Marieb Anatomy + Physiology Chapter 9: Muscles + Muscle Tissue

Muscle Fibers

- Skeletal + smooth muscle (except cardiac) are elongated, that's why they are called "muscle fibers".

- Muscle fibers ARE muscle cells.

- HUGE cells

- Diameter is 10 to 100 micrometers long

- Up to 10 times the size of an average body cell

- Can get as long as 30cm long

Muscle Cells

Are muscle fibers

Skeletal Muscle

- Voluntary muscle

- Muscles that attach to bones

- LONGEST muscle cells

- Striated

- Responsible for body mobility

- Multinuculate

- Cylindrical

Cardiac Muscle

- Heart Muscle

- Involuntary Muscle

- Striated

- Branching

- Intercalated discs

Smooth Muscle

- Involuntary Muscle

- In walls of hollow organs

- Not striated

- Elongated cells

- SPINDLE shaped

4 Special Characteristics of Muscle Tissue

1.) EXCITABILITY (Responsiveness): The ability to receive + respond to a stimulus. In muscles, the stimulus is usually a chemical + the response is an electrical impulse that will contract the muscle.

2.) CONTRACTILITY: The ability to shorten forcibly when stimulated during muscle contraction.

3.) EXTENSIBILITY: The ability to extend or stretch. Muscles SHORTEN when contracted but they can STRETCH when relaxed.

4.) ELASTICITY: The ability of a muscle cell to RECOIL + RESUME its resting length after stretching.

5 Muscle Functions

1.) Producing Movement

2.) Maintaining Posture + Body Position

3.) Stabilizing Joints

4.) Generating Heat

5.) Additional functions: Protect internal organs. Smooth muscle regulates the movement of substances threw hollow organs, dilates + constricts the pupils of eyes + forms arrector pili muscles attached to hair follicles.

Skeletal Muscle: Nerve + Blood Supply

- One nerve, one artery + one or more veins serve EACH muscle.

- Skeletal muscle has a rich blood supply.

- Enter/exit near CENTRAL part + branch through connective tissue sheaths.

- Huge nutrient + oxygen needs.

- Generates a large amount of waste.

Skeletal Muscle: 3 Connective Tissue Sheaths

External to internal:

1.) Epimysium: Dense irregular connective tissue that covers OUTSIDE the WHOLE muscle. Sometimes blends with the deep fascia.

2.) Perimysium + Fasciles: Muscle fibers are wrapped into FASCILES + around EACH fascile is PERIMYSIUM made of fiberous connective tissue.

3.) Endomysium: Wispy sheath of connective that surrounds EACH muscle fiber. Made of areolar connective tissue.

Epimysium

Dense irregular connective tissue that covers the WHOLE muscle. Sometimes blends with the deep fascia.

Perimysium + Fasciles

Muscle fibers are wrapped into FASCILES + around EACH fascile is PERIMYSIUM made of fiberous connective tissue.

Endomysium

Wispy sheath of connective that surrounds EACH muscle fiber. Made of areolar connective tissue.

Direct (fleshy) Attachments

The epimysium of skeletal muscle is FUSED to the periosteum of a bone OR perichondrium of cartilage.

Indirect Attachment

The muscle's connective tissue wrapping extend beyond the muscle either as a ropelike TENDON or a sheetlike APONEUROSIS. They both anchor a muscle to the connective tissue covering of a skeletal element (bone or cartilage) or to the fascia of other muscles.

Tendon + Aponeurosis

- Indirect attachments

- Both anchor a muscle to the connective tissue covering of a skeletal element (bone or cartilage) or to the fascia of other muscles.

Aponeurosis

- Joins muscle to muscle

- Sheetlike

- Indirect attachment

Insertion

Movable bone

Orgin

Immovable (or less movable) bone

Sarcolemma

Plasma membrane of skeletal muscle fiber (cell)

Sarcoplasm

- CYTOPLASM of muscle cell.

- Contains GLYCOSOMES: Granules of stored glycogen that provide glucose during muscle cell activity

- Contains MYOGLOBIN: A red pigment that STORES oxygen. Similar to hemoglobin in blood.

