Lecture 8 - Muscles Flashcards
What makes muscle tissue unique (4)?
Extensibility
- ability to stretch in response to a force
Elasticity
- recoil when stretch is removed and return to its resting length
Contractibility
- ability to shorten/contract
Irritability
- ability to respond to a stimulus
Hierarchical structure
Sarcomere Myofibril Fibres (joined by endomycium - continuous with cap + nerves) Fasicles (joined by perimycium) Muscles
What creates motion?
- CNS sends signal to motor unit
- Muscle shortens and applies force on bones
- sliding filament theory - relative movement between actin and myosin
- crosslinks flip over and shorten muscle –> sum of contractions of all individual sarcomeres - Moment generated around joint
- muscle contracts in the middle and pulls on both bones
Components of a sarcomere
Actin - thin filament (5nm)
Myosin - thick filament (15nm)
Titin - maintains structure (like a molecular spring)
Hill muscle model:
What are represented by:
- contractile element
- elastic element in series/parallel
What is the force equation relating them?
Contractile element = actin/myosin
Elastic element in series = tendon
Elastic element in parallel = connective tissues
F(active) + F(passive) = F(tot)
What affects the force production?
Tension depends on:
- amount of stimulation
- length of muscle
- velocity of muscle shortening
Maximum tension (i.e. maximum overlap of actin and myosin) is at resting length –> striation spacing = 2-2.5um
Draw the tension-length curve for a muscle:
Active tension:
- max at ideal length
- negative parabola
- -> shortened muscles = less tension produced
Passive tension:
- kicks in when muscle is lengthened only
- due to tendons and connective tissues
- longer –> resists tension
What is active insufficiency?
Failure to produce force when the muscle is too short
Difference between an agonist, antagonist and synergist?
Example of an agonist and antagonist?
Agonist - responsible for movement
Antagonist - opposes the movement, adds control
Synergist - assists the agonist in performing the movement
Example:
bicep (flexion) tricep (extension)
Concentric contraction
Shortening of muscle causes joint movement
–> muscle moment the same direction as joint angle change
e.g. (on chair) quads contract
Eccentric contraction
Lengthening of muscle decelerates joint movement
–> muscle moment opposite direction to change in joint angle
e.g. quads contract, but moment due to external weight if more than that due to muscle force - muscle lengthens
Isometric contraction
Contraction of muscle with no movement
–> muscle stays the same length
e.g. posture
Of the three types of contraction, which produced the greatest force?
Eccentric > isometric > concentric
Due to longer contraction time:
- more cross bridging
- more tension in elastic components
- recruitment of motor neurons
Velocity tension curve - relationship between eccentric and isometric contraction?
max T(eccentric) = 1.25 max T(isometric)
Muscle fibre types:
Fibre types allow for muscle adaptation
Type I:
- recruited first
- slow contraction
- good blood supply (red)
- difficult to fatigue
- endurance
- small diameter (low tension)
Type IIA:
- moderately fast contraction
- variable contractile force
- long term anaerobic
- moderately good blood supply
- intermediate fibres (between I and II)
Type IIB:
- fast contraction
- powerful contraction (greater force than type I)
- anaerobic
- poor blood supply (white in colour)
- rapidly fatigued
What affects muscle movement (2)?
Length of muscles moment arm
- |_ distance between muscle and point of rotation
- smaller moment arm = larger excursion
Length of fibres composing the muscles
- muscle fibre can shorten by 50-60% of its length
- total shortening depends on # sarcomeres in series
Physiological cross sectional area (pCSA) and its force relation
Area |_ to fibre direction
pCSA = muscle volume / fibre length
F(max) = pCSA x 37N/cm2
Pennation angle - what is it and how does its value affect muscle architecture?
Angle at which the fibres are attached to tendon
Fmuscle = Ffiber x cos(a)
- allows more fibres to be packed in –> more force
- high a = shorter fibres, long tendons, static tasks
- low a = longer fibres, more shortening, motion tasks
Four different forms of muscle architecture
Fusiform
- v small pennation angle
- quick movement
- easily fatigued
Unipennate
- larger pennation angle
- slower movement
- powerful
Bipennate
- multiple pennation angles
- static contraction
- stability
Multipennate
- short and long fibres
- multiple angles
- stability and movement
Muscle adaptation in strength training
- bulk up - high force, low reps
- increase pCSA
- bigger fibres, more contractile protein content
- hypertrophy of fibres (increase size, not #)
- improved innervation
Muscle adaptation in endurance training
- adapt by changing energy supply (not fibre size)
- increase # capillaries and mitochondria
Sore muscles- inflammatory response
- tensile stress –> structural injury
- diffusion of cell contents into interstitial fluid
- macrophages come clean up
- elevated pressure, swollen fibres
- delayed onset (24-48hr)
- most severe for eccentric contractions
What affects muscle strength?
- muscle size
- moment arm
- stretch
- contraction velocity
- level of fibre recruitment
- fibre type
Determining muscle forces: optimisation techniques (5)
Minimise total muscle force
- only muscles with longest lever arms are active
Maximum total muscle stress
- max stress equivalent for all muscles –> once max stress reached, synergistic muscle activates
- muscles with longest lever arms are active
Minimise max muscle stress
Minimise muscle power
Maximise endurance
EMG:
What does it measure?
How does it measure it?
Determining force from EMG?
What affects EMG signals?
Measures
- muscle activity (V) - timing and magnitude, not force
Mesure using
- surface EMG (summation of action potentials, non invasive)
- fine wire EMG (specific motor units, invasive - good for small and deep muscles)
Fi = (EMGi x pCSAi) / (EMGpm x pCSApm)
–> pm = prime mover
Factors affecting signals
- cross-talk between muscles
- changes in geometry
- tissue impedance
- external noise
Disuse atrophy
- decrease pCSA
- affects both type I and II fibres
- muscle dependent
