excitation and contraction Flashcards
1
Q
myofibril
A
- longitudinally with in the muscle fibers
- Z line
- ACH in the neuromuscular junction releases CALCIUM
2
Q
sarcomeres
A
- composed of this and thick filaments
3
Q
contraction
A
- causes no change in A BAND
- shortening of I an H BAND
4
Q
I BAND
A
- ACTIN
5
Q
H ZONE/BAND
A
- MYOSIN
6
Q
A BAND
A
- ACTIN and MYOSIN
7
Q
ACH in the neuromuscular junction releases CALCIUM
CALCIUM descends into
A
- T-tubule
8
Q
sarcolemma
A
- covering of myofibril
9
Q
sarcoplasmic reticulum
A
- dumps calcium into the T-tubules
10
Q
T- tubules take calcium into the
A
- muscles
11
Q
ACTIN
A
- THIN filaments
12
Q
MYOSIN
A
- THICK filaments
13
Q
tropomyosin
A
- covers the binding site
- blocks the myosin head for attachment
- prevents cross linking to actin
14
Q
calcium binds to
A
- troponin
15
Q
troponin
A
- functions is to move tropomyosin
16
Q
hydrolysis of ATP causes
A
- cross bridge to gain energy and affinity for actin
- loss of affinity for actin
17
Q
SARCOPLASMIC RETICULUM
A
- STORAGE SITE FOR CALCIUM
18
Q
2 ATP’s are needed
A
- to start mechanical contraction
19
Q
ATP split are needed for
A
- relaxation and contraction
20
Q
skeletal muscle action potential
A
- SHORT
- causing multiple action potential
21
Q
complete TETANUS is obtained
A
- when sufficient free calcium is available
- everything is engaged
22
Q
complete tetanus vs rigor mortis
A
- tons of calcium , actin and myosin are engaged (TETANUS)
- no ATP it doesn’t detached (RIGOR MORTIS)
- SAME
23
Q
ABSOLUTE REFRACTORY PERIOD
A
- is already depolarized
- -70mV
- happening
24
Q
relative refractory period
A
- going back to normal
- earliest time that can have a new stimulus
- can get new depolarization
25
preload
- load on a muscle in a relaxed state prior to contraction
- causes muscle to STRETCH
- causes muscle to develop PASSIVE TENSION
26
AFTERLOAD
- how much effort to push to get the blood out 100lb
| - the HIGHER THE BLOOD PRESSURE the MORE THE LOAD
27
```
drugs that decrease renin angiotensin aldosterone (CHF)
decrease AFTERLOAD (lowers amount of ischemia, arrhythmias, and death)
```
- spironolactone
- ACE inhibitors
- beta blocker
- ARB
28
more preload
- more passive tension
29
stretch too much loose (DILATED CARDIOMYOPATHY)
over stretch the actin and myosin filaments
PASSIVE
- FORCE
- cannot generate force of contraction
- causing low EF
30
no stretch
- straight contractility
31
muscle contract when
- they are moderately streched
32
active
- actin, myosin filaments are contracting
| - consuming ATP
33
passive, more stretch more passive
- pulling muscles apart
| - loosing active
34
FORCE- VELOCITY CURVE
- preload can go up
35
Vmax is determined by
- muscle ATPase activity
36
maximum force generated
- is determined by muscle mass
37
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
38
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
39
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
40
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
41
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