GLYCOSOMES

- Granules of stored glycogen that provide glucose during muscle cell activity

- Located in sarcoplasm of muscle cell

MYOGLOBIN

- A red pigment that STORES oxygen. Similar to hemoglobin in blood.

- Located in sarcoplasm of muscle cell

Structural Levels of Muscle Tissue from Outside to Inside

- Epimysium

- Muscle

- Perimysium

- Fascicle

- Endomysium

- Muscle Fiber (muscle cell)

- Sarcolemma

- Myofibril (composed of bundles of myofilaments. PARALLEL to length of muscle)

- Sarcomere (segment of myofibril): The FUNCTIONAL (contractive) unit of muscle

Striations of Skeletal Muscle

Made of repeating series of DARK ("A" bands) + LIGHT ("I" bands).

Sarcomere

- Smallest contractile unit of a muscle fiber (the FUNCTIONAL unit of skeletal muscle)

- Made up of TWO successive "Z" discs in a myofibril

- Contains an "A" band flaked by HALF an "I" band.

Thick Filaments

- Contain 300 MYOSIN molecules

- Tails are within the central part + the heads face outward a the END of each thick filament

- The central part is smooth + the ends are studded

- The myosin heads contain the actin + ATP BINDING SITES

- The myosin heads also have ATPase activity, which is an enzyme that SPLITS ATP to generate energy for the muscle.

- The myosin heads link the thick + thin filaments together to form CROSS BRIDGES which act as motors to generate force + contract the muscle

Thin Filaments

- Contain ACTIN

- Actin contains GLOBULAR ACTIN (G Actin) which bear the active sites in which the myosin heads attach to during muscle contraction. These are the "pits" inside the actin.

- Globular actin subunits are POLYMERIAED into long actin filaments called FILAMENTOUS (F Actin). The G + F actin filaments twist to form the backbone of each thin filament

- Tropomyosin + troponin help control the cross bridge formations of myosin + actin during muscle contraction.

- TROPOMYOSIN (a rod shaped polypeptide) spirals in the actin core to help stabalize it. They are arranged end to end along the actin filaments. When the muscle is relaxed, tropomyosin BLOCKS the myosin binding sites.

- TROPONIN (a globular polypeptide complex). Made of THREE parts: One part is TnI and is an INHIBITORY subunit that binds to actin. The second is TnT and it binds to tropomyosin and helps position it on actin. The third is TnC and it binds to calcium ions.

TROPOMYOSIN

- Located within THIN filaments

- Rod shaped polypeptide

- Spirals in the actin core to help stabalize it. They are arranged end to end along the actin filaments. When the muscle is relaxed, tropomyosin BLOCKS the myosin binding sites.

TROPONIN + its 3 parts

- Located within THIN filaments

- A globular polypeptide complex.

Made of THREE parts:

1.) TnL: INHIBITORY subunit that binds to actin.

2.) TnT: Binds to tropomyosin and helps position it on actin.

3.) TnC: Binds to calcium ions.

Dystrophin

- A structural protein that LINKS the thin filaments to the INTEGRAL PROTEINS of the sarcolemma.

- Lack of dystrophin causes muscular distrophy

Other proteins that bind filaments or sarcomeres together

- Nebulin

- Myomesin

- C Proteins

Elastic Filaments

- Contain TITIN

- Exist within thick filaments + forms its core to attach it to the "M line"

- Holds the THICK FILAMENTS in place to maintain the organization of the "A band"

- Helps muscle spring back into shape after stretching

- Stiffens as it uncoils to help the muscle resist excessive stretching

Cross Bridges

Myosin + Actin binding

Intermediate (desmin) Filaments

Extend from the Z disc + connect each myofibril to the next throughout the width of the muscle cell.

I Band

Contains THIN filaments ONLY

H Zone

Contains THICK filaments ONLY

M Line

Contains THICK filaments linked by accessory protiens

Outer Edge of the "A" Band

Contains THICK + THIN filaments overlapping

Titin

- Holds thick filaments IN PLACE + helps them SPRING BACK into place after stretching.

