thick filaments; describe composition.
made up of many MYOSIN molecules that have PROTRUDING HEADS at opposite ends of filament
- connect with THIN STRANDS of ACTIN to form CROSS BRDIGES - for MUSCLE CONTRACTION
“pulling motion”
thin filaments; describe composition.
has TWO STRANDS of ACTIN with a TWISTED HELIX STRUC.
- TWO REGULATORY PROTEINS: TROPONIN & TROPOMYOSIN
- has SPECIFIC MYOSIN ATTACHMENT SITES
*look like little blueberries :)
troponin
aids greatly in MUSCLE CONTRACTION in SKELETAL & CARDIAC MUSCLE
tropomyosin
aids in the CONTRACTION of SKELETAL MUSCLE
Titin
helps hold the THICK FILAMENTS in PLACE, helps with the RECOIL/GREATER RESISTANCE
dystrophin
aids with the LINKING OF FILAMENTS TO PROTEINS of the SARCOLEMMA
sarcoplasmic reticulum
triad
composed of T TUBULES & TERMINAL CISTERNS of the SR
terminal cisterns
t tubules
a TUBE that is FORMED by the PROTRUSION OF SARCOLEMMA DEEP into CELL INTERIOR
what is the sliding contract mechanism?
this is where we begin to see CHANGES within the I BAND & H ZONE - during MUSCLE CONTRACTION
- where MYOSIN BEGINS TO PULL ACTIN (making the SARCOMERE SHORTEN - Z DISCS MOVE TOWARDS EACH OTHER
what is the sliding filament model of contraction? name each step!
(***remember to note where our CALCIUM COMES FROM first - released by the SR due to ACTION POTENTIAL from the NMJ)
PHASE TWO
1. AP first TRAVELS across the entire SARCOLEMMA
2. AP TRAVELS along the T TUBULES
3. SR RELEASE of CALCIUM which BINDS TO TROPONIN (TROPONIN+CALCIUM)
4. TROPONIN PULLS TROPOMYOSIN - EXPOSED ACTIN BINDING SITES
5. MYOSIN HEAD BIND TO ACTIN (CROSS-BRIDGING)
6.’‘SWIVELING” MOTION - creation of the “POWER STROKE” **sliding filament action
7. COMPLETED POWER STROKE - ATP attachment again to MYOSIN/BACK TO ORIGINAL POSITION
*this process is repeated all over again as ATP is broken down by ATPase
*important - CALCIUM + ATP
the 4 steps of describe muscle contraction.
describe the nerve stimulus and the events that occur during the NMJ.
[context. always heavily getting stimulations from our skeletal muscles - sends then through alpha motor neurons all the way to the NMJ]
PHASE 1
1. AP arriving at AXON TERMINAL of MOTOR NEURON
2. VOLTAGE GATED CALCIUM enters AXON TERMINAL
3. CALCIUM ENTRY causes ACH (acetylcholine) RELEASe through EXOCYTOSIS (vesicles)
4. DIFFUSION of ACh in the SYNAPTIC CLEFT - binding of SARCOLEMMA RECEPTORS
5. PASSAGEWAY OF SODIUM-POTASSIUM PUMPS (3 sodiums in, 2 potassiums in) - creation of END PLATE POTENTIAL (also changes POLARITY of CELL
*local DEPOLARIZATION that helps DIFFUSE AP to PHASE 2
role of acetylcholinesterase
the breakdown of ACh is due to the enzyme acetylcholinesterase & stops contractions
muscle twitch
the SIMPLEST CONTRACTION due to MUSCLE FIBER’S RESPONSE to a SINGLE AP from MOTOR NEUTRON
what are the myogram phases?
*phases can vary from SIZE of muscles, or other METABOLIC NEEDS
wave (temporal) summation
results from 2 DIFFERENT STIMULI recieved from the MUSCLE due to RAPID SUCCESSION
*not enough time to RELAX - creation of MORE TENSION
tentanic contraction/fused (complete) tetanus
muscle tone
the CONSTANT, SLIGHTLY CONTRACTED STATE OF ALL MUSCLES
- gets input from stretch receptors in muscles - keeping muscles FIRM, HEALTHY, & RESPONSIVE
what is excess postexercise oxygen consumption (EPOC) or oxygen debt?
this is where if you continue to BREATHE HEAVILY for a long time
- replenishing of CP reserves
- conversion of lactate to pyruvate
- lactic acid to pyruvic acid
- reloading of oxygen into myoglobin
what are the type of stimulus?
*range of MOTOR UNITS depending on stimulus (goes from small, medium, to large fibers)