Download 2 Muscle Performance and Contraction Process

Anatomy and Physiology
Muscular System
Part # 2
Muscle Performance and
The Contraction Process
Fall 2008
Muscle Performance
Power and endurance determined by two
factors
1. Physical state of muscle conditioning/training
2. Genetically determined proportions
of types of muscle fibers within
muscle
Types of Muscle Fibers
Fast vs. Slow
Twitch Fibers
Types of Muscle Fibers/Cells
1.
Fast Twitch
Contract rapidly/powerfully
Need lots of energy (ATP)
Do have large glycogen reserves
Large densely packed cells
Fewer blood vessels
Less myoglobin
Holds less Oxygen
“Color”? More “white meat” appearance
Fewer mitochondria make and store less ATP
Quickly resort to anaerobic respiration
Fatigue quickly
Athletic activities?
Good sprinters, weight lifters – requires
anaerobic endurance
2. Slow Twitch
Contract slowly
Small cells
More blood vessels
More myoglobin
Holds high Oxygen reserves
“Color”? More “red/dark meat”
appearance
More mitochondria make and
store lots of ATP
Can run longer on aerobic
respiration
Fatigue resistant
Athletic activities?
Good long distance
runners
3. Intermediate Twitch
Properties between fast and slow twitch
Intermediate in terms of blood capillaries
Have less myoglobin
Resemble pale “white” fast fibers
Intermediate as far as fatigue resistance,
contraction speed and strength
Human Muscles
Genetically determined
proportions
Amount/type also varies at
different body locations
Area of fast twitch?
Ex: Eye – fast twitch =
brief, swift movements;
tire easily ie. Reading
Area of slow twitch?
Ex: Back and
abdominal muscles –
slow twitch = slow,
longer sustained
contractions to maintain
body posture for long
periods
Eye vs. Back – number of
fibrils controlled by one
motor unit neuron??
Working Out
Can one change the type of fibers in
one’s body?
Working out can somewhat cause fast
twitch fibers to develop appearance and
functional capabilities of intermediate
fibers
Result?
More fatigue resistant, more tone,
hypertrophy
Hypertrophy = more filaments,
mitochondria, ATP and glycogen
reserves
Huxley’s Sliding Filament Theory
How do muscles contract?
Contraction occurs at the level of the
sarcomere
Sarcomeres
Sarcomere –
repeating pattern
of arrangement
of actin and
myosin fibers
Billions extend
along fibril (cell)
length
Actual site of
contraction
Sarcomere Review
Uncontracted Sarcomere
Process involves sarcomere filaments
sliding over each other from both ends
toward the center
Goal to make actin meet in the middle
Result – shortens length of sarcomere
Occurring in billions of sarcomeres,
shortens overall length of muscle and
muscle pulls
Contracted Sarcomere
What’s Involved?
A.
B.
Myosin
Thick, dark filament with protoplasmic crossbridge
extension shaped like a golf club head
(“sticky finger”)
Has bonding sites for actin and ATP molecules
Can flex in a powerstroke when energized
by splitting of an ATP molecule
(rubberband analogy)
Actin
Thin, light filament
Has bonding site for myosin crossbridge – called: Active Site
Active site has protective (inhibiting) proteins wrapped around it
Called: troponin and tropomyosin (rubber glove analogy)
Calcium ions can remove (“unlock”) these proteins and make active
site available for bonding
Contraction Process
1. Neurotransmitter (acetylcholine) stimulation at motor point
2. Calcium ions diffuse deep into muscle
3. Calcium ions unwinds/removes inhibiting proteins from actin,
exposing active site
4. A molecule of ATP is split, releasing energy
5. Energy allows the myosin crossbridge to extend and cock (like a
mousetrap spring or gun trigger)
6. Crossbridge bonds to active site on actin
7. Crossbridge “springs” and pulls actin to sarcomere center
(rubber band analogy)
8. Second ATP is split releasing energy
9. Energy allows the crossbridge/actin bond to break
Entire process takes about 1/20 to 1/40 of a second
Muscle
Contraction # 1
Muscle Contraction
Neuromuscular
Junction
Sarcomere Contraction
Continued…
As long as ATP remains high, cycle repeats over
and over
Crossbridges bond to active sites farther out on
actin, again pulling the toward the sarcomere
center
Occurs all along both sides of the sarcomere
End result: the actin finally touch in the center,
entire sarcomere is contracted
Occurs to BILLIONS of sarcomeres along entire
muscle length
Finally, entire muscle is contracted or shortened
Sarcomere/Muscle Relaxation
Basically a passive process
Requires final ATP molecules to break actin/crossbridge
bond and filaments slide back to normal condition
Calcium ions are actively transported back in SR;
inhibiting proteins recover active sites on actin
Sarcomere/muscle lengthens
What if all ATP is depleted?
Cramp = Contracture (“Charley Horse”)
How do we get muscle to relax?
Massage? Works why?
Muscle “Fun Facts”
One sarcomere has about 500 myosin and
900 actin filaments !!
One muscle fibril (cell) has about 40 – 50
billion total filaments !!
Each myosin require about 2500 ATP
molecules per second during contraction !!
All – or – None Law
Law of physiology that applies to one single
muscle cell (fibril) or one single neuron
Given an appropriate level of neurotransmitter
stimulus, a single muscle fibril will always
contract or shorten fully
Appropriate stimulus called: Threshold
Only if not fatigued
In other words – there is no partial contraction of
a sarcomere or fibril
It shortens/contracts fully or not at all.
Not true for an entire muscle.
Muscle Pathology
Botulism
Bacterial food poisoning
Scientific name: Clostridium botulinum
“Cousin” of C.tetani
Anaerobic bacteria
Means what?
Produces spores shed in feces that can survive
aerobically
Produces a toxin
Usually found in canned foods
Bacteria produces gas that makes can bulge
Ingested, it prevents the release of acetylcholine at
NMJ
Can contract from a wound
Highly fatal
Can paralyze diaphragm and intercostal muscles
Patient dies why?
Botox
Use toxin from C. botulinum
Injected in small amounts into
facial muscles
Prevents acetylcholine
release and muscle
contraction
Eliminates “lines” on face
Why not poisonous to entire
body?
Costly; wears off in a few
months
Clostridium tetani
Anaerobic bacteria
Reproduces by spores shed in feces that
can survive aerobically
Contracted how?
NOT rusty nails
Usually a puncture wound
Must be contaminated with bacterial
spores
Usually from soil/water with feces
Produces toxin that acts on neurons that
control muscles
Result: muscle spasms and rigidity
Often masseter is first affected “lockjaw”
Can impact respiratory muscles and be
fatal
Should be vaccinated about every 10
years
Polio
Viral disease
Virus attacks brain and spinal cord neurons that
control muscles
Neurons can’t stimulate muscles
Leads to paralysis and atrophy
Often affects large leg skeletal muscles and sometimes
respiratory muscles
Patients often require leg braces, wheelchairs or even “iron lung”
Usually recover and may improve but often left with limp or
muscle damage
Epidemics in 40’s and 50’s
Jonas Salk developed vaccine in 1955 and helped to eradicate
disease from much of world by 1979
Making a comeback in some parts of world, especially Africa
Africa – some poorly educated parents afraid to vaccinate
children due to false fear that vaccines spread HIV and cause
infertility
Iron Lung Images
Salk and the Polio Vaccine