- Part of elastic filaments that are continuous with thick filaments.

2 Intercellular tubles that REGULATE muscle contraction

1.) Sarcoplasmic reticulum

2.) T Tubles

- Together they form TRIADS

Sarcoplasmic Reticulum

- REGULATES calcium

- STORES calcium

- RELEASES calcium on demand when the muscle fiber is stimulated to contract

- Smooth endoplasmic reticulum that loosely surrounds each myofibril longitudinally

- Communicates with each other along the "H zone"

- TERMINAL CISTERNS form larger, perpindicular cross channels at the A + I band junctions + always occur in pairs.

- Contain large amount of mitochondria + glycogen granules to provide energy for muscle during contraction

Terminal Cisterns

- Part of Sarcoplasmic reticulum closest to the T Tubules

- Form part of the TRIADS along with the T Tubules

T Tublues

- At each A + I band junction

- Increases the mucle fiber's surface area

- Protrudes deep into the muscle cell interior

- "T" stands for "transverse"

- Continuous with the extracellular space (possibly the result of fusing tubelike caveolae with the lumen (cavity) of t tubule)

- CONTINOUS WITH SARCOLEMMA

- Sandwiched in between 2 terminal cisters to form TRIADS

- Encircle EACH sarcomere

- Conduct impulses to the DEEPEST regions of the muscle cell + each sarcomere

- SIGNAL FOR THE RELEASE OF CALCIUM from the adjacent terminal cisterns.

Triads + its 3 parts

- Working together the triads signals for muscle contraction

- At the triads, where they come closest into contact, integral proteins protrude into the intermembrane spaces

- Integral proteins act as voltage sensors

3 Parts:

- 2 Terminal Cisterns (on outside)

- 1 T Tubule (Sandwiched between the 2 terminal cisterns)

What is the "go" for muscle contraction?

Calcium (Ca+)

Sliding Filament Model of Contraction + Four Steps

- States that during contraction the THIN filaments SLIDE PAST the THICK filaments so that the ACTIN + MYOSIN filaments OVERLAP to a greater degree:

1.) Myosin binds to actin to form CROSS BRIDGES + the sliding begins

2.) These cross bridge attachments between myosin + actin BREAK SEVERAL TIMES during contraction, acting like tiny ratchets to generate tension + propel the thin filaments towards the CENTER of the sarcomere.

3.) This happens throughout the cell + the muscle cell shortens

4.) Thin filaments (actin) slides CENTRALLY + the "z discs" are pulled TOWARDS the "m line". The "I bands" shorten, the "h zones" DISAPPEAR + the "a bands" move CLOSER together but their length does not change.

Contraction

- "Shortening"

- The activation of cross bridges (formed by myosin + actin), which are force generating sites

4 things needed for a muscle fiber (cell) to contract

1.) Fiber must be stimulated by a nerve ending so that a change in membrane potential occurs.

2.) It must generate an electrical current called an ACTION POTENTIAL in its sarcolemma.

3.) The action potential moves along the sarcolemma.

4.) As a response, intracellular calcium ion levels must RISE breifly, providing the final trigger for contraction

The 2 phases (9 steps total) that lead to muscle fiber contraction

Phase 1: Motor neuron stimulates muscle fiber

1.) Action potential (AP) arrives at axon terminal at neuromuscular junction

2.) ACh released; binds to receptors on sarcolemma

3.) Ion permeability of sarcolemma changes

4.) Local change in membrane voltage (depolarization) occurs

5.) Local depolarization (end plate potential) ignites AP in sarcolemma

Phase 2: Excitation-contraction coupling occurs

6.) AP travels across the ENTIRE sarcolemma

7.) AP travels along T tubules

8.) SR releases Ca+ and it beinds to troponin; myosin-binding sites (active sites) on actin exposed

9.) Myosin heads bind to actin; contraction begins

Neuromuscular Junction

- Also called "end plate"

- Where axon (of motor neuron) meets a SINGLE muscle fiber

- Each muscle fiber only has ONE neuromuscular junction, located approximately in the middle

- Close- about 50-80nm apart

- Separated by small space called the SYNAPTIC CLEFT that is filled with gel like extracellular rich in glycoprotiens + collagen fibers.

