Lecture 4, Skeletal Muscle Function Flashcards
Muscle Contraction - Types
a muscle contraction refers to the generation of tension by a muscle
three main types:
1. isotonic contraction - maintained muscle tension (amount of force generated by muscle is the same), with a change in muscle length
A. concentric - decrease in muscle length (usually decrease in muscle angle as well)
B. eccentric - increased in muscle length (eccentric is not relaxing is just opposite of concentric (slowly bringing it down, not bringing it down right away))
2. isometric contraction - decreased/maintained/increased muscle tension, no change in muscle length
3. isokinetic contraction - the change in muscle length occurs at a constant velocity
* force is added, tension is going up but length is not changing for isometric
* constant velocity is constant - there is no jerking in movements (change is muscle length is constant
Isotonic, Concentric Contraction vs. Isometric Contraction
muscle tension > load
decrease muscle length
VS.
muscle tension = load
static muscle length
Overview of Muscle Contraction
- a skeletal muscle cell contracts only when activated by a neuron
- electrical activity passes over the sarcolemma, and down the t tubules, triggering the release of Ca2+ from the sarcoplasmic reticulum
- Ca2+ triggers interaction between thick and thin filaments, causing them to contract the muscle myofibril
- as an myofibrils shorten, the cell length shortens, and it generates active tension
Neuromuscular Junction
- the synapse between the somatic motor neuron and the muscle cell is called neuromuscular junction (NMJ)
◦ motor end plate of the muscle cell (landing pad for axon where connection happens)
◦ synaptic end bulb of the neuron (aka somatic or alpha motor neuron) - each skeletal muscle cell is controlled by a single nerve cell (only innervated ever by one nerve cell)
Neuromuscular Junction (2)
the axon terminal of the motor neuron contains synaptic vesicles containing acetylcholine (ACh)
* acetylcholine: a neurotransmitter (chemical messenger)
the region between the axon terminal (neuron) and the motor end plate (muscle) is called the synaptic cleft
* contains the enzyme acetylcholine esterase (AChE)
◦ degrades ACh when it is no longer needed
recall: schwann cells support neurons in the PNS and create myelin sheath
◦ schwann cell would not be seen in central nervous system
Action Potential Transmission at the NMJ (steps 1-3)
- action potential is transmitted down the axon of the motor neuron to the axon terminal
A. neuron resting potential = -70mV
B. the signal sent down the axon occurs is an action potential (+30mV) - the depolarization of the synaptic end bulb causes Ca2+ to flood into the end bulb via voltage-gated channels
A. voltage-gated channels: a type of protein embedded in the plasma membrane that, when activated allows for passage of chemicals/molecules across the membrane - Ca2+ binds with the synaptic vesicles, causing them to merge with the plasma membrane
A. exocytosis of ACh into the synaptic cleft
action potential -> calcium -> acetylcholine
Neuromuscular Junction (4-6)
- ACh crosses the synaptic cleft and binds with ion channels on the motor end plate, causing them to open
◦ crosses the cleft by passive diffusion - opening of the ion channels allows for entry of Na+ into the muscle cell
◦ depolarization of the sarcolemma
◦ the interior of the muscle cell is also negative at rest - depolarization of the sarcolemma triggers more ion channels to open
◦ ion channels to adjacent to the motor end plate open
◦ more Na+ enters the cell
Neuromuscular Junction (7-9)
- depolarization creates an action potential within the muscle
- action potential travels down the sarcolemma to the T tubules
◦ when the action potential reaches the T tubules, Ca2+ is released by the sarcoplasmic reticulum to initiate contraction of the sarcomere - ACh in the synaptic cleft is degraded by AChE
◦ AChE is normally present within the synaptic cleft
◦ degrades ACh so that the ion channels can close
◦ Na+/K+ pumps reset the muscle’s resting potential
◦ reset and ready for the next signal
Excitation-Contraction Coupling
the action potential is propagated across the entire membrane surface of the muscle fiber
* T tubules connect the sarcolemma to deeper myofibrils
* the action potential reaches all the myofibrils along the whole length of the muscle fiber
excitation-contraction coupling: the close coupling between the action potential of the motor neuron and the synchronous contraction of the myofibrils
* the mechanism that links sarcolemma stimulation and cross-bridge force production
Sarcomere Contraction
during a muscle contraction, the Z lines of the sarcomere are pulled closer together
* this happens due to cross-bridge cycling of the thin and thick filaments
during a muscle contraction:
* myosin “walks” along the actin filament pulling it to the M line
* the Z lines of the sarcomere are pulled closer together
* the zones of overlap get wider
* H zones gets narrower
* I band gets narrower
* A band stays the same
Cross-Bridge Cycling
individual actin molecules are spherical, but come together to form a helical arrangement with the regulatory proteins tropomyosin and troponin
* each actin molecule has a myosin binding site
at rest, tropomyosin rests overtop of the myosin binding sites
* prevents myosin from binding and forming a cross bridge with actin
* tropomyosin is a thin, strand-like protein
troponin is a cluster protein that anchors tropomyosin to the actin filaments
* troponin has 3 binding sites, one each for actin, tropomyosin and calcium
* when calcium is present, it will bind to troponin, causing it to lose its anchoring hold on tropomyosin
Cross-Bridge Cycling (at rest vs when calcium is present)
at rest:
* Ca2+ is not available to bind to troponin
* troponin anchors tropomyosin to actin, so that the myosin-sites are blocked
* myosin heads are energized and ready to bind, but are blocked to tropomyosin
when Ca2+ is present:
* Ca2+ binds to troponin, causing it to change its hold on tropomyosin
* tropomyosin shifts off actin, exposing the myosin-binding sites
* the myosin head are able to bind to actin, forming a cross-bridge
* formation of a cross-bridge automatically initiates a cross-bridge cycle, which generates forc
Cross-Bridge Cycling (1-2 steps)
he sarcoplasmic reticulum releases Ca2+ into the cell
A. Ca2+ binds with troponin, causing tropomyosin to shift off the myosin-binding sites on the actin filament
B. myosin heads bind to the actin filaments
a. binding of the myosin heads to actin initiates the cross-bridge cycle
C. myosin heads are already bound to an ADP molecule and inorganic phosphate
a. myosin heads are “energized”
2. ADP and Pi are released from the myosin
A. the myosin heads change shape, pulling the actin filament downwards, towards the M line
a. power stroke or working stroke
B. myosin will remain bound to actin in this position until another ATP molecule is available
-> no ADP or Pi means no energy
Cross-Bridge Cycling
- ATP binds to the myosin, allowing for the myosin head to release the actin
A. cross-bridge detaches - the ATP is hydrolyzed into ADP and Pi
A. provides the energy for the myosin heads to return to its original position
B. reset and ready to bind to the next binding site on actin
rigor mortis: stiffening of the muscles of the body caused by the depletion of ATP in the muscle
* usually occurs a few hours after death, but is temporary
* ATP binding to myosin allows for it to detach from actin (step #3)
* no ATP = stuck in the cross-bridge
Cross-Bridge Cycling Configuration
when the myosin heads are bound to ATP = low-energy configuration
when myosin heads are bound to ADP, Pi and actin = high-energy configuration
