Skeletal Muscle

steps for a muscle contraction

1. neuromuscular junction (NMJ) 2. excitation-contraction (E-C) 3. contraction relaxation cycle

steps for E-C coupling

1. somatic motor neuron releases Ach at NMJ 2. net entry of Na+ through Ach receptor channel initiates a muscle AP 3. AP in t-tubule alters conformation in DHP receptor 4. DHP receptors open RyR Ca2+ releases channels in SR and Ca2+ enters cytoplasm 5. Ca2+ binds to troponin allowing actin and myosin binding 6. myosin heads execute power stroke 7. actin filament slides toward the center of sarcomere

sarcomere length equation

1/2 (A+I-H)

ATP binds and myosin detaches

ATP binding decreases the actin binding affinity of myosin

major E-C coupling events

- Ach is released from the somatic motor neurons -Ach initiates and AP in the muscle fiber - the muscle AP triggers Ca2+ release from the SR - Ca2+ combines with troponin and initiates contraction

skeletal muscle structure

- largest cells in the body -fusion of individual muscle cells -multinucleated -sheathed in connective tissue -adjacent fibers bound together into fascicles

What is required for the transduction of the electrical signal into a Ca signal

-DHP: voltage sensing L-type Ca channel in t-tubule membrane -RyR: ca2+ release channel in the SR

structure of sarcomere

-Z disk -I band -A band -H zone -M line

latent period

-a short delay between muscle and action potential and the beginning of muscle tension development -time required for E-C to take place

twitch

-a single contraction-relaxation cycle in a skeletal muscle -latent period, contraction phase, relaxation phase

Duchenne muscular dystrophy

-absence of dystrophin that link actin to protein in the cell membrane -tiny tear in the membrane allow Ca2+ to enter the fiber -intracellular enzymes are activated causing breakdown of fiber

What happens to type IIA fibers during endurance training? Why?

-aerobic capacity of fiber can be enhanced until they are fatigue resistant as slow twitch fibers - endurance training increases the number of capillaries and mitochondria in the muscle tissue allowing oxygen carrying blood to increase aerobic capacity of muscle fibers

tendons

-attach skeletal muscle to bone -dense connective tissue made of collagen

skeletal muscle

-attach to the bones of -40% of total body weight -control body movement -striated -sarcomeres -multinucleated -has t-tubules and sarcoplasmic reticulum -fiber proteins: actin, myosin, troponin, tropomyosin -needs Ach to initiate contraction

motor units

-basic unit of contraction -one somatic motor neuron and its muscle fibers -number of motor units in a muscle fiber depends on gross motor or fine motor -must have same fiber type

Ca2+ and muscle contraction

-ca2+ initiates the powerstroke -Ca2+ binds to troponin to initiate muscle contraction -troponin controls the position of tropomyosin

possible causes of muscle fatigue

-central fatigue mechanism in CNS -peripheral fatigue mechanism in NMJ and contractile elements -E-C failure in the muscle fiber

H zone

-central region of A band -has only thick filaments

crossbridge

-connection formed when myosin head of thick filaments binds to actin molecules of the thin filament -g-actin molecule has single myosin binding site -myosin head has one actin and one ATP binding site

contraction

-creation of tension in the muscle -need ATP

contraction phase

-crossbridges interaction increases -increase in tension

A band

-darkest area of sacromere -entire length of thick filament (H zone) -outer edges thin and thick filament

fatigues within the muscle fiber

-depletion of muscle glycogen which cause lack of ATP and decrease Ca2+ release from SR -increased levels of inorganic phophate altering the power stroke and decrease Ca2+ from SR -ion imbalance alter membrane potential change Na+-K+ ATPase activity

M line

-divide A band in half -form attachment sites for thick filaments -has accessory proteins

elastic components

-elastic fibers in the tendons and connective tissues that attach muscle to bone -elastic cytoskeleton proteins between myofibrils

titin

-elastic molecule -stretch from Z disk to M line -stabilize position of contractile filaments -return stretched muscles to their resting state

terminal cisternae

-enlarged regions at the ends of the tubules concentrate and sequester Ca2+

neural causes of fatigue

-failure in the NS command neurons (physiological fatigue) -communication failure at NMJ -Ach is not synthesized in axonal terminal fast enough so cant reach threshold so no AP and no contraction

speed of fast-twitch fibers

-fast twitch fibers develop tension the fastest -due to myosin ATPase splitting ATP more rapidly

duration of fast twitch fibers

-fast twitch fibers during contraction -determined by how fast SR removes Ca2+ from cytosol -fast twitch fibers pump Ca2+ into their SR more rapidly -Ca2+ ATPase more effective in type II so removes Ca2+ faster

nebulin

-inelastic protein alongside thin filaments -attach to Z disk -help align actin filaments

What influences muscle fatigue

-intensity and duration of contraction activity -use of aerobic or anaerobic metabolism -composition of muscle -fitness of the individual

What do the bones and joints function as?