- In the axon terminal

- SYNAPTIC VESICLES are sacs in the axon terminal that contain ACETYLCHOLINE (ACh)

- Highly folded. These folds are called JUNCTIONAL FOLDS and provide a larger SURFACE AREA for the millons of ACh RECEPTORS

- Includeds the axon terminals, synaptic cleft + junctional fords

- After ACh binds to ACh receptors its effects are terminated by ACETYLCHOLINESTERASE, an enzyme located in the synaptic cleft that BREAKS DOWN ACh to its building blocks (acetic acid + choline). This provides continual muscle fiber contraction in the absence of additional nervous system stimulation.

SYNAPTIC VESICLES

Sacs in the axon terminal that contain ACETYLCHOLINE (ACh)

JUNCTIONAL FOLDS

- Located in the neuromuscular junction.

- Provide a larger SURFACE AREA for the millons of ACh RECEPTORS

ACETYLCHOLINESTERASE

An enzyme located in the synaptic cleft that BREAKS DOWN ACh to its building blocks (acetic acid + choline). This provides continual muscle fiber contraction in the absence of additional nervous system stimulation.

Synaptic Cleft

- A space (or cleft) located between the axon terminal and the muscle at the neuromuscular junction (or end plate)

- Made up of a gel like extracellular substance rich in glycoproteins + collagen fibers

End plate

The Neuromuscular Junction

What is acetylcholine made of?

Acetic acid + choline

Myasthenia Gravis

- Disease characterized by drooping upper eyelids, difficulty swallowing + talking + generalized muscle weakness

- Caused by a SHORTAGE of ACh receptors

- Serum analysis reveals antibodies to ACh receptors, suggesting that this is an autoimmune disease

Resting Sarcolemma

Is POLARIZED, meaning that there is a potential difference in voltage across the membrane + the INSIDE is negative relative ot the outer membrane surface.

6 Events at the Neuromuscular Junction

1.) Action potential arrives at the axon terminal of motor neuron

2.) Voltage-gated Ca+ channels open + Ca+ enters the axon terminal moving DOWN its electrochemical gradient

3.) Ca+ entry causes ACh to be released by exocytosis

4.) ACh diffuses across the synaptic celft + binds to its receptors on the sarcolemma

5.) ACh binding opens ion channels in the receptors that allow simultaneous passage of Na+ into the muscle fiber and K+ ions exit, which produces a local change in the membrane potential called the END PLATE POTENTIAL

6.) ACh effects are TERMINATED by its breakdown by acetylcholinesterase + diffusion AWAY from the junction.

Depolarization

- Muscle contracion

- Due to Na+ entry

- Sarcolemma becomes LESS NEGATIVE

- Also called an END PLATE POTENTIAL

Repolarization

- Muscle relaxation

- Due to K+ exit

- Also called the REFRACTORY PERIOD

3 Steps in Generating an Action Potential Across the Sarcolemma

1.) GENERATION OF AN END PLATE POTENTIAL: ACh binding to the ACh receptors opens CHEMICALLY (ligand) GATED ION CHANNELS. Na+ and K+ will pass. The driving force for Na+ is greater than K+ so MORE Na+ diffuses out. This change in membrane potential occurs as the interior of the sarcolemma becomes less negative (DEPOLARIZATION). This depolarization is called an END PLATE POTENTIAL.

2.) DEPOLARIZATION: GENERATION + PROPAGATION OF AN ACTION POTENTIAL: The end plate potential ignites an action potential by spreading to ajacent membrane areas + opening voltage gated sodium changes. Na+ enters (following its electrochemical gradient) + once THREASHOLD is reached an action potential is GENERATED. The action potential PROPAGATES in ALL directions FROM THE NEUROMUSCULAR junction. As it propagates, the local depolarization wave of the action potential spreads to other areas repeating step one followed by this step.

3.) REPOLARIZATION: RESTORING THE SARCOLEMMA TO ITS INITIAL POLARIZED STATE

Refractory Period

- Happens during REPOLARIZATION

- Happens because the cell cannot be stimulated again until repolarization is complete.

