Download Chapter 9 Muscle

Survey
yes no Was this document useful for you?
   Thank you for your participation!

* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project

Document related concepts
no text concepts found
Transcript
Chapter 9 Muscle
Functions of Skeletal Muscle
•
•
•
•
movement
maintain posture
stabilize joints
heat production
Gross anatomy
•
•
•
muscle cell
–
= muscle fiber
myofibrils
fascicle
many myofibrils
cylindrical units within each cell
contain sarcomeres
= bundle
many cells
muscle
many fascicles
microanatomy
•
•
•
•
sarcolemma
–
T tubules
cell membrane
run deep into SR
stores Ca++
sarcoplasmic reticulum
–
–
surrounds myofibrils
terminal cisternae
sarcoplasm
–
–
= cytoplasm
glycogen
myoglobin
sarcomere
unit of contraction
sarcomere
•
•
•
•
•
•
unit of contraction
many along length of myofibril
Z disc
-
“striations”
ends of sarcomere
A band (dark)
myosin and overlapping actin
I band
non-overlapping actin
(light)
contractile proteins
actin ; myosin
contractile proteins
•
•
thick filament
–
–
myosin
tail
shaft
heads
2 binding sites for actin
thin filament
–
–
–
actin
helical chain of actin molecules
myosin binding sites
tropomyosin
covers actin – myosin binding sites
troponin
binds tropomyosin to actin
has Ca++ binding sites
Contraction of Sarcomere
•
•
•
•
sarcomere gets shorter ; not the filaments
Sliding Filament Model
actin and myosin slide past each other
Z discs get closer = sarcomere shortens
Ca stimulates filament sliding
•
•
•
•
•
++
Ca binds to troponin
troponin changes shape
pulls tropomyosin off the actin
exposes actin
actin and myosin bind
Who does what to who ?
•
•
•
myosin vs ADP
–
–
w/ ADP
myosin extended
w/o ADP
myosin bends
actin vs ATP
–
–
ATP
knocks actin off myosin
Actin
knocks ADP off myosin
Ca
actin and myosin bind
put it together
•
•
•
resting
myosin extended w/ ADP
stimulus
Ca
cross bridge formation
myosin and actin bind
actin knocks off ADP
•
power stroke
w/o ADP, myosin bends
myosin bend pulls actin
•
detachment
ATP binds to myosin head
breaks bond with actin
•
“cocking” of myosin heads
ATP  ADP + P
ADP extends myosin
•
repeats
•
•
•
•
•
some myosin always in contact with actin
cycle repeats several times –
pulling actin further
1 power stroke shortens muscle about 1%
muscles shorten ~ 30 – 35 % of their resting length
continues as long as Ca++ and ATP present
Neuromuscular junction
•
•
•
= motor neuron + muscle fiber
control cell = neuron
–
neurotransmitter
transport
axon terminal
acetylcholine (Ach)
synapse
•
target cell
–
(post-synaptic cell) muscle
motor end plate
sarcolemma at synapse
• receptors
• action potential
for Ach
sarcolemma
Neuromuscular excitation
•
•
•
•
•
•
GOAL:
sarcomere contraction
Muscle vs Nerve :
NT depolarizes target cell
effect of action potential:
target cell = nerve
NT release
target cell = muscle
Ca from sarcoplasmic reticulum
Sarcolemma
•
polarized
•
Na channels
•
–
–
+ outside / - inside
chemically-gated
at motor end plate
voltage-gated
receptors
sarcolemma, T-tubules
for Ach
motor end plate only
Sarcolemma acts like an axon
•
polarized
•
Ach opens Na ligand-gated channel
•
•
•
–
at rest
+ outside / - inside
Na / K
nature wants ?
depolarization
+ in / - ouside
+
Na inside opens voltage-gated Na channels
action potential
entire sarcolemma and T-tubules
same as axon
action potential causes calcium release
•
•
•
•
T-tubules next to terminal cisternae
T tubules depolarize
Na+ inside opens voltage gated Ca channels in SR
sarcoplasmic reticulum releases Ca++
excitation-contraction coupling – short version
•
•
•
•
neuron stim sarcolemma
action potential
Ca released
sarcomere shortens
excitation-contraction coupling
•
•
•
•
•
neuron depolarizes
depolarization reaches axon terminal
rush of Ca++ into axon terminal
Ca++ causes release of Acetylcholine into synapse
Ach binds with receptors on motor endplate
•
•
•
•
•
•
•
•
•
•
Ach opens ligand-gated Na channels
Na+ inside opens voltage-gated Na+
action potential along sarcolemma and T-tubules
Na+ inside causes sarcoplasmic reticulum to release Ca ++
Ca++ binds to troponin
pulls tropomyosin off actin
actin and myosin bind
cross bridge
myosin bends
power stroke
sarcomere shortens
How do you stop this darn thing?
•
Acetylcholinesterase destroys Ach at motor end plate
–
–
Na channels close
sarcolemma repolarizes
•
Na - K+ pump
•
Ca++ pump
•
•
+
•
Ca++ into SR via active transport
troponin and tropomyosin cover actin
ATP - detachment
•
myosin extends
sarcomere lengthens
ATP uses
•
•
•
Na pump
