Neural Control of Muscle Flashcards
Motor Unit Types: Size, Mitochondria, Myosin ATPase, and Force Properties
Size from smallest to largest: type I, type IIA, type IIB
Type I – slow oxidative or slow; oxidative means that it has a lot of mitochondria and able to produce energy from this; twitch = force profile; relaxes and contracts more slowly
Type IIa – fast oxidative glycolytic (more dependent on glycolytic with some oxidative) contracts rapidly; fatigue resistant
Type IIb – fast glycolytic or fast fatigue; used for more powerful movements that don’t last long; contracts rapidly
Types I and IA have a lot of mitochondrial enzymes whereas type IIB does not
Types IIA and IIB have a lot of myosin ATPase and type I does not
Motor Unit Recruitment and Discharge Rate
Recruitment starts with type I, then type IIA, then type IIB = happens with intensity of muscle contraction and need more units to maintain contraction/force
As you progressively get tired, you recruit more of these fibers to try to maintain the force output
As one produces more force more fibers are recruited as force increases, but also the individual motor units are firing faster as force increases
Recruitment, Fatigue, and Force Graph
Type I: see that they do not fatigue quickly, can stay contracted for long periods, but are slow in contraction, and do not produce a lot of force
Type IIA: don’t fatigue as quickly, contraction time is shorter side of intermediate, and generate more force than type I but less than type IIB
Type IIB: fatigue quickly but generate a lot of force rapidly
Biophysical Basis of Motor Unit Recruitment
V = I * R
Ohm’s law: nerves are essentially electrical
V = change in membrane potential
I = input current; how much excitatory signal are we giving
R = key; larger vs. smaller diameter
When I is the same: smaller diameter will reach threshold first; smaller = more resistance which means greater difference in membrane potential (V), but it conducts slower because more resistance, which is the same reason is reaches threshold first
Garden hose analogy
Excitability of Nerves
Axon hillock is the key if the threshold is reached or not = all or none
Dendrites = many synaptic inputs; some are excitatory (E), and some are inhibitory (I); can have a lot of E, but if have a lot I as well then threshold will not be reached
If you increase E only then threshold can be reached = key to understanding the spinal reflexes
Deep tendon reflexes: mediated by muscle spindles; how delicate balance of muscle contraction and relaxation works
Functional Importance of Orderly Recruitment
Order: type I, type IIA, and then type IIB
Minimizes development of fatigue by allowing the most fatigue resistant fibers to be used most of the time, holding the more fatigable fibers in reserve until needed for higher forces.
Allows for greater fine motor control
NMJ Transmission and Synaptic Physiology
- APs comes down nerve terminal
- Ca2+ on outside and AP comes down and triggers Ca2+ to flow in
- Ach vesicles dock and fuse (regulated by SNARE complex) to nerve terminal so Ach spills out into NMJ (exocytosis)
- Ach docks onto Ach receptors (2 Ach per receptor)
- Channel opens to allow for 3Na+ in and 2 K+ out to create the threshold to get propagation of AP across muscle fiber
Botulism
Mechanism of neuromuscular blockade by botulinum toxin
Flaccid paralysis occurs when SNARE proteins are cleaved by botulinum toxin, resulting in inhibition of synaptic vesicle fusion and absence of acetylcholine release
Results in paralysis/inability of muscle to contract by integrating SNARE proteins so Ach vesicles cannot dock and fuse correctly creating spastic muscle
Myasthenia Gravis
Autoimmune disorder where Ab bind to AchR so that so Ach cannot bind
Excitation Contraction Coupling: T-Tubules to SR
T tubules are next to two terminal cisternae of SR = TRIAD and the close proximity together is important; located at each end of the A band
T tubule membrane = have Ca2+ channel with DHP expressed in t tubule networks; DHP are L-type Ca2+ channels
DHPR gets activated by voltage (AP) and signals/couples with RyR in SR membrane = physical interaction in skeletal muscle and this activates Ca2+ release from SR
Excitation Contraction Coupling: SR to Contraction
Ca2+ released in cytoplasm and looks for target = troponin C on actin filament
On borders of A bands so the Ca2+ can find the troponin quickly because of close proximity
Troponin T binds causes a conformation change on tropomyosin to move and exposure myosin head binding sites on actin
Myosin head binds onto actin to cause contraction, but the myosin heads are NOT synchronized
SERCA
The sarcoplasmic endoplasmic reticulum Ca2+ pump (SERCA) is an ATPase; it uses the energy of ATP splitting to pump Ca2+ back into the SR and keep the resting [Ca2+] low
Calsequestrin
Is a calcium-binding protein of the sarcoplasmic reticulum. The protein helps hold calcium in the cisterna of the sarcoplasmic reticulum after a muscle contraction, even though the concentration of calcium in the sarcoplasmic reticulum is much higher than in the cytosol
Parvalbumin
The affinity of parvalbumin for Ca2+ is as high as that of troponin, but it binds Ca2+ more slowly
After initial binding of Ca2+ to troponin, mass action transfers some of the Ca2+ to parvalbumin, yielding relaxation
PLN
SERCA is modulated by phopholamban – when not phosphorylated then SERCA doesn’t uptake Ca2+, but when it is P, then Ca2+ uptake is greatly increased
It’s modulation is regulated by epinephrine via protein kinase A, which is particularly important in cardiac muscle in affecting relaxation rate
