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Muscle Contraction

KIN 290 - Berry College - Dept. of Kinesiology
by

David Elmer

on 4 February 2014

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Transcript of Muscle Contraction

Muscle Contraction
Chapter 11
excitation-contraction coupling
sarcoplasmic reticulum
terminal cisternae
Ca++
+++
+++
DHPR
RYR
t-tubule
- - - - - - - -
+ + + + + + + +
+ + +
- - -
voltage sensor
calcium channel
may mechanically or chemically open RYR
junctional feet
IP
3
(inositol triphosphate)
run inward toward center of muscle
meet with each other to form continuous structure
located at juncture of A and I bands
2 per sarcomere
speed of activation signal = 7 cm/sec
Ca -ATPase
2+
Ca -ATPase
2+
calsequestrin
binds calcium when it enters S.R.
Ca++
terminal cisternae
sarcoplasmic reticulum
binds lots of calcium - efficient storage
2 Ca in, 2 K out
2+
+
slow - 20 ions/sec
densely packed in S.R. membrane
stimulated by magnesium ions
Ca++
100 fold increase in concentration
initiates muscle contraction
sliding filament and cross-bridge theory
amount of force developed depends on the number of cross-bridges formed
myosin
two globular heads and a coiled tail
several hundred myosin molecules associate together to form a single myosin filament
have a pocket for binding and hydrolyzing ATP
open cleft = weak binding to actin
closed cleft = strong binding to actin
regulatory chain
essential chain
provide structural stability
phosphorylation causes myosin head to swing out and get closer to actin
increase force & velocity of shortening
actin
g-actin combines to form f-actin
polarity ensures they all line up the same way
spans 7 g-actin molecules
double helix conformation, stiffens actin chain
T - binds to tropomyosin
I - holds troponin to actin
C - binds 4 calcium ions, undergoes conformational change to move tropomyosin off actin-myosin binding sites
blocks the actin-myosin binding sites
role of ATP
before arrival of calcium...
ATP bound to myosin head - weak binding (dissociation) with actin
ATP partially hydrolyzed to ADP
Pi
myosin head "cocked"
1.
2.
calcium arrives
myosin weakly binds actin
3.
Pi released - strong binding and power stroke
4.
ADP released, replaced by ATP - weak binding (dissociation) with actin
5.
ATP is required for cross-bridge release
(rigor mortis)
usually 1-10 ms
twitch
smallest contractile response that can be elicited
1x =
used to determine different fiber types and characteristics of motor units
force
time
1/2 relaxation time
peak rate of force development
peak relaxation rate
contraction time
what if you stimulate the fiber again before it relaxes all the way?
summation & tetanus
time
fusion frequency
stimulation frequency when peaks fuse together
peak force
force-velocity relationship
velocity
force
power = force x velocity
length-tension relationship
longer neck = faster velocity
"lever arm" action
changes shape of associated cleft
type I
type IIa
type IIx
twitch
EMG
weak effort
max effort
twitch
EMG
weak effort
max effort
activity dependent potentiation:
aka postactivation potentiation
twitch response is greater for a few minutes following a tetanic contraction
possible causes:
phosphorylation of myosin light chain
elevated calcium in the cytosol of the muscle
"positive staircase"
result:
fast twitch
slow twitch
1. what do PAP, HPAP, LPAP, TPT, and HRT stand for?
2. what is the mechanism responsible for PAP?
3. what were the two hypotheses for this study?
4. describe the timeline for the protocol.
5. describe the correlation between PAP and fiber type found in this study
6. describe the correlation between PAP and TPT found in this study
7. describe the relationship between HPAP and TPT in this study
8. what are the two lines of evidence indicating a relationship between fiber type and PAP?
9. what is the physiological reason for the difference in results for TPT and HRT?
Full transcript