Mod 3 Physiology
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What are the basic functions of muscle?
- 1) movement
- 2) posturing
- 3) internal motility and storage
- 4) heat
What is the basic organization of skeletal muscle?
Muscle->muscle fasicle->muscle cell (fibre)->myofibril
List some of the key structures in the muscle fibre
- 1) sarcolemma (cell membrane)
- 2) sarcoplasm (cytoplasm)
- 3) T-tubules (invaginations in the sarcolemma)
- 4) Sarcolasmic reticulum (Ca++ storage)
Describe the organization and components of a sarcomere
Explain the function of the following in a sarcomere: tropomyosin; tropinin, actin, myosin
- Tropomyosin: covers the myosin binding sites on actin
- tropononin: Ca++ causes a conformational change in this and causes the tropomyosin to move.
- actin: thin helical filaments attached to Z-line (move)
- myosin: two heads each with an actin binding site and an ATP binding site
What is a motor unit?
One motor nueron and all of the muscle fibres that it innervates.
Describe how signalling happens at the NMJ
- 1) AP comes down motor neuron
- 2) Causes influx of Ca++ in neuron
- 3) Causes ACh vesicles to fuse with the cell membrane and release ACh into the neurosynaptic cleft
- 4) ACh binds to ligand-gated Na+ channels (2/channel) on the muscle cell
- 5) Causes depolarization and eventually action potential
- 6) ACh is eventually taken back up by neuron or degraded by AChE
Describe Excitation Contration Coupling (what happens when an AP is running along sarcolemma)
- 1) AP runs down the T-Tubules into the cell
- 2) AP causes a conformational change in DHPR membrane protein on T-Tubule surface
- 3) DHPR mechanically causes conformational shape change in ryanodine receptors on the sarcoplasmic reticulum
- 4) ryanodine receptors allow Ca++ to rapidly leave the SR into the sarcoplasm
- 5) Ca++ is taken up by the SERCA pump (away from T-tubule - SR interface)
Describe the cross-bridge cycle
- 1) The Ca++ binds to the troponin, which causes the tropomyosin to be moved off the binding sites
- 2) The (cocked) myosin head binds to one of these sites
- 3) The ADP and P detach and the head flexes (power stroke)
- 4) New ATP binds to the head, causing to to detach from the actin
- 5) ATP dephosphorylates, causes the myosin head to "cock" (now ready to bind to a new actin site) and on and on...
How do: botox, succinylcholine, and myasthenia gravis affect the NMJ?
botox: prevents the ACh vesicle from fusing with the presynaptic membrane, thus preventing its release.
succinylcholine: ACh receptor agonist (i.e. it binds to the same receptors, causing them to open and in this case STAY OPEN), prevent any further action potentials
myasthenia gravis: autoimmune condition where antibodies bind to the ACh receptors. This prevents the ACh from binding, and also causes the destruction of the ACh receptors.
How does the cross-bridge cycle generate force?
Force is generated during the power stroke.
What are the 5 factors that influence force generation
- 1) Motor Unit size: how many muscle fibres are innervated by one neuron?
- 2) Motor Unit Recruitment: smaller motor units recruited first, larger motor units added as more strength is needed. Smooth movements
- 3) Muscle Length/Stretch: There is a "peak" contractile force at resting length
- 4) Muscle fibre diameter: more sarcomeres added in parallel will generate a larger force
- 5) Frequency of stimulation: contraction can sum on top of previous contractions (stronger force)
Name and describe the three energy sources for muscles
- 1) Creatine Phosphate: In all muscle types; used up quickly and replenished quickly;
- 2) Glycolysis: predominantly in IIb fibres; small capacity; fairly rapid
- 3) Oxidative Phosphorylation: Predominantly in I and IIa; slow supply, but can make lots of ATP
What causes muscle fatigue?
- ATP depletion
- impaired Ca++ release from SR
- depletion of O2
- central fatigue
- impaired AP conduction
Contrast AP generation in smooth and skeletal muscles
- Smooth muscle doesnt NEED a nerve to depolarize
- -CAN use NMJ transmission
- -Graded response (due to local factors or mechanical stim)
- -Spontaneous depolarization (fluctuation of ions over membrane)
- Smooth muscle doesnt need depolarization to contract
- -ligand gated receptors that release second messenger that cause Ca++ release in SR
Difference in cell components between smooth and skeletal muscle
- -calmodulin and myosin light chain kinase (MLCK)
- -actin and myosin not organized like in skeletal (no striations)
- -it is the interaction of calmodulin and MLCK that allow the myosin-actin cross bridging to occur (activate myosin and make it ready to bind)
difference in activation of contraction between skeletal and smooth muscle
- 1) how Ca++ increases:
- i)VG Ca++ channels on membrane open because of AP
- ii)Excell Ca++ enters and stimulates Ca++ release from SR
- iii) second messenger signal to SR
- iv) auxillary Ca++ channels can open if SR Ca++ is depleted
- 2) effect of Ca++ influx
- Ca++ binds calmodulin -> activated calmodulin activates MLCK -> MLCK hydrolyses ATP -> loose Pi binds and activates myosin -> myosin is now ready to go
Difference in cross bridge cycling between skeletal and smooth muscles
smooth: much slower because there is much lower ATPase activity on the myosin molecule
Difference in termination of contraction between smooth and skeletal muscle.
- Requires two events:
- 1) Removal of Ca++ from sarcoplasm
- 2) Dephosphorolization of myosin
- -deactivate MLCK
- -dephosphorylate myosin
- -myosin returns to inactivated state
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