Biomechanics of musculotendinous unit Flashcards
Tissues
are groups of similar cells and their extracellular products, organised to perform a common function.
Tissue types
- Epithelial Tissue-covers body surfaces, lines cavities & forms glands
- MuscleTissue responsible for movement, interaction with the environment
- Nervous Tissue – receives, transmits & integrates information to control the
activities of the body - ConnectiveTissue–supportstheother3tissues
A muscle (organ) = muscle tissue + connective tissue
ECM
Extracellular matrix (ECM)
• A substance produced by the cells of a specific tissue
• Can contain protein, salts, H2O, and dissolved macromolecules • Located outside of cells
• Respond to physical stresses
Muscle tissue has very little (if any) ECM – rather, it is surrounded by connective tissue **referred to as ECM in Oatisandsomeothersources.
Connective tissue has a significant ECM
Microstructure of muscle:
- Muscle is made up of a large number of bundles (fascicles) of muscle fibres (muscle cells), surrounded by connective tissue.
- A single muscle fibre (cell) is very long. It runs parallel to other fibres.
- The fibre is made from a large number of fused embryonic cells, therefore a single muscle fibre has many nuclei
- Inside each cell is a bundle of myofibrils (muscle – slender fibre), that lie in parallel
- These are the contractile filaments that convert the electrical signal (action potential) initiated in the nervous system to muscle force are within the myofibril
- A series of sarcomere’s make up each myofibril
- The sarcomere is the basic contractile unit of skeletal muscle.
Microstructure of muscle 2:
Thin filaments (actin) attach at the Z line Thick filaments (myosin) anchor at the M line in the centre of the sarcomere
When at rest, actin and myosin overlap partially
Whole muscle shortening results as the filaments overlap more, pulling the Z line’s closer
Whole muscle lengthening results as the filaments overlap less
Contraction can occur during lengthening or shortening
**Elastic filament: Titin - anchors myosin to the Z line, contributes to passive force in muscle.
PCSA
Different muscles have different force generating capacity.
Greatest predictor of force is the muscles physiological cross sectional area (PCSA)
PCSA = Muscle volume / Fiber length
or
PCSA =Muscle volume x CosΦ Fiber length / fiber length
Fiber length and pennation angle [CosΦ] changes with contraction and joint angle… PCSA will change depending on muscle condition when measured
Individual muscle force (N) is influenced by
Muscle architecture, muscle length
Muscle fibre length, pennation angle - PCSA Specific tension – fibre types Number/discharge rate of active motor units
i.e. neural drive
Type of contraction i.e. isometric, concentric, eccentric
speed of contraction, force relative to length Passive force
Muscle fatigue and damage
MORE FORCE TRANSFER WHEN PARALLEL 2 MUSCLE FIBRES
muscle volume
Muscle volume does not change with contraction and joint angle…
MUSCLe length changes with contraction and joint angle…
have overlap of actin and myosin occuring actively > contraction and passive shortening
fascile length longest at greater angle
Pennation angle changes with contraction and joint angle…
Muscle force transfer to tendon is reduced when muscle fascicles insert with a greater pennation angle
Changes in pennation angle during contraction make a small difference to overall force within a muscle.
What is specific tension?
Specific tension (Tspe)= the maximum force exerted by the fibers per unit of PCSA
Total muscle force = PCSA x Specific tension
Tspe depends on muscle typology, with a higher specific tension associated with Type II muscle fibres.
Skeletal muscles contain different proportions of Type I, IIA and IIB motor units depending on their function:
POSTURAL MUSCLES: high proportion Type I (e.g. soleus 86% slow twitch)
DYNAMIC MUSCLES: high proportion Type II (e.g. gastrocnemius 56% fast twitch)
Most human muscles are mixed (40% - 60% fast twitch)
motor neuron
Each muscle fibre is innervated by a motor neuron (from the spinal cord) at a neuromuscular junction (motor point).
