Biochemistry of muscle contraction Flashcards
the muscle cell
- what do you call a muscle cell
- why is it multinucleated
- hierarchical structure of a muscle fiber
- what organelle is very abundant in muscle cells
- structure of a sarcomere
- other proteins in a sarcomere
- myocyte
- due to fusion of myoblasts during development
- sarcomeres are the contractile units of myocytes. many sarcomeres and myocytes make up a myofibril.
many myofibrils make up a fasicle.
many fasicles make up a muscle fiber - mitochondria for aerobic ATP synthesis
- thick filament/protein myosin, thin filament/protein actin, tropomyosin, troponin)
- M line = myomesin and M-protein, Z-line = a-actinin
role of Ca2+ in muscle contraction
- Ca2+ released from sarcoplasmic reticulum
- Calcium binds to TnC causing change in its conformation
- TnL detached from actin
- Tropomyosin moved to expose actin binding sites for myosin
what is cross-bridge cycling and sliding filament theory?
- ATP hydrolysed and releases free energy energising myosin heads (S1) to lengthen and then bind to actin.
- Pi released strengthening cross bridge.
- Power stroke occurs (due to converting the free energy to kinetic energy) shortening the muscle, generating tension.
- ADP dissociates from myosin, but cross bridge still intact.
- ATP binds to empty active site of ATPase causing detachment of actin and myosin.
- S1 is then ready for another cycle.
lengths of bands during sliding filament theory
- same - A band (length of myosin)
- shorten - I band (thin filaments only), H zone (gap between actin), gap between z lines
myosin
- what chains make it up
- what does light meromyosin do
- what does heavy meromyosin do
- what is s1 fragment
- 2 heavy chains and 4 light chains
- forms filaments spontaneously
- forms cross bridges
- contains ATPase which hydrolyses ATP and binds to actin
actin -
- 2 main components
- what is the relationship between them
- what does the end actin form do
- G (globular) actin and F (fibrous) actin
- g actin forms f actin
- F actin monomers intertwine and form the trunk of thin filaments to which tropomyosin and troponin attach, also increases the rate at which ADP and Pi are released from the active site increasing rate of ATPase
sarcomere at rest
- tropomyosin physically blocks the actin-binding site due to no calcium. therefore no actin and myosin binding
myosin isoforms and fiber type
- how does variation occur in proteins
- 3 different myosin heavy chains
- alternate splicing or RNA editing forming isoforms
- type 1 (slow twitch), type 2a and 2x (fast twitch)
myosin ATPase activity of each type
type 1- lower, 2a- intermediate, 2x- higher
Maximal shortening velocity of each type
type 1- lower, 2a- intermediate, 2x- higher
Economy and fatigue resistance of each type
type 1- higher, 2a- intermediate, 2x- lower
the regulatory subunits of troponin
- Tnl binds to actin
- TnC binds Ca2+
- TnT binds tropomyosin
role of Calcium in muscle recovery/relaxation post contraction
- Calcium taken back up by sarcoplasmic reticulum using energy from ATP
- Calcium detached from TnC causing another change in conformation (reversing)
- Attachment of TnL to actin
- Movement of tropomyosin concealing myosin binding sites on actin
- Relaxation
- signalling from the brain to the muscle
- what is the gap between the neuron and the muscle called
- Signals are carried out chemically in motor units (motor neurons and the muscle cells they innervate)
- As motor neuron reaches muscle, splits into thousands of branches ending with neuromuscular junctions (NMJ)
signal transmission at NMJs
- how is resting potential reached
- what happens to acetylcholine after excitation
1 - APs arrive at the pre synaptic membrane.
- a neurotransmitter, acetylcholine is released from synaptic vesicles into synapse
- Acetylcholine diffuses across synapse and binds to 2a subunits of acetylcholine receptors on the motor end plate and dilate its core
- Many Na+ ions inflow with fewer K+ leaving
- When depolarisation threshold is met voltage gated Na+ channels in membrane open and increase Na+ entry and signal is carried across
- When returning resting membrane potential VG K+ channels open letting K+ out of the cytosol
- free acetylcholine is hydrolysed in the synaptic cleft by acetylcholinesterase and the receptor returns to its original conformation
