Muscles Flashcards
properties of muscle
40% body mass
extensibility
elasticity
force production
generates movement
cardiac muscle
actin and myosin cross bridges
sliding filament mechanism
node cells produce spontaneous action potentials (autorhythmicity)
electrical coupling between cells via gap junctions
refractory period to prevent tetanic contraction
smooth muscle
surround hollow structures
sliding filament mechanism with actin and myosin
regulated by Ca2+ which is controlled by autonomic nervous system
spontaneous action potentials
skeletal muscle
moves skeleton
sliding filament mechanism with actin and myosin
controlled by motor neurones
tendon
attach muscle to bone
form aponeurosis as all muscles fibres connect to tendoninous structure
transmit force from muscle to skeleton and vice vera
mainly collagen
no metabolic energy required
transmission of muscle force
generated within fibres of muscle belly and transmitted to connective tissue (aponeurosis). sheets of aponeurosis come together to form the tendons of the muscle and force is transmitted through these to skeletal
if muscle changes length, this is translated to the skeleton and the bone (lever) will move
muscle resistance
when an external load is applied to body, muscles resist effect of force. tendons stretch to allow joint to flex and muscles will generate force to absorb the energy of the impact
concentric contraction
force causes shortening
muscle generates more force as what it is trying to move
isometric contraction
same length
external force = force muscle generates
eccentric contraction
external force is greater than the force muscle generates
muscle lengthens while still producing tension
muscle absorbs energy
powerstrokes go in opposite direction
characteristics of skeletal muscle fibres
multinucleated
many mitochondria
transverse tubules
myofibrils (smallest functional elements) and sarcomeres (smallest force capacity)
structure of skeletal muscle
muscle belly
muscle fibre (single muscle cell)
myofibril with sarcomeres
z line
boundary defining ends of sarcomere
complex of proteins
maintains structural integrity
anchors actin filaments
A-band
dark band
contains actin and myosin
remains constant length during contraction
I band
lighter region
only actin
shortens during contraction
H zone
lighter region within A band
no overlap
only myosin
becomes narrower during contraction
M line
centre of sarcomere
attachment site for myosin-stability
actin
thin protein filaments
actin (globular) and tropomyosin (fibrous regulatory protein)
troponin complexes
myosin
thick protein filaments
sliding filament theory
muscle force and length change is generated by the overlapping and interaction of actin and myosin filaments
tropomyosin
regulatory protein that overlaps binding sites on actin for myosin and inhibits interaction when in relaxed state
troponin
regulatory protein that binds to Ca2+ reversibly
conformational change causing it to pull tropomyosin away from the binding sites
T-tubules
projections of sarcolemma into the cell/fibre to get closer to the sarcoplasmic reticulum
action potential comes into vicinity of sarcoplasmic reticulum, depolarises the membrane and stimulates release of Ca2+
role of Ca2+ (excitation-contraction coupling)
binds to troponin, tropomyosin removed
crossbridges bind and generate force
Ca2+ taken up again
tropomyosin restored
if ATP is present, the crossbridge will detach
connection between T-tubules and sarcoplasmic reticulum
junctions comprised of two integral membrane proteins (one in each of the membranes)
the protein in the T-tubule membrane is a modified voltage-sensitive Ca2+ channel (DHP receptor). detects depolarisation and triggers protein in SR to release Ca2+
contraction mechanism
AT propagated into T-tubules
Ca2+ released from lateral sac of SR
Ca2+ binding to troponin removes blocking action of tropomyosin
cross bridges form between actin and myosin and generate force by moving through power strokes
ATP causes release of myosin head and its return to original state
if Ca2+ and ATP still present, myosin head will attach to another binding site
AT complete, Ca2+ taken back into sarcoplasmic reticulum
binding sites blocked
ATP in contraction
ATP binds to myosin head=conformation change=reduced affinity for actin=detachment from binding site
ATP hydrolysed to ADP and Pi by myosin ATPase, providing the energy to reposition the myosin head back to its high-energy state
motor neurones
innervate skeletal muscle
cell bodies located in brainstem or spinal cord
myelinated axons
terminal branches create junctions with thousands of muscle fibres
motor unit
motor neurone and the skeletal muscle fibres it innervates
many motor units within a muscle
activate different number of motor units to control level of force
if the threshold of a motor unit is reached all of the fibres in that motor unit will generate their maximal force (for their length and velocity).