Motor unit = 1 motoneuron, its motor axon and all of the muscle fibres it innervates
Action Potential
Motoneuron receives excitatory and inhibitory input from descending pathways, spinal interneurons & afferent fibres
When sufficient excitatory input to reach firing threshold, an action potential is generated
Every action potential generated in the motor neuron generates an action potential in the motor units muscle fibres
» actin/myosin cross-bridging»_space; active force production
Single MOTOR UNIT SMU
Force is altered by number & discharge rate of single motor units (SMU)
Henneman’s size principle
Small motor units (within a motor unit pool) are recruited first
Same input = greater change in membrane potential in the smaller units»_space; reaches threshold sooner
With greater excitatory input the number of motor units increase, and the size of the recruited motor units increase
Assumption: Motor units within the same pool receive the same drive.
Increased drive = more motor units and bigger motor units
RECRUIT SMALLER MOTOR UNIT FIRST BECAUSE REQUIRE EXCITATORY NEURON
FORCES
Force opposing the contraction is larger than the contraction force.
Decelerates the movement (absorbing energy)
STATIC -Isometric (same length)
DYNAMIC - Concentric (shortening)
Eccentric (lengthening)
Isotonic (constant force) Isokinetic (constant angular velocity)
The maximum force that can be produced is dependent on the direction such that: ECCENTRIC > ISOMETRIC > CONCENTRIC; and rate of change of muscle length such that the faster you contract concentrically the less force is produced
ABSOLUTE force produced depends on the motor task
An eccentrically contracting muscle can produce more force at the same muscle length than a concentrically contracting muscle
Eccentric = higher torque for same motor drive
in Same torque in each condition below
• Motor unit discharge rate lower during eccentric torque matched contractions
• For each motor unit discharge more torque is produced during eccentric contractions
In eccentric movements actin and myosin ‘hold on’, more stretch of the elastic components (eg titin) > more force for same energy (# action potentials)
Decreased rate of cross-bridge detachments»_space; greater force production on the eccentric bout.
Force-velocity Relationship
The force generated by a muscle is also dependent on its (lengthening/shortening) velocity.
- Mechanisms for higher muscle force at lower shortening speed:
- The force generated by a muscle depends on the total number of actin-myosin cross bridges
It takes time for cross-bridges to attach.
- As filaments slide past each other faster (i.e. as the muscle shortens with increased velocity), fewer cross bridges are able to attach and generate force.
As the relative filament velocity decreases, more cross bridges have time to attach and generate force.
What makes up the muscle-tendon unit and why are these components important when considering muscle force?
TOTAL muscle force = ACTIVE + PASSIVE tension
Active Tension = Force produced by active sarcomeres, driven by CNS
Passive Tension = Force produced by stretched connective tissue, cross bridges
Hill’s mechanical model of the muscle-tendon unit.
Contractile component (CC) – muscle fibers, actin and myosin cross bridges Series elastic component (SEC): intracellular titin, tendon Parallel elastic component (PEC): connective tissue - epimysium and perimysium, endomysium & passive cross bridge connections
Muscle fatigue:
exercise-induced reduction in ability to produce force peripheral (muscle): failure to produce force appropriate to drive
central (brain, spinal cord): failure to drive motoneurons adequately
Exciting stimuli can increase maximal performance
Peripheral mechanisms will be task dependent, peripheral sites may include:
neuromuscular junction [reduced release of Ach]
changes in the muscle cell membrane potential [Na+/K+ pump] excitation-contraction coupling due
to a change in the calcium release
accumulation of metabolites [build up of lactate and H+ will change the pH and alter cell membrane]
depletion of fuels [ATP]
Muscle damage reduces ability to generate force
Some sarcomeres resist the stretch more than others: Overstretched, disrupted sarcomeres > Membrane damage»_space; uncontrolled release of calcium >
- shift in optimal length (stretched sarcomeres)
- fall in active tension (less force generated with AP)
- rise in passive tension
- inhibition of motor signal through odema, nociceptor sensitization
