Muscles 2 Flashcards
What is tetanus?
When many stimuli are given repeatedly and rapidly to the muscle fiber, the result is an amplified, sustained contraction called tetanus
How do skeletal muscles regulate force?
- Temporal summation
2. Spatial summation (recruitment)
Explain the physiology behind a single twitch
- Action potential causes Ca2+ release
- Release of Ca2+ evokes muscle contraction
- Muscle membrane has completely repolarized before relaxation of the muscle
For this reason, the muscle fiber could be activated again before the muscle has relaxed. The duration of mechanical contraction allow individual twitch contractions to be summed temporally (Temporal Summmation) to enhance the contractile force generated by a muscle fiber
What is a temporal summation?
Second summation
- after the refractory period
- before complete muscle relaxation
Second contraction is stronger than first
- frequency of stimulation
- increased total force
Tetanus in the final stage becomes fused and sustained
- subsequent stimulation increase force, until tetanus (max force)
- Called physiologic tetanus- tetanus in the disease-also have maximal force
Summated the fir not the action potential
What is a motor unit?
- A single motor neuron and all the muscle fibers it innervates
- The muscle fiber contraction is controlled by innervation
- Precision of movement is determined by the number of fibers innervated by a motor neuron ( innervation ratio)
- Fine motor control- skeletal muscle fibers innervated by a single motor neuron varies from about 10-100 (eye-low ratio) to more for coarse movements > 1000( back to high ratio)
What is recruitment (spatial summation)?
The number of motor units active at any one time determines the total force produced by a muscle
- As more motor units are recruited the force increases. This is called Recruitment or spatial summation
- This type of modulation of muscle function endows a large muscle group with the ability to deal with light loads with an economy of function
Force is controlled by motor unit recruitment
Note: spatial and temporal summation can co-exist
Force is controlled by…
Motor unit recruitment
Compare skeletal and cardiac muscle
Skeletal: Absolute refractory potential< muscle contraction duration
- tetanic contractions (temporal summation-increase force)
- fastest contraction
Cardiac: ARP~= muscle contraction duration
-Tetanic contraction does not occur. (Temporal summation not an option) (protective: heart cannot fill if contracts continuously and NOT relax)
Explain the process of excitation contraction coupling
- when Action potential passes over the sacrolemma and down the T-tubules
- This trigger the entry of calcium into the cell via the DHP/L-type calcium channels in the T-tubules
- An increase in intracellular Ca2+ concentration induces calcium release via the Ryanodine-sensitive calcium release channels on the junctional SR
- When the intracellular free Ca 2+ concentration is high (>1.0 uM), cross-bridges form between the thick and thin filaments found within the muscle
How does the heart contract?
Depolarization due to automaticity(SA node) and spreads via gap junctions (synctium). Entire heart contracts at the same time.
Ca2+ from extracellular and intracellular sources
- L-type Ca channel -acts as a channel. Extracellular Ca2+ enter cell
Not all SR Ca2+ released (normal conditions Ca2+ 0.5-2 uM vs 10 skeletal) . Intracellular calcium levels titrated to increase contraction force (inotropy- later lectures)
-fraction of all crossbridges from (~40% maximal, not “all or none” like skeletal muscle)
Why is this the only way cardiac muscle increases force of contraction?- gap junctions, refractory period
What are the functions of Na+-Ca+ exchanger and Ca+-ATPase pump in excitation contraction coupling ?
Ca2+ unbind to troponin
-About 80% of the calcium is actively taken back up into the SR by the action of SERCA pumps
- About 20% of the calcium is extruded from the cell into the extracellular fluid either via:
- Na+-Ca2+ exchanger
- Ca2+-ATPase pumps
Summarize excitation contraction coupling
- Action potential enters from adjacent cell
- Voltage-gated Ca2+ channels open. Ca2+ enters cell
- Ca2+ induces Ca2+ release through ryanodine receptor-channel (RyR)
- Local release causes Ca2+ spark
- Summed Ca2+ sparks create a Ca2+ signal
- Ca2+ ions bind to troponin to initiate contraction
- Relaxation occurs when Ca2+ unbinds from troponin
- Ca2+ is pumped back into the sarcoplasmic reticulum for storage.
- Ca2+ is exchanged with Na+
- Na+ gradient is maintained by the Na+-K+-ATPase
What is inotropism?
The ability of myocardial cells to change the strength of contraction at the level of the cell.
How does inotropin lead to modulation?
Modulation of the influx of calcium through :
- DHP channels
- G protein-linked receptor (ANS)
- Non- receptor mediated events
give rise to the capability of modulation of the inotropic state of a single myocardial cell
How can inotropism occur?
This modification of force-generating capacity can occur independently
-At any given loading condition, the heart exposed to an Inotrope can potentially generate more isotonic force and move a greater load faster and farther