- Restores the ELECTRIAL CONDITIONS of the resting (polarized) state. The Na+ and K+ pump restores the ICONIC CONDITIONS of the resting state, but hundreds of action potentials can occur before ionic imbalences interfere with contractile activity

Excitation-Contraction Coupling: 4 Steps

- Sequence of events by which TRANSMISSON OF AN ACTION POTENTIAL along the sarcolemma causes the MYOFILAMENTS TO SLIDE

- This action potential is brief and ends before any signs of contraction are obvious

- This action potential does NOT act directly on the myofilaments. It instead causes the RISE in intracellular levels of clcium ions, which allows the filaments to slide.

1.) Action potential propogates along the sarcolemma + down the T tubules

2.) Calcium ions are released

3.) Calcium binds to troponin + removes tropomyosin to reveal the binding sites on action

4.) Contraction begins when the myosin heads bind to actin (forming cross bridges + creating the "power stroke" that causes muscles to contract)

What triggers the release of ACh into the synaptic cleft?

Calcium (Ca+)

What opens the chemically gated Na+ and K+ channels?

When ACh binds to ACh receptors

What causes the "end plate potential"?

Greater influx of Na+

What happens when intracellular calcium levels are low?

The muscle is relaxed

To activate a group of SEVEN actins, troponin must bind to _______ calcium ions?

Two

By how much do contracting muscles shorten compared to their resting length?

30-35%

How many of the myosin heads are pulling and attached to actin at the same time during muscle contraction?

Half, the rest are RANDOMLY seeking their next binding site

Rigor Mortis

- Illustrates that cross bridge DETACHMENT is ATP driven

- Happens 3-4 hours after death

- Peak regidity occurs 12 hours after death

- Relaxes 48-60 hours after death

- Happens because dying cells are UNABLE to EXCLUDE calcium + the calcium influx into muscle cells PROMOTES THE FORMATION OF CROSS BRIDGES.

- After death, ATP synthesis ceases but ATP begins to be consumed + therefore, cross bridge DETACHMENT is impossible as cross bridge detachment is ATP driven. No ATP = No Detachment

- As muscle tissue begins to degrade, rigor mortis ceases

Muscle Tension

The force exerted by a contracting muscle ON AN OBJECT

Load

The opposing force EXTERTED ON the mucle by the WEIGHT of an object to be moved

Isometric

Happens when a muscle contracts and develops a MUSCLE TENSION but is UNABLE to move the LOAD

Ex. Trying to move a 2000lb car

- INCREASING MUSCLE TENSION is measured for isometirc contractions

Isotonic

Happens when a muscle contracts and develops a MUSCLE TENSION but is ABLE to move the LOAD

Ex. Moving a 5lb bag of sugar

- AMOUNT OF MUSCLE SHORTENING is measure for isotonic contractions

When is the "increase of muscle tension" measured?

During ISOMETRIC contractions (or when a muscle develops muscle tension + cannot move a load)

When is the "amount of muscle shortening" measured?

During ISOTONIC contractions (or when a muscle develops muscle tension + successfully moves the load)

Motor Unit

Consists of ONE motor neuron + ALL the muscle fibers it innervates (supplies)

- When a motor neuron fires, ALL the muscle fibers it innervates contract

- The # of muscle fibers may be as high as SEVERAL HUNDRED or as log was FOUR.

- Muscles with fine control (fingers + eyes) have SMALL motor units

- Muscles that are large + weight bearing (hip muscles) have LARGE motor units

Muscle Twitch + three phases

- The SIMPLEST contraction

- A SINGLE action potential of its motor neuron

- Used in a laboratory setting in order to measure muscle contraction using a MYOGRAM (a record of contractile activity). The line reading the activity is called a TRACING.

- Not the way our muscles normally operate

Three phases:

1.) LATENT PERIOD: first few milliseconds after stimulation when excitation-contraction coupling is occurring. Muscle tension is not yet measurable.

2.) PERIOD OF CONTRACTION: Cross bridges are active. If the tenseon becomes great enough to overcome the resistance of the load, the muscle shortens.

