what are the 2 key molecules required for cross-bridge formation and cycling
Ca2+
- enables myosin heads to attach to actin by revealing myosin binding sites on actin molecules
-> high force contraction molecule
ATP
- binds to myosin and is hydrolyzed to ADP+Pi
(myosin is an ATPase)
- ATP hydrolysis provides energy for the myosin powerstroke
- ATP binding to myosin allows it to detach from actin (cross bridge cycling)
what happens in the absence of Ca2+
- myosin and actin cannot form a secure cross bridge
- troponin is inactive
- tropomyosin partially blocks myosin binding site on G actin molecules
- myosin heads can bind to actin but only weakly (low force cross bridge)
what happens when Ca2+ is present
- increase in [Ca2+] will activate troponin
- pulls tropomyosin away from the myosin binding site on actin(conformation change)
- allows stronger (high force) cross bridge formation
- myosin binds strongly to actin and completes power stroke
- actin filament moves
what are the steps of the contraction cycle
- ATP binds to myosin, myosin releases actin
- myosin hydrolyzes ATP, energy from ATP rotates the myosin head to the cocked position, myosin binds weakly to actin (ADP and Pi remain bound)
- power stroke begins when tropomyosin moves off the binding site due to Ca2+ signal
-> actin filament moves toward M line
-> myosin releases Pi - myosin releases ADP at the end of power stroke
-> tight binding in the rigor state
what is rigor mortis
- muscle cant release myosin because no more ATP binding (when dead)
explain the sliding filament model of contraction (what shortens/stays the same)
- sarcomere shortens during contraction
- actin and myosin do not change length but slide past each other
- thick and thin filaments do not change length
- contraction due to filaments sliding past each other by cross bridge cycling
- A band length maintained
- I band and H band shorten
- sarcomere shortens (Z lines closer together)
what is muscle tension, load, contraction, and relaxation
muscle tension = force created by muscle
load = weight or force opposing contraction
contraction = creation of tension in muscle
relaxation = release of tension
summary map of muscle contraction (what is excitation contraction coupling)
- events at neuromuscular junction
- excitation contraction coupling (depolarization of the muscle fiber occurs at the motor end plate and spreads through the muscle fiber, via t tubules, this depolarization leads to Ca2+ release from SR = trigger for contraction)
- Ca2+ signaling
- Contraction-relaxation cycle
what are the events at the NMJ that lead to muscle cell depolarization
- somatic motor neuron releases ACh at NMJ
- net influx of Na+ through nAChR causes end plate potential which is a graded potential
-> EPP is always suprathreshold and activated nearby voltage gated Na+ channels to trigger action potential
what are the steps of excitation-contraction coupling
- action potential in t tubule alters conformation of DHP (dihydropyridine L-type calcium channel) receptor (voltage gated)
- DHP receptor opens RyR (ryanodine receptor) Ca2+ release channels in SR and Ca2+ enters the cytoplasm
- Ca2+ binds to troponin allowing actin-myosin binding
- myosin heads execute power stroke
- actin filament slides toward center of sarcomere
what are the steps of the relaxation phase
- sarcoplasmic Ca2+-ATPase (SERCA) pumps Ca2+ back into SR
- decrease in free cytosolic [Ca2+] causes Ca2+ to unbind from troponin
- tropomyosin re covers binding site, when myosin heads release elastic elements pull filaments back to their relaxed position
explain action potentials in the Axon terminal (motor neuron) and in the muscle fiber and how that leads to a muscle twitch
- motor neuron action potential has a resting membrane potential of -70 and goes to +30
- muscle fiber action potential has a resting membrane potential of -80 and goes to +20
- a muscle twitch is a single contraction-relaxation cycle
- axon terminal (motor neuron) AP is shorter than muscle fiber AP (2msec)
explain how summation allows for increased force of contraction in a single muscle fiber (unfused and complete tetanus)
- summation = stimuli closer together do not allow muscle to fully relax
- unfused tetanus = stimuli are far enough apart to allow muscle to relax slightly between stimuli
- complete tetanus = muscle reaches steady tension, if muscle fatigues tension decreases rapidly
What causes muscle fatigue
- fatigue causes muscle to lose tension despite continuing stimuli
- low glycogen
- excitation contraction failure such as SR calcium leak
- lactate or acid accumulation
- NMJ failure
- not due to low ATP which is always abundant in a living cell
what is a motor unit (size, number and order)
- one motor neuron and the muscle fiber it innervates
- size of motor units is related to the need for refined movement
-> more refined movement = fewer fibers per motor unit - number in order of motor units recruited is related to the power needed to generate movement
- smaller motor units always recruited first
what is the relation between contractile force and motor unit size
- larger motor units contain more muscle fibers and therefore generate more force/tension when activated
- tension can also be increased by recruitment of multiple motor units within a muscle (X + Y)
- muscles involved in fine movements have small motor units (lower threshold)
- larger muscles have many motor units some which may be quite large (higher threshold)
explain the size principle of motor unit recruitment
- smaller motor units (MU X) have smaller motor neurons
-> lower threshold for activation
-> activated at lower frequency of stimulation from CNS - as frequency of stimulation from CNS increases
-> action potential frequency and tension in MU X increases
-> larger motor units brought to threshold and contribute to total muscle tension - total muscle tension reflects some of motor unit activation in a motor neuron pool
explain length tension relationships in skeletal muscle contraction
- sarcomeres contract with maximum force when they are at their optimal resting length just prior to contraction
-> provides optimal number of cross bridges - normal resting length of muscle usually ensures that this happens
- if sarcomere length is very long = very few cross bridges
- at optimal sarcomere length (2.1-2.2) = lots of cross bridges
- if sarcomere shorter than optimal length = thick and thin filaments have too much overlap
- if sarcomere so short that the thick filament runs into the Z disks = myosin unable to find new binding sites
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