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Muscle contraction
Relevant literature- physiology of muscles by Katz
Three types of muscle:
• Skeletal-voluntary (also unconscious movement like posture control):
Type I- slow oxidative (“slow twitch”), red (many capillaries, myoglobin and
mitochondria), good for aerobics.
Type II- “fast twitch”- divided to type IIa (like I-aerobic). IIb-anaerobic,
white. IIx- between red and white, specialized for fast and short-lasting
contractions.
• Smooth muscle- involuntary. Wall of organs like stomach, uterus. blood
vessels.
• Cardiac muscle- involuntary, specialized.
Cardiac and skeletal muscle are "striated" in that they contain sarcomers and
are packed into highly-regular arrangements of bundles; smooth muscle has
neither. While skeletal muscles are arranged in regular, parallel bundles,
cardiac muscle connects at branching, irregular angles.
What should we explain:
A muscle can contract and creates tension.
Analogy- tension on a string (one dimension, zero mass)
Calculating tension- connecting the muscle to a spring F=-K*x
(K- spring constant, known to us, x- shortening of muscle, Fforce).
A muscle can produce Isometric force (increasing force, hand
length stable-maintaining weigh at a given position) and
isotonic force (shortening muscle, stable force-lifting
weigh)
How does the muscle contracts
• How does a Nerve-Ach release- controls contraction
• How come we can have both isometric and isotonic forces
• Why is there an optimal muscle length
• Why load interferes with speed (the heavier the load the
slower the run)
• How building up muscles aids performance
• Why pre-training (“warming up”) aids performance
Striated skeletal muscle
Striated muscle is made of
Myofiber- multinucleated,
composed of 2 m myofibrils (coiled coil proteins)
• Packed in a membrane network- Sarcoplasmatic
Reticulum (SR)
• Outer membrane has invaginationsTransverse tubular system
(locations close to SRterminal cisternea
# of myofibrils- determine genetically,
can only decrease (atrophy)
Striated skeletal muscle-fiber structure
functional unit: sarcomere (defined from one Z disks to another)
Interleaving thin (actin) and thick (myosin) filaments.
Actin-G actin monomers form
F-actin polymer,each Actin is
composed of 2 F-actin (in coiled
coil) , lined with a tropomyosin
Molecule in the groove of the coil
(every 7 g-actin)
actin attached to z-disks by
Titin, the biggest protein known!
Filaments
troponin complex: Tropomyosin
Attaches to troponin C-troponinT
-troponin I that attaches back to Actin
(close circuit). Troponin C has 4 Ca sites,
unoccupied at rest (2 are occupied by Mg -unfavorably)
Myosin-Composed of myosin (2 heavy chains forming coiled coil,
Head domains with ATPases on one side, actin binding site on
other with motile “Neck” (90 degree deviation from “body” at
rest), and 4 light Chains (associated to
neck, regulatory)
The actual contraction- what causes
muscle shortening (Sliding filaments theory)
• Sarcomeres shorten by 70%
• Shortening is preceded by
creation of cross-bridges
How?
Starting at rigor actin-myosin
connection
1 ATP binding dissociates rigor state
2 ATP hydrolysis causes binding of head to new binding site
Small movement
3 Pi release produces power stroke
Large movement
4 ADP release completes the cycle
The force is with them
• every time actin and myosin attach/detach, thereby moving
sites and causing muscle shortening. This is termed isotonic
work.
• Sometime we want to hold something steady (no
movement)=isometric work- no change in muscle length but
an increase in its mechanical tension. (actually all isotonic
work is partially isometric- there is always some weight to
maintain).
In that case, actin and myosin will connect and de-connect at
the, same site, and ATP energy is be used for stability
(tension).
Excitation-contraction coupling (how
the nerve control contraction)
• Ach cause action potential which causes contraction through
calcium mediationAP’s depolarization open voltage sensitive calcium channels
(dihydropyridine) on transverse tubular system. They
machanically open ryanodine (Ca dependent Ca channels)
that releases Ca from reservoir in
sarcoplasmatic Reticulum.
Later- slow Ca reuptake.
The coupling more illustrative
Why is the calcium important?
The role of Ca2+- is to allow actin myosin
connection
Myosin binding sites on actin
are covered by tropomyosin.
Ca binds Troponin C, release
troponin complex to reveal
the binding site for actin.
Note I- depolarization is required only
for Ca entry, Ca entry only for
ryanodine.
Note Ii-doesn’t example muscle
sequence
The speed-load trade off
explained
1. The lighter the weight, the faster the run-> (Hyperbolic) inverse
relationship between speed and strength. why?
Maximal speed-the ATP turnover
Maximal strength- # of cross bridges
Why connected?
Whenever there is a weight (always)
Some cross bridges stay at same
location (tension)->less shortening
The optimal muscle length
explain (is it?)
2. Length-tension curveA muscle has optimal length,
Which is the length more crossbridges are in chance of contact
I- no bridges (or less then max)
II- optimal
III- less optimal directionally
IV- myosin bumps into Z disks,
Mechanical distortion.
But there are other elements to regard:
The first is the spring like properties of the
sliding filaments
When measured on real muscle, tension-length curve has double
peak. If measured WITHOUT ANY WORK, it is increasing.
Meaning- Passive spring like (rigid, non- elastic, resistive, creates
tension) properties. These are the properties of the actin and
myosin filaments without any work.
This is what
pre training
does
So overall tension
depends on more
then the worksubstrate the
passive tension!
There is Another spring like element
Example-the difference between twitch
and tetanus
• One AP cause a small contraction (a twitch)
• A train of AP, much larger contraction(tetani)
Hill suggested that: a single AP causes enough
calcium release for tetani, but the energy is
wasted.
His test: stimulating a muscle immediately
when pulling it (thereby
normal shortening after
the pull shifts connecting
tissue and no energy is
required. In this case, one
AP was enough for tetani.
The other spring like element is the
muscle’s connecting tissue-Hill’s model
Connecting tissue (proteins) occupies most of
the muscles volume and determine its shape.
They are rigid and resist muscle shortening, and
energy is wasted on moving them.
So in order to shorten the muscle one must first
Overcome the parallel spring of connective
tissue ,so that energy will arrive at the actinmyosin. Then, energy is spend on the passive
elastic properties of the actin-myosin complex
(the serial spring) and then move.
In isometric work- only the passive element is
relevant.
• This is why big muscles do more workthey are already more tensed and less
energy is needed to move them (# of muscle
fiber is fixed, This is the only improvable
element).
• Why do connective tissue grow- Either
response to
micro-damage to the muscle during exercise or
direct response to lactic acid)
Muscle-summery
• Actin and myosin attach and detach , using ATP to promote
either muscle tension or sliding on each other (muscle
shortening).
• Therefore, a muscle has optimal length and there is speedstrength trade off.
• Calcium is necessary to reveal actin binding sire. Calcium is
dependent of depolarization, and therefore, the amount of
action potentials will control the amount of muscle
contraction (how is thecontraction patttern set? Good question).
• In order to create work, more elements are to be considered:
1.the elasticity of the actin-myosin complex (there is partially why
warm-up aid performance)
2.The elasticity of the connecting tissue (this is why bulking up
aids performance)
Smooth muscle contraction
The interaction of sliding actin and myosin
filaments is similar in smooth muscle. There are
differences in the contraction cause -In Smooth
muscle contractions are initiated by calcium that
acitvate myosin phosphorylayion, that releases
energy.