3.) PERIOD OF RELAXATION: Initiated by reentry of Ca+ into SR. Contractile force is declining. Muscle tension decreases to zero + tracing returns to baseline.

Graded Muscle Responses + 2 ways it can be graded

- Variations needed for proper control of skeletal movement

2 ways:

1.) Changing the FREQUENCY of stimulation

2.) Changing the STRENGTH of stimulation

Muscle Response to Changes in FREQUENCY of Stimulation

- Way of GRADING MUSCLE RESPONSES

- The SECOND twitch will be stronger than the first

- WAVE (or TEMPORAL SUMMATION): Muscle contractions are ADDED to other contractions. For instance, the SECOND twitch will be STRONGER than the first. This happens because before the SECOND contraction begins, the muscle is already PARTIALLY contracted + more calcium added to the cytosol to replace that being reclaimed by the SR, this will cause MORE shortening than the first.

- UNFUSED (INCOMPLETE TETANUS): Happens if the stimulus strength is held constant + the muscle is stimulated at an increasingly faster rate. The relaxation time between twitches becomes shorter + shorter The concentration of Ca+ rises higher + higher. The degree of wave summation becomes greater + greater. This produces a sustained but quivering contraction.

- FUSED (COMPLETE TETANUS): Maximal tension. Smooth, sustained contraction plateau in which all evidence of muscle relaxation disappears. Very unlikely to happen under normal circumstances. Happens when someone shows superhuman strength lifting a fallen tree limb off a person.

WAVE (or TEMPORAL SUMMATION)

Muscle contractions are ADDED to other contractions. For instance, the SECOND twitch will be STRONGER than the first. This happens because before the SECOND contraction begins, the muscle is already PARTIALLY contracted + more calcium added to the cytosol to replace that being reclaimed by the SR, this will cause MORE shortening than the first.

UNFUSED (INCOMPLETE TETANUS)

Happens if the stimulus strength is held constant + the muscle is stimulated at an increasingly faster rate. The relaxation time between twitches becomes shorter + shorter The concentration of Ca+ rises higher + higher. The degree of wave summation becomes greater + greater. This produces a sustained but quivering contraction.

FUSED (COMPLETE TETANUS)

Maximal tension. Smooth, sustained contraction plateau in which all evidence of muscle relaxation disappears. Very unlikely to happen under normal circumstances. Happens when someone shows superhuman strength lifting a fallen tree limb off a person.

Muscle Response to Changes in STRENGTH of Stimulation

- Way of GRADING MUSCLE RESPONSES

- RECRUITMENT (MULTIPLE MOTOR UNIT SUMMATION: Controls the FORCE of contraction more precisely than WAVE (TEMPORAL SUMMATION). This is achieved in the laboratory by delivering shocks of increasing voltage to the muscle, calling more + more muscle fibers into play.

- SUBTHRESHOLD STIMULI: Produce NO observable contractions.

- THRESHOLD STIMULUS: Stimulus at which the FIRST observable contraction occurs.

- MAXIMAL STIMULUS: Strongest stimulus that INCREASES contractile force. It represent the point at which ALL the muscle's motor units are recruited. Increasing the stimulus intensity beyond the maximal stimulus does NOT produce a stronger contraction.

- Guided by the SIZE PRINCIPAL

RECRUITMENT (MULTIPLE MOTOR UNIT SUMMATION

Controls the FORCE of contraction more precisely than WAVE (TEMPORAL SUMMATION). This is achieved in the laboratory by delivering shocks of increasing voltage to the muscle, calling more + more muscle fibers into play.

SUBTHRESHOLD STIMULI

Produce NO observable contractions.

THRESHOLD STIMULUS

Stimulus at which the FIRST observable contraction occurs.

MAXIMAL STIMULUS

Strongest stimulus that INCREASES contractile force. It represent the point at which ALL the muscle's motor units are recruited. Increasing the stimulus intensity beyond the maximal stimulus does NOT produce a stronger contraction.

Size Principal

- Motor units with the SMALLEST muscle fibers are activated FIRST because they are controlled by the smallest, most highly excitable motor neurons.

