 235-248.