-lever and fulcrum -muscles exert force to move or resist a load

transverse (t-tubules)

-linked to terminal cisternae of SR -triad: 1 t-tubule and 2 surrounding terminal cisternae -rapidly move AP from cell surface to interior of the fiber

two states of crossbridges

-low force (relaxed muscles ) -high force (contracting muscles)

sarcoplasmic reticulum (SR)

-modified form of endoplasmic reticulum that wrap around the myofibril -contain longitudinal tubules and terminal cisternae -only ER that releases and stores Ca2+

antagonistic muscle group

-muscle contraction can pull on a bone, but not push the bone away (pull the bone in opposite directions) -flexor-extensors pairs move bones in opposite directions

botulinum toxin

-muscle disorder -decrease the release of Ach

complete (fused) tetanus

-muscle fiver that does not have time to relax between stimuli -reaches maximum tension

elastic components in isometric contraction

-muscle has not shortened -sarcomeres shorten generating force -elastic elements stretch allowing muscle length to remain the same

McArdle's disease

-myophosphorylase deficiency -lack of enzyme that converts glycogen to glucose 6 phosphate -muscles lack usable glycogen energy supply

ATP hydrolysis provides energy fro the myosin head to rotate and reattach to actin

-myosin head forms a 90 angle along the long axis of the thick filament -both ADP and P remain bound to myosin -myosin binds to a new actin -resting muscle fibers in this state

rigor state

-myosin heads are tightly bound to g-actin -no ATP or ADP is bound to myosin -muscle freezing due to immovable crossbridges

What happens to ATP after E-C coupling?

-need to restore Na+ and K+ levels -Na+ and K+ pump uses ATPase

What happens if there is too much overlap of crossbridges?

-no tension produced -there is room for powerstroke because thin filaments cross M line the myosin head becomes nonfunctional

How can a dysfunction in skeletal muscle arise?

-problem from nervous system -miscommunication at NMJ -defect in the muscle

What happens to ATP during relaxation?

-pump Ca2+ into SR through Ca2+ pump -ATPase

I band

-region that contains only thin filaments -Z disk runs through every I band

power stroke

-released P allows myosin head to swivel -the head swing sliding the thin filament toward the M line -ATP provides energy for the power stroke

type II B fibers and their ability to resist fatigue

-rely on anaerobic glycolysis to produce ATP - fatigue more easily -accumulation of H+ from ATP contributes to acidosis

type IIA and type I fibers and their ability to resist fatigue

-rely on oxidative phosphorylation for ATP production -harder to fatigue -have more mitochondria -more blood vessels to bring oxygen to cells -more myoglobin

contractile cycle

-rigor state -ATP binds and myosin detaches -ATP hydrolysis provides energy for the myosin head to rotate and reattached to actin -powerstroke -myosin releases ADP

Z disk

-sarcomere is made of 2 Z disks -zig zag protein structure -attachment site for thin filaments

elastic components in isotonic contraction

-sarcomere shorten -elastic elements are already stretched the entire muscle must shorten

sliding filaments

-sarcomere shortens during contractions -length of A band remains constant -Z disk moves closer/further

subtypes of skeletal muscle

-slow twitch oxidative fibers (type I) -fast twitch oxidative glycolytic fibers (type IIA) -fast twitch glycolytic fibers (type IIB)

How do muscle twitches vary by fibers?

-speed -maximum tension -duration

How are skeletal muscle subtypes classified?

-speed of contraction -resistance to fatigue with repeated stimulation

muscle cramp

-sustained painful contraction of skeletal muscle -caused by hyperexcitability of somatic neurons

myofibrils

-the main intracellular structure -highly organized bundles of contractile and elastic proteins that carry out work of contraction -made of thin and thick filaments

load-velocity relationship

-the speed of muscle contraction depends on the type of muscle fiber and on the load being moved -contraction and velocity is faster when load is zero -contraction and velocity is slower when load is equal to the ability of the muscle to create force (isometric contraction)

What does contraction force depend on?

-the types and numbers of motor units -changing the types of motor units that are active -changing the number of motor units that are responding

myosin

-thick filament -motor protein that can create movement -has a long tail (still), hinge region (elastic), two heads

actin

-thin filament -has one globular protein (g-actin) -multiple g-actins polymerize to form long chains (f-actin) -two f-actin polymers twist together to create the thin filament

How many thick and thin filaments surround each other?

-thin filaments surrounded by 3 thick filaments -6 thin filaments surround a thick filament

phosphocreatine

-used as a backup energy source -create creatine kinase (CK) and creatine phosphokinase (CPK) by transferring phosphate group between phosphocreatine and ADP

conclusions of skinned muscle experiment

-when Ca2+ os removed the myofibrils relax even with ATP -crossbridges only produce tension when ATP and Ca2+ are present in the cytosol

steps for synaptic transmission at the NMJ

1. APs arrive at the axon terminal and open voltage gated Ca2+ channels in the pre-synaptic membrane 2. Ca2+ diffuses into the cell down its electrochemical gradient triggering the release of Ach-containing synaptic vesicles (exocytosis) 3. Ach diffuses across the synaptic cleft and binds to the nicotinic receptors on the muscle membrane 4. Ach bound to nicotinic receptors allow K+ and Na+ to flow through 5. net Na+ depolarizes the muscle fiber triggering an AP to cause a muscle contraction

