Muscular System Part 2: structure of a skeletal muscle fiber Flashcards
plasma membane
sarcolemma
= tunnel-like extensions of the sacrolemma
transverse tubules
cytoplasm
sarcoplasm
a cytoplasmic protein that binds oxygen
myoglobin
a polymer of glucose
glycogen
a network of membranous sacs around the myofibrils, stores calcium ions.
Sarcoplasmic Reticulum
Contracts organelle
myofibrils
Membranous sacs encircling each myofibril
Loaded with Ca++
Release of Ca++ triggers myofibril contraction
Sarcoplasmic Reticulum
Generate force during contraction
Contractile proteins
Switch the contraction process on and off
regulatory proteins
Align the thick and thin filaments properly
Provide elasticity and extensibility
Link the myofibrils to the sarcolemma
structural proteins
Thick filaments
Functions as a motor protein which can achieve motion
Convert ATP to energy of motion
Projections of each molecule protrude outward (___)
Myosin (Myosin Head)
Thin filaments
molecules provide a site where a myosin head can attach
Tropomyosin and troponin are also part of the thin filament
In relaxed muscle
Myosin is blocked from binding to it
Strands of tropomyosin cover the myosin-binding sites
Calcium ion binding to troponin moves tropomyosin away from myosin-binding sites
Allows muscle contraction to begin as myosin binds to it
Actin
Stabilize the position of myosin
accounts for much of the elasticity and extensibility of myofibrils
Extends from Z disc to M line
Titin
Links thin filaments to the sarcolemma
links actin in outermost myofilaments to transmembrane proteins and eventually to fibrous endomysium surrounding the entire muscle cell
transfers forces of muscle contraction to connective tissue around muscle cell
genetic defects in this produce disabling disease muscular dystrophy
Dystrophin
Covers myosin-binding sites, keeps myosin from engaging actin
tropomyocin
Bind to tropomyocin
In the presence of Ca++, causes tropomyosin to uncover myosin binding sites, allowing contraction to begin.
Troponin
The presence of Calcium ++ causes:
Myosin heads attach to and “walk” along the thin filaments at both ends of a sarcomere
Progressively pulling the thin filaments toward the center of the sarcomere
Leading to shortening of the entire muscle
Hardening of muscles and stiffening of the body, beginning 3-4 hours after death
peaks 12 hours after death and then diminishes over the next 48 to 60 hours
rigor mortis
Release of acetylcholine
Nerve impulse arriving at the synaptic end bulbs causes many synaptic vesicles to release ACh into the synaptic cleft
Step 1 of muscle contraction
Activation of ACh receptors
Binding of ACh to the receptor on the motor end plate opens an ion channel
Allows flow of Na+ to the inside of the muscle cell
Step 2 of muscle contraction
Production of muscle action potential
The inflow of Na+ makes the inside of the muscle fiber more positively charged triggering a muscle action potential
The muscle action potential then propagates to the SR to release its stored Ca++
Step 3 of muscle contraction
Termination of ACh activity
Ach effects last only briefly because it is rapidly broken down by acetylcholinesterase (AChE)
Step 4 of muscle contraction
Interface of the motor neuron and muscle fiber
neuromuscular jusnction
