Lecture 9.3 main points Flashcards
briefly describe the events involved in initiating muscle conttraction
nerve impulse reaches axon terminal, voltage gated calcium channels open, Ach is released to the synaptic cleft, Ach binds to receptors in sarcolemma which opens ligand gated Na and K channels, end plate potential causes voltage gated Na channels to open causing depolarization, if threshold is reached an AP is activated causing propagation across the sarcolemma down into the T-Tubules. DHP receptors (proteins) in the t-tubules change shape and activate the ryanodine receptors causing a release of calcium from the SR into the sarcoplasm
when intracellular (sarcoplasmic) calcium concentrations are low the muscle fiber is in a relaxed state, why is this
because tropomyosin blocks the active sites of myosin binding sites on the thin filaments. Myosin heads of the thick filament are required to bind to the thin filaments to cause contraction
when sarcoplasmic calcium increases due to release of Ca from the SR, what does calcium bind to the in the sarcomere
calcium binds to troponin C of the troponin-tropomyosin complex
what change occurs in the thin filament due to the binding of calcium and troponin C?
what can the thick filament do?
troponin changes shape and moves tropomyosin away from the myosin binding sites
myosin can then bind to actin and undergo power stroke causing sarcomere shortening
what happens when nervous system (motor neuron) stimulation of the skeletal muscle ceases
no more calcium pumping into sarcoplasm therefore no Ach release and no AP stimulation
what is the name of the SR pump that removes calcium from the sarcoplasm
SERCA pumps
what are the names of the pumps in the sarcolemma that remove calcium from the sarcomplasm
Ca pumps
how is the position of the troponin-tropomyosin complex affected by low sarcoplasmic calcium
low sarcoplasmic calcium causes the tropomyosin to block myosin binding sites on actin on thin filaments
how is the position of the troponin-tropomyosin complex affected by high sarcoplasmic calcium
the troponin C binds to calcium and moves tropomyosin away from the myosin blocking sites
define cross bridge formation
myosin heads bind to actin of thin filaments. Sliding of thin filaments with respect to the thick begins as power stroke of the myosin head takes place
cross bridges from and break several times ratcheting thin filaments toward the center of sarcomere
this causes shortening of the muscle fiber
briefly describe the process of cross bridge cycling and the change in location of the z-discs relative to the M- line
z-disc is pulled toward the m-line. This causes the I bands to shorten, the Z discs move closer, the H zones disappear, A bands of adjacent sarcomeres move closer together but the A length stays the same
what sarcoplasmic ion concentration allows for cross bridge cycling to continue in the contracting muscle cell
as long as sarcoplasmic Ca stays high and adequate ATP is present
in order for cross bridging between a g-actin subunit of the thin filament and the myosin head of the thick filament to form. what two molecules must be bound to the myosin head
ADP and an inorganic phosphate
define power stroke and what molecules are released in the process
when inorganic phosphate is released changing the shape of the myosin head this initiates the power stroke, then ADP is released
where the myosin head pivots and pulls thin filament toward the M line
release ADP and Pi in the process
how does the myosin head release from the g-actin subunit of the thin filament post power stroke
ATP attaches to myosin head weakening the link between actin and myosin and cross bridge detaches
how is the myosin re-energized post detachment
energy from the hydrolysis of ATP into ADP and inorganic phosphate cocks the myosin head into a high energy state
what two molecules must be bound to myosin head for it to be in the high affinity state for the binding site on the g-actin subunit
inorganic phosphate and ADP
what molecule initiates power-stroke when released from the myosin head
inorganic phsophate
the release of which molecule completes the process of power-stroke of the myosin head
ADP
which molecules must bind to the myosin head in order for it to release from its binding site on the g-actin subunit of the thin filament
ATP
what must myosin do to ATP in order to reset back into high affinity state
hydrolyze ATP into ADP and Pi
when sarcomeres shorten and elastic filaments are stretched what is produced
muscle tension
what particular features relating to the position of the thin and thick filaments determine the tension a muscle fiber is capable of producing
dependent on the amount of overlap between the thin and thick filaments
how is max tension affected if the muscle fiber is too short (under-stretched)? why is this?
there is too much overlap between thin and thick filaments, tension is decreased when the muscle is shortened, thin filaments begin to overlap
how is max tension affected if the muscle fiber is too long (over-stretched)? why is this?
there is too little overlap between thin and thick filaments therefore not enough cross bridges can be formed causing tension to decrease the more a muscle is stretched
define optimal resting length and why is produces max tension in the muscle fiber when contraction occurs
allows for maximum number of actin/myosin cross bridge formations, allows for max tension generated during contraction
-muscles rest at this length
how long post expiration (after death) does rigor mortis begin to occur
3-4 hours post death, maximum stiffness around 12 hours post death, can take 48-60 hours to subside
describe the process of rigor mortus as it relates to sarcoplasmic calcium control, decrease in available ATP, and cross- bridge cycling
when the heart stops, blood flow stops and oxygen/nutrient delivery is halted, therefore ATP production declines causing cell death
ATP is no longer available to bind to the myosin head for detachment of myosin head from active site on actin. ATP is no longer available to power the calcium pumps that remove calcium from the sarcoplasm into the terminal cisternae. This means that intracellular calcium stays high enough to allow the active sites on thin filaments to remain unblocked
how can rigor mortis be used by law enforcement and medical professionals
can be used to determine time of death