Ca pump
break myosin and actin bond
Motor unit
•
•
•
•
•
motor neuron + muscle cells it stimulates
1 neuron has several branches of its axon
strength of contraction
–
–
more motor units =
stronger contraction of muscle
recruitment
control of movements
–
–
small motor units (4-10)
fine control
fingers
large motor units (100)
poor control
thigh
alternation
one stimulus
•
•
twitch = single contraction due to a single stimulus
3 parts:
–
latent period
time from excitation to contraction
no change in myogram
~ 3 ms
–
contraction
begin contraction to max. force
myogram increases
~ 10-100 ms
–
relaxation
myogram decreases
sarcomere relaxes
~ 10-100 ms
myogram
•
•
•
recording of muscle activity
tension , not voltage
muscles vary in speed and length of twitch
size of motor unit
repeated stimuli
•
graded response =
•
wave summation
•
–
–
–
varied strength of contraction
number of motor units
repeat stim w/o full relaxation
nd
2 twitch is a stronger contraction (summed)
increased Ca++ available
tetanus:
smooth, sustained contraction
normal muscle contraction
stronger stimuli
•
•
•
motor unit summation
–
–
=
in vivo:
more neurons
lab:
more electricity (mV)
recruitment
threshold stimulus
–
minimum stim to cause contraction
maximal stimulus
–
–
strongest stim that increases force of contraction
all motor units recruited
muscle tone
•
muscle tone
–
–
–
slight, constant contraction of all skeletal muscles
posture
stabilize joints
heat production
treppe
•
“warming up”
treppe
–
–
gradual increase strength of 1st few contractions
increase Ca++
and enzyme activity
length - strength
•
•
•
•
resting length vs strength
ideal resting length
–
80 – 120 % of resting length
too short
–
sarcomeres already short
too long
–
actin and myosin too far away
force of muscle contraction
•
affected by:
–
–
–
–
recruitment
size of muscle fibers
wave summation (frequency)
muscle length
types of muscle contraction
•
•
•
•
muscle tension
force
load
weight of object (bone)
isometric contraction
tension w/o movement
isotonic contraction
tension w/ movement
–
–
concentric
tension while shortening
eccentric
tension while lengthening
Energy production
•
•
•
stored ATP
3 – 4 seconds
creatine phosphate (CP)
10 – 15 sec
– creatine-P
+ ADP  creatine + ATP
CPK
new ATP:
– glycolysis
=
anaerobic respiration
• fastest, but only 2 ATP made
• strenuous activity
30 – 40 sec
• when decreased O2 and blood flow
• lactic acid
– aerobic respiration =
cell respiration
• glucose + O2  ATP + CO2 + H2O + heat
• 36 ATP made
• mild, or prolonged activity
fuel for ATP
•
•
fatty acids
main source at rest
glycogen
stored in muscle
moderate to heavy exercise
•
glucose
blood
minimal source in muscle
•
pyruvic acid
liver converted lactic acid
replaces ATP after exercise
•
oxygen
myoglobin
hemoglobin
effects of ATP use
•
fatigue
low ATP
lactic acid - low pH inhibits enzymes
inability to contract
•
contractures
lack ATP
can’t detach cross-bridges
decrease blood flow
•
Oxygen debt
replace O2 stored in myoglobin
O2 for lactic acid  pyruvic acid
increased respiratory rate
decreased pH
CO2 , lactic acid
•
•
increase body temp
types of skeletal muscle fibers
•
slow oxidative fibers (type I)
–
–
–
–
aerobic (cell respiration)
myoglobin ; mitochondria
slow , prolonged contraction
little fatigue
(red)
•
•
fast glycolytic fibers (type II x)
–
–
–
anaerobic
little myoglobin or mitochondria
(pale)
fast contraction ; quick fatigue
fast oxidative fibers (type II a)
–
(pink)
intermediate speed, strength, and fatigue
Exercise
•
•
•
endurance exercise
–
–
–
–
aerobic
increase mitochondria , myoglobin , capillaries
slow, oxidative fibers
less fatigue
no increase mass
resistance exercise
–
–
–
increase myofibrils , not # muscle cells
= hypertrophy
stores glycogen
split ends theory
atrophy
–
–
disuse
nerve damage
homeostatic responses to exercise
•
•
•
•
•
•
vasodilation
increase O2 , glucose
remove CO2
increase heart rate
same
increase respiration
remove CO2 , raise pH
remove heat
repay oxygen debt
acid-base mechanisms
remove H+ , raise pH
sweat
decrease body heat
thirst
replace water loss
smooth muscle
•
•
•
•
•
no sarcomeres
network of sliding thick and thin filaments
Ca++ stim sliding
–
SR and caveoli (pouch of extracellular Ca++)
gap junctions
no fatigue
slow contraction
low ATP requirement
•
neural stim
acetylcholine
norepinephrine
•
other controls
α ß
hormones
O2 , CO2 , pH
histamine , paracrines
cardiac muscle
•
see heart chapter
diseases
•
•
•
Muscular Dystrophy
myasthenia gravis
atrophy