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, F-

force).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 invaginations-

Transverse tubular system

(locations close to SR-

terminal 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!

Filamentstroponin complex: TropomyosinAttaches 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

connection1 ATP binding dissociates rigor state2 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 mediation-

AP’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 curve-

A muscle has optimal length,

Which is the length more cross-

bridges 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 work-substrate 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 enoughcalcium 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, oneAP 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, andenergy is wasted on moving them.

So in order to shorten the muscle one must firstOvercome the parallel spring of connective

tissue ,so that energy will arrive at the actin-myosin. 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 work-

they 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 speed-strength 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.