- As motor units with LARGER + LARGER muscle fibers begin to be excited, contractile strength INCREASES.

- The largest motor units have as much as 50 TIMES the contractile force of the smaller ones. They are controlled by the largest, least excitable (highest-threshold) neurons + are activated only when the most powerful contraction is necessary.

- Allows the increases in force during weak contractions (ex. maintaining posture) to happen in SMALL STEPS.

- Explains how the same hand that lightly pats your cheek can deliver a stinging slap at the volleyball

- Although its possible that all the motor units of a muscle may be recruited simultaneously to produce an exceptionally strong contraction, motor units are MORE COMMONLY activated ASYNCHRONOUSLY. This helps PROLONG a strong contraction by preventing or delaying fatigue.

Isotonic Contractions + 2 ways

Muscle length changes + MOVES A LOAD. Tension remains relatively CONSTANT through the rest of the contractile period.

Occurs one of two ways, either:

1.) Concentric Contraction: Muscle shortens + does work

2.) Eccentric Contraction

- Bicep curls are an example of how concentric + eccentric contractions work together

Concentric Contractions

- Type of Isotonic Contraction

- The muscle shortens + does work, such as picking up a book or kicking a ball

Eccentric Contraction

- Type of Isotonic Contraction

- Muscle GENERATES FORCE as it LENGTHENS.

- 50% MORE forceful than concentric contractions at the same load

- More often cause delayed-onset muscle soreness

- Ex. Occurs in the calf muscle as you walk up a steep hill.

- May cause soreness due to microtears in the mucles due to the stretching.

Isometric Contractions

- Tension builds to the muscle's peak tension-producing capacity but the muscle does NOT shorten or lengthen.

- Occurs when a muscle attempts to move a load that is GREATER than the force (tension) the muscle is able to develop.

- Ex. Trying to lift a piano on one's own.

- Ex. Knee bend- When you squat for a few seconds, the quadricepts muscles of your anterior thigh contract ISOMETRICALLY to HOLD your knee in a flexed position. While you rise, they CONTINUE to contract isometrically until their tension exceeds the load, at that point concentric contraction begins:

1.) Flex knee (eccentric)

2.) Hold squat (isometirc)

3.) Extend knee (isometirc THEN concentric)

Muscle Tone

- Skeletal muscles are voluntary but even when relaxed, the muscles are almost always slightly CONTRACTED.

- Due to spinal reflexes that first activate one group and then another in response to activated stretch receptors

- Does NOT produce active movements but keeps the muscles firm, healthy, and ready to respond to stimulation

- Helps stabilize joints + maintain posture.

How much ATP do muscles store?

- About 4 to 6 seconds worth.

- Why muscles must generate their own energy using the three pathways: 1.) Direct Phosphorylation 2.) Anerobic Pathway 3.) Aerobic Pathway

3 Pathways for Generating ATP During Muscle Activity

After ATP is HYDROLYZED to ADP + inorganic phosphate in muscle fibers, it is REGENERATED within a fraction of a second by one OR MORE of these three pathways:

1.) Direct Phosphorylation

2.) Anerobic Pathway

3.) Aerobic Pathway

Creatine Phosphate (CP)

- A unique high-energy molecule store in muscles that is tapped to REGNERATE ATP while the metabolic pathwyays adjust to the suddenly high demand for ATP.

- Muscle cells store two to three times more CP than ATP.

- Used during the DIRECT PHOSPHORYLATION pathway

- Provides maximum muscle power for about 15 seconds, ex, for a 100 meter dash.

- This reaction is readibly reversible

Cretine Phosphate + ADP = Creatine + ATP ( this reaction is CATALIZED by the enxyme CRETINE KINASE)

Direct Phosphorylation

- Provides maximum muscle power for about 15 seconds, ex, for a 100 meter dash or sprinting

- This reaction is readibly reversible

- NO oxygen use

- Produces 1 ATP for every 1 CP

Cretine Phosphate + ADP = Creatine + ATP ( this reaction is CATALIZED by the enxyme CRETINE KINASE)