Physiology of Muscle -Brownell Flashcards
What are the 3 types of motor proteins?
- myosin: actin==> basis of skeletal, cardiac and smooth mm contraction
- kinesins: microtubule motors that walk intracellular organelles along microtubules
- dyneins: microtibule motors that cause the bending of cilia and flagella
defects in any of these will lead to diseases
What is a muscle fiber? How is it developed?
Muscle fiber=1 muscle cell
developed by fusion of myoblasts into multinucleate myotubes, differentiation into mm fibers
fixed # of mm fibers at birth
Which myofibril band is where actin and myosin overlap?
A band- think of it as the “active” band
What is titin?
The large elastic protein that connects thick filaments to A discs in mm myofibrils
What does CapZ do?
form the Z disc, and binds the (+) end of actin
What couples electrical depolarization to contraction?
the DHP/ryanodine complex
Describe the process of muscle contraction
ACh from the motor neuron is released in to the neuromuscular junction (short distance). this binding of the ACh receptor allows for the depolarization of the mm through Na+ influx and the formation of an action potential. The action potential propagates and in the t-tubule changes the DHP receptor conformation, releasing Ca2+ from the sarcoplasmic reticulum
The Ca2+ binds to trpoonin allowing actin-myosin binding and a power stroke formation–> actin slides towards the center of the sarcomere
What can cause an increase in muscle contraction tension?
increase in frequency of action potentials
==> can lead to tetany=maximum contraction
What is the rate limiting factor for most physiological processes? How is this overcome in muscle contraction?
diffusion distance
for muscle contraction, the distance must be in micrometers or smaller (between motor neuron terminal and ACh receptor on mm).
=> the T-tubule and DHR and RyR allow for the Ca2+ to be held right next to them so it can be released quickly and effectively
How is the initiation of contraction different in smooth muscle from skeletal mm?
smooth mm couples electrical depolarization to contraction by a second messenger mediated process (MLCK) (myosin light chain kinase)
much SLOWER than skeletal mm
How can ATP for muscle contraction be generated (3)?
- creatine phosphate (quickly release stored energy–> only enough for 8 twitches)
- glycolysis
- oxidative phosphorylation
What are the major differences in fast and slow twitch muscle fibers?
Fast twitch:
- glycolytic, anaerobic ATP synthesis
- large diameter
- pale in color
- easily fatigued
- e.g. escape reflex mm, jumping mm.
Fast oxidative:
- fast
- oxidative phosphorylation
- fatigue resistant
- e.g. walking
- medium diameter
slow twitch:
- beta oxidative (aerobic ATP synthesis)
- smaller diameter
- dark red color due to myoglobin (vascularized)
- fatigue resistant –> sustained contraction
- e.g.: postural mm.
- numerous mitochondria
How is negative feedback used in controlling muscle contraction?
-ALL skeletal mm contraction is under negative feedback control.
-the set point (intended movement) is the central command to move.
the body senses current movement and amplifies (motor neurons) the signals to get output appropriate for the set point .
this output can be affected by environmental factors–> negative feedback of movement (sensory)
cannot have precision without negative feedback!!!!
what are the fastest nerve fibers? Where are these found and why?
1a (muscle spindle)
1b (golgi tendon organ)
largest diameter, fastest fibers here because need fast feedback in the somatosensory system!
these fibers are responsible for sending the afferent information to cerebellum
what is responsible for the re-efference (error correction) in muscle movement?
the cerebellums signals to the alpha and gamma* motor neurons
When does muscle fatigue occur? What are the 2 types of fatigue?
30% ATP depletion
central and peripheral fatigue
What is myasthenia gravis? How is it treated?
autoimmune suppression of the post-synaptic NACh receptors–> will present with weakness (fatigue)
tx: pharmacological inhibition of ACh esterase
What is Lambert-Eaton Syndrome?
Autoimmune attack of presynaptic Voltage-gated channels for Ca2+ which blocks ACh vesicle exocytosis (triggered by Ca2+)
also leads to less NT release and weakness
What is the difference between Duchennes Muscular Dystrophy and Beckers Dystrophy?
Duchennes (x-linked) =unexpressed gene for dystrophin protein
Beckers (x-linked) =Dystrophin is partially functional
What is the function of dystrophin? How is the body affected in pt’s with Duchennes?
dystrophin gives the body structural integrity
normally, nNOS (attaches to dystrophin) triggers NO release when there is tension on dystrophin which causes vasodilation
without dystrophin, you lose this vasodilation reflex and get less NO generation and less vasodilation
What is Amyotrophic Lateral Sclerosis?
Degenerative motor neuron diseases with associate effects on muscle atrophy.
Progressive degeneration from lower motor neuron to upper motor neuron
What are the differences between fatigue and rigor mortis?
peripheral fatigue:
- 30% ATP depletion
- sufficient ATP to drive Ca2+ transport
- [ADP]/[ATP]=too high to drive crossbridges–> no movement
rigor mortis:
- complete depletion of ATP
- no Ca2+ transport
- crossbridges cannot dissociate (stuck in contracted state)
- occurs 3 hours postmortem and persists up to 72 hours
What determines muscle fiber type, distribution and size? How was this proven?
The motor neuron that innervates it! (determined during development)
when you take a fast motor neuron and attached it to a slow muscle, it will become fast muscle
What does denervation atrophy lead to?
What does disuse atrophy (e.g. bedridden) lead to?
denervation: type grouping–> fast and slow muscle fibers will group together
disuse atrophy: smaller, “angular” fast fibers