contractile cycle steps

1. ATP binds to myosin in rigor state causing myosin to release from actin 2. myosin hydrolyzes ATP and the myosin head rotates and binds to actin 3. power stroke 4. myosin releases ADP

steps for Ca2+

1. Ca2+ levels increase in cytosol 2. Ca2+ binds to troponin 3. troponin-Ca2+ complex pulls tropomyosin away from actin's myosin-binding site 4. myosin binds to actin to complete powerstroke 5. actin filament moves

equation to calculate force

F1xD1=F2xD2

How is a muscle fiber modeled?

a contractile element arranged in parallel with one elastic component and in series with another elastic component

length-tension relationship

a single twitch tension is determined by the length of the sarcomere

how does recruitment work?

a weak stimulus activates only the neurons with the lowest thresholds controlling the fatigue resistant slow twitch fibers as the stimulus increases additional neurons with higher threshold composed of fatigue resistant type IIA fibers and so on

load

a weight/force that opposed a contraction of a muscle

recruitment

addition of motor units to increase the force of contraction

Which are the most common ways to produce energy for muscles?

anaerobic glycolysis and beta oxidation

flexion

centers of the connected bones are brought closer together when the muscle (flexor) contracts

flexion

centers of the connected bones are brought closer together when the muscle contracts

What is skeletal muscles made of ?

collection of muscle vesicles which contain a collection of muscle cells (fibers)

myofibril proteins

contractile, regulatory, accessory

isometric contraction

contractions crease force without moving a load

isotonic contraction

contractions create force to move a load

structure of muscle subtypes

diameter: type IIB> type IIA> type I myoglobin content: type I> type IIA> type IIB capillary density: type I> type IIA> type IIB

asynchronous recruitment

different motor units take turns maintaining muscle tensions to avoid fatigue

relaxation phase

elastic components return the sarcomeres to resting length

internal vs external tension

external tension develops more slowly than internal tension

What are fast twitch fibers used for?

fine, quick movements

types of movement

flexion and extension

muscle tension

force created by contracting a muscle

phosphocreatine ar rest

high energy phosphate bonds of phosphocreatine are created from creatine and ATP by creating kinase

Why does dehydration cause muscle cramps

hyperkalemia there is more K+ outside of the cell making Ek less negative and AP more likely to fire because it closer to threshold

How can tension be increase?

increasing the frequency of muscle AP

summation

interval of time between AP shorten and muscle fiber does not have enough time to relax causing more forceful contraction

types of muscle contraction

isotonic and isometric

muscle fiber structure

long cylindrical cell with several nuclei on the surface

What are slow twitch fibers used for?

maintaining posture, standing, walking

advantages of the lever and fulcrum system

maximizes speed and mobility

insertion

more distal/mobile attachment

incomplete tetanus

muscle fibers partially relax between contraction

disadvantages of the lever and fulcrum system

muscles required to make a large amount of force to move or resist a small load

ultrastructure of muscle fiber

myofibrils, SR (sarcoplasmic reticulum), sarcolemma, mitochondria, t-tubules

How do muscles get ATP during contraction?

myosin ATPase

contractile proteins

myosin and actin

Does skeletal muscle have an unlimited amount of ATP?

no a muscle fiber can only generate enough ATP for 8 twitches

Is tension produced is Ca2+ is absent and ATP is added?

no, tension decreases because without Ca2+ tropomyosin blocks the actin binding site for myosin

sliding filament theory of contraction

overlapping actin and myosin filaments of a fixed length slide past one another in an energy-requiring process

myoglobin

oxygen binding pigment with high affinity for oxygen

longitudinal tubules

release Ca2+

muscle fatigue

reversible condition when a muscle is no longer able to generate or sustain power output

ultrastructure of myofibril

sarcomere, myosin, actin, titin, nebulin, troponin, tropomyosin, g-actin molecule

types of muscles

skeletal, smooth, cardiac

tetanus

stimulation of muscle fibers at short intervals and relaxation of contraction decreases until muscle reaches maximal contraction

Is tension produced if Ca2+ is present, but ATP is removed?

tension remains the same because the myosin is in the rigor state

extension

the bone moves away when the muscle contracts

extension

the bones moves away when the muscle (extensor) contracts

origin

the end of the muscle that is attached closest to the trunk or stationary bone

phosphocreatine active

the high energy phosphate group of phosphocreatine is transferred to ADP to create more ATP by creatine kinase

relaxation

the release of tension created by a contraction

sliding filament theory

the tension a muscle fiber can generate is directly proportional to the number of crossbridges formed between thick and thin filaments

What happens to Ca2+ when a muscle fiber is stimulated?

there is an increase of Ca2+ going in

What happens if there is no overlap of crossbridges?

there is no tension produced

accessory proteins

titin and nebulin

regulatory proteins

tropomyosin and troponin