excitation and contraction Flashcards
myofibril
- longitudinally with in the muscle fibers
- Z line
- ACH in the neuromuscular junction releases CALCIUM
sarcomeres
- composed of this and thick filaments
contraction
- causes no change in A BAND
- shortening of I an H BAND
I BAND
- ACTIN
H ZONE/BAND
- MYOSIN
A BAND
- ACTIN and MYOSIN
ACH in the neuromuscular junction releases CALCIUM
CALCIUM descends into
- T-tubule
sarcolemma
- covering of myofibril
sarcoplasmic reticulum
- dumps calcium into the T-tubules
T- tubules take calcium into the
- muscles
ACTIN
- THIN filaments
MYOSIN
- THICK filaments
tropomyosin
- covers the binding site
- blocks the myosin head for attachment
- prevents cross linking to actin
calcium binds to
- troponin
troponin
- functions is to move tropomyosin
hydrolysis of ATP causes
- cross bridge to gain energy and affinity for actin
- loss of affinity for actin
SARCOPLASMIC RETICULUM
- STORAGE SITE FOR CALCIUM
2 ATP’s are needed
- to start mechanical contraction
ATP split are needed for
- relaxation and contraction
skeletal muscle action potential
- SHORT
- causing multiple action potential
complete TETANUS is obtained
- when sufficient free calcium is available
- everything is engaged
complete tetanus vs rigor mortis
- tons of calcium , actin and myosin are engaged (TETANUS)
- no ATP it doesn’t detached (RIGOR MORTIS)
- SAME
ABSOLUTE REFRACTORY PERIOD
- is already depolarized
- -70mV
- happening
relative refractory period
- going back to normal
- earliest time that can have a new stimulus
- can get new depolarization
preload
- load on a muscle in a relaxed state prior to contraction
- causes muscle to STRETCH
- causes muscle to develop PASSIVE TENSION
AFTERLOAD
- how much effort to push to get the blood out 100lb
- the HIGHER THE BLOOD PRESSURE the MORE THE LOAD
drugs that decrease renin angiotensin aldosterone (CHF) decrease AFTERLOAD (lowers amount of ischemia, arrhythmias, and death)
- spironolactone
- ACE inhibitors
- beta blocker
- ARB
more preload
- more passive tension
stretch too much loose (DILATED CARDIOMYOPATHY)
over stretch the actin and myosin filaments
PASSIVE
- FORCE
- cannot generate force of contraction
- causing low EF
no stretch
- straight contractility
muscle contract when
- they are moderately streched
active
- actin, myosin filaments are contracting
- consuming ATP
passive, more stretch more passive
- pulling muscles apart
- loosing active
FORCE- VELOCITY CURVE
- preload can go up
Vmax is determined by
- muscle ATPase activity
maximum force generated
- is determined by muscle mass
white muscle
- large
- powerful muscles
- utilized short term
- LEG muscle of a sprinter, ocular muscles
- large mass
- high ATPase activity
- high capacity for anaerobic glycolysis
- low myoglobin
- fast energy
red muscle
- smaller
- less powerful muscle
- utilized long term
- for endurance
- postural muscles
- small mass
- lower ATPase activity
- slower
- high capacity for aerobic metabolism
- high myoglobin (red color) provide O2 to the cell
skeletal muscle
- striated (Z lines)
- actin myosin form sarcomeres
- sarcolemma lacks junctional complexes bet fibers
- each fiber innervated
- must be separately/ individually innervated
- one muscle at a time
- troponin to bind to calcium
high ATPase activity - fast muscle
- extensive sarcoplasmic reticulum inside the sarcomere
- T-tubules form TRIADIC at A I junctions
- lack Ca channels
cardiac muscle
- actin myosin form sarcomeres
- striated (Z lines)
- junctional complexes bet fibers including Gap junctions
- electrical syncytium
- troponin to bind to calcium (MI increase troponin)
- intermediate ATPase activity
- intermediate sarcoplasmic reticulum
- T tubules form dyadic contact near Z lines
- voltage gated calcium channels
- plateau phase 200 msec
smooth muscle
- non striated (no Z lines, no sarcomeres)
- actin myosin not organized into sarcomeres
- gap junctions ( fast bidirectional)
- electrical syncytium
- detrusor, esophagus, diaphragm
- calmodulin ( calcium modulation)to bind Ca2+
- low ATPase activity
- slow muscle
- limited sarcoplasmic reticulum
- lack T- tubules because their is a electrical syncytium to deliver electricity to the whole muscle simultaneously
- sarcoplasmic reticulum controlled by 2nd messenger
- voltage gated calcium channels