each motor unit has an all or nothing response
neuromuscular junction
junction of an axon terminal of motor neurone with motor end plate (region of muscle fibre plasma membrane directly under the neurone)
neuromuscular junction events
AT through motor neurone=Ca2+ enters via voltage gated channels
acetylcholine released and binds to nicotinic receptors on muscle fibre
opens ion channels in motor end plate. more Na+ in than K+ out
Na2+ entry depolarises motor end plate
spreads to adjacent sarcolemma
AT propagates along sarcolemma
latent period between AT and twitch contraction
time for excitation-contraction coupling
twitch contraction
brief, single contraction of a muscle fibre in response to a single action potential from a motor neuron
phases of twitch contraction
latent period
contraction phase (takes a while to build up as more cross bridges form with more Ca2+)
relaxation phase (due to how long it takes to take up all Ca2+, longer than contraction period)
tetanic contraction
when the frequency of stimulation is high enough for force to remain constant for the period of activation
sustained contraction-Ca2+ doesnt return to SR
summation
multiple action potentials to a muscle fibre before it relaxes causes summation in tension
incomplete tetanus
fluctuation in force generated as muscle stimulated repeatedly at high frequency
tetanic vs twitch contractions
in reality, muscle fibres are stimulated by multiple action potentials
by stimulating a fibre repeatedly before its gone through relaxation, more force is generated that becomes sustained
factors determining how much force is generated in tetanic contraction
number of cross bridges formed which is influenced by the length of the muscle fibres/sarcomeres and the contraction velocity
level of activation (number of motor units stimulated) and time since onset of activation also have influence
force-length relationship graph
actin and myosin cant overlap if actin is overlapping with other actin (very short)
optimum overlap=maximum number of binding sites=maximum force
decrease in force as length increases past optimum as overlap decreases
why does the force generated by the whole muscle differ from that produced by individual sarcomeres
muscles fibres are connected via collagen tendons and themselves contain collagen which is stretchy/elastic. when you stretch a muscle beyond its resting length while the tension produced by the sarcomeres is decreasing, the amount of force produced by the elastic tissues increases
region of muscle function
just below and above optimum length
effect of velocity of contraction on muscle force generated
quicker cross bridges have to form=fewer crossbridges bonded at any given time=less force
why is more force generated in eccentric contraction than concentric
lengthen=more force from elastic tissue whether done slow or fast
fast eccentric contraction dangerous
how motor units affect level of force generation
how many motor units activated
different motor units are activated at different times so the time since inset of activation also influences force
types of skeletal muscle fibres
slow/fast/very fast (maximal velocities of shortening)
oxidative or glycolytic (major pathway used to form ATP)
slow vs fast muscle fibres
contain different isomers of myosin that attach and detach from actin at different speeds.
differ in maximal rate at which ATP is used
heavy chain responsible for this
determines maximal rate of crossbridge cycling and maximal shortening velocity
3 pathways of ATP synthesis
Phosphorylation of ADP by creatine phosphate- when muscle first activated
Oxidation phosphorylation of ADP in mitochondria (Aerobic)
Glycolytic phosphorylation of ADP in the absence of oxygen (Anaerobic)
oxidative fibres
high number of mitochondria so high capacity for oxidative phosphorylation
dependent on blood flow to deliver oxygen
glycolytic fibres
fewer mitochondria
high concentration of glycolytic enzymes and a large store of glycogen
can produce a lot of force quickly
muscle fatigue once glycogen runs out
3 types of skeletal muscles fibres, based on the 2 determining characteristics
Slow-oxidative fibres (Type I) combine low myosin-ATPase activity with high oxidative capacity.
Fast-oxidative-glycolytic fibres (Type IIa) combine high myosin-ATPase activity with high oxidative capacity and intermediate glycolytic capacity.
