INTRODUCTION TO MUSCLE Movement is a fundamental

characteristic of all living things Cells capable of shortening and

converting the chemical energy of ATP into mechanical energy

Types of muscle skeletal, cardiac and smooth

Physiology of skeletal muscle basis of warm-up, strength, endurance and

fatigue11-1

THE FUNCTIONS OF MUSCLES

Movement of body parts and organ contents

Maintain posture and prevent movement

Communication - speech, expression and writing

Control of openings and passageways Heat production

11-2

CHARACTERISTICS OF MUSCLE Responsiveness (excitability)

to chemical signals, stretch and electrical changes across the plasma membrane

Conductivity local electrical change triggers a wave of

excitation that travels along the muscle fiber

Contractility -- shortens when stimulated

Extensibility -- capable of being stretched

Elasticity -- returns to its original resting length after being stretched

11-3

SKELETAL MUSCLE Each muscle is composed of muscle

tissue, blood vessels, nerve fibers, and connective tissue

The three connective tissue sheaths are: Endomysium – fine sheath of

connective tissue composed of reticular fibers surrounding each muscle fiber

Endomysium surrounds muscle fiber Perimysium – fibrous connective tissue

that surrounds groups of muscle fibers called fascicles

Perimysium surrounds fascicles of muscle fibers

Epimysium – an overcoat of dense regular connective tissue that surrounds the entire muscle

Epimysium surrounds entire muscle 11-4

Perimysium

Epimysium

Endomysium

Tendon

Deep fascia

MUSCLE ATTACHMENTS

Direct (fleshy) attachment to bone epimysium is continuous with periosteum intercostal muscles

Indirect attachment to bone epimysium continues as tendon or aponeurosis

that merges into periosteum as perforating fibers

biceps brachii or abdominal muscle Attachment to dermis Stress will tear the tendon before pulling the

tendon loose from either muscle or bone11-5

SKELETAL MUSCLE Voluntary striated muscle with multiple

nuclei Muscle fibers (myofibers) as long as 30

cm Exhibits alternating light and dark

transverse bands or striations reflects overlapping arrangement of

internal contractile proteins Under conscious control (voluntary)

11-6

MUSCLE FIBERS Multiple flattened nuclei inside cell membrane

fusion of multiple myoblasts during development unfused satellite cells nearby can multiply to produce a small

number of new myofibers Sarcolemma has tunnel-like infoldings or transverse (T) tubules

that penetrate the cell carry electric current to cell interior form triad with sacoplasmic

reticulum (SR)

11-7

MUSCLE FIBERS 2 Sarcoplasm is filled with

myofibrils (bundles of myofilaments) glycogen for stored energy and myoglobin for binding oxygen

Sarcoplasmic reticulum = smooth ER network around each myofibril dilated end-sacs (terminal cisternea) store calcium triad = T tubule and 2 terminal cisternae

11-8

THICK FILAMENTS

Made of 200 to 500 myosin molecules 2 entwined polypeptides (golf clubs)

Arranged in a bundle with heads directed outward in a spiral array around the bundled tails central area is a bare zone with no heads

11-9

THIN FILAMENTS Two intertwined strands fibrous (F) actin

globular (G) actin with an active site Groove holds tropomyosin molecules

each blocking 6 or 7 active sites of G actins

One small, calcium-binding troponin molecule on each tropomyosin molecule

11-10

ELASTIC FILAMENTS

Springy proteins called titin Anchor each thick filament to Z disc Prevents overstretching of sarcomere

11-11

STRIATIONS = ORGANIZATION OF FILAMENTS

Dark A bands (regions) alternating with lighter I bands (regions)

A band is thick filament region lighter, central H band area contains no thin filaments

I band is thin filament region bisected by Z disc protein called connectin, anchoring elastic and thin

filaments from one Z disc (Z line) to the next is a sarcomere

11-12

STRIATIONS AND SARCOMERES

11-13

OVERLAP OF THICK AND THIN FILAMENTS

11-14

CONTRACTILE AND REGULATORY PROTEINS

Myosin and actin are contractile proteins Tropomyosin and troponin = regulatory proteins

switch that starts and stops shortening of muscle cell contraction activated by release of calcium into

sarcoplasm and its binding to troponin, troponin moves tropomyosin off the actin active sites

11-15

RELAXED AND CONTRACTED SARCOMERES

Muscle cells shorten because their individual sarcomeres shorten pulling Z discs

closer together pulls on

sarcolemma Notice neither thick nor

thin filaments change length during shortening

Their overlap changes as sarcomeres shorten

11-16

Animation

NEUROMUSCULAR JUNCTIONS (SYNAPSE)

Functional connection between nerve fiber and muscle cell

Neurotransmitter (acetylcholine/ACh) released from nerve fiber stimulates muscle cell

Components of synapse (NMJ) synaptic knob is swollen

end of nerve fiber (contains ACh)

junctional folds region of sarcolemma with ACh receptors

synaptic cleft = tiny gap between nerve and muscle cells

basal lamina = thin layer of collagen and glycoprotein over all of muscle fiber 11-17

ELECTRICALLY EXCITABLE CELLS Plasma membrane is polarized or

charged resting membrane potential due to Na+

outside of cell and K+ and other anions inside of cell

difference in charge across the membrane = resting membrane potential (-90 mV)

Stimulation opens ion gates in membrane ion gates open (Na+ rushes into cell and K+

rushes out of cell) quick up-and-down voltage shift = action

potential spreads over cell surface (both in muscle

and nerve cells)

11-18

MUSCLE CONTRACTION AND RELAXATION

Four actions involved