Fast-glycolytic fibres (Type IIx) combine high myosin-ATPase activity with high glycolytic capacity.
prolonged stimulation of slow oxidative fibres
constant force
50ms contraction phase (long time)
10mN (low)
fatigue resistant
prolonged stimulation of fast oxidative glycolytic fibres
greater force and a bit quicker than slow oxidative fibres
over time produces less force as glycolytic pathway out of fuel
prolonged stimulation of fast glycolytic fibres
lots of force generated and quick contraction period
force drops off quickly, cannot sustain
whole muscle contraction, size principle of motor unit activation
Each muscle has a combination of all of the fibre types. Proportion of the types vary.
Fibre types differ in threshold of activation, lower in small/slower muscle fibres
(time since onset of activation)
force-time curve of muscle activation
if not all motor units within a muscle are activated = submaximum contraction
activate all units=maximum force
there is a period of ramping up to that activation as more motor units are recruited
electromyography
measures action potentials in muscle fibres
motor control defintion
The co-ordinated activation of muscles to produce controlled movement
involves neurones organised into hierarchal levels
motor control system
Voluntary movement is initiated by the higher centres in the brain
These signals are then relayed to the middle areas of brain which co-ordinate the movement
And onto the MOTOR NEURONS which activate the MUSCLES (efferent signals)
SENSORY FEEDBACK comes back from SENSORY RECEPTORS in the muscles and joints (afferent signals) to modulate the movements
proprioceptors
sensory receptors within muscles and joints
tell CNS what is happening in muscles
responsible for reflex actions
muscles spindles
proprioceptors that provide feedback on muscle length
wrap around fibres
golgi tendon organs
proprioceptors that provide feedback on muscle force
found where muscles join to tendon, stimulated when tendon stretches
involuntary movement: stretch reflex
When muscle is stretched afferent signal from muscle spindle to spinal cord
Synapes with motor neuron of stretched muscle which causes it to contract to resist the stretch (monosynaptic)
Also synapses with inhibitory interneuron which inhibits motor neurons to the flexor muscle
Afferent signal from muscle spindle also goes to higher centres (brain) so movement becomes ‘conscious’
PROTECTS MUSCLE FROM TOO MUCH STRETCH
withdrawal reflex
Painful stimulus
Pain detected by nociceptor and signal sent to spinal cord
Synapses with motor neuron of flexor muscle to flex knee and withdraw foot
Inhibitory interneuron results in inhibition of ipsilateral extensor muscle to facilitate this movement
Reflex also crosses to contralateral side to increase weight support on that side
Excitatory interneuron to contralateral extensor
Inhibitory interneuron to contralateral flexor
Afferent signal from nociceptor also goes to higher centres (brain) and pain becomes conscious
sensory feedback
responsible for reflexes
regulation
exercise associated muscle cramp
Painful, spasmodic and involuntary contraction of skeletal muscle that occurs during or immediately after exercise
Occurs in activated muscle groups
Can be relieved by passive stretching and massage. Resets inhibitory pathways
2 hypothesis for cramps
Electrolyte depletion and dehydration
Change in sodium potassium, magnesium or calcium concentration in plasma, disrupted ion balance in muscles, affecting ability to turn on/off
No prospective studies to support this theory
Altered neuromuscular control
Altered reflex control due to fatigue
Excitatory input overwhelms inhibitory input
delayed onset muscle soreness
Microdamage to muscle which results in minor inflammation and pain, but is normal and important for muscle adaptation
Occurs as a result of overload of muscle
Particularly due to eccentric exercise
Results in up regulation of protein synthesis and adaptation of muscle to new load
muscular dystrophy
weakening and breakdown of muscle over time
Duchennes muscular dystrophy
Genetic condition caused by mutation in the gene for the protein dystrophin on X chromosome
Dystrophin important in linking myofibrils to sarcolemma
Lack of dystrophin results in muscle fibre disorganisation and death
Affects muscles of pelvis and lower limb first progressing to the upper limbs and respiratory muscles
Results in premature death
CNS disorders
Toxins
Autoimmune conditions (attack motor neurones)
Multiple sclerosis (reduction in insulation)
Cerebral palsy (damage to brain affects sensory feedback)
Motor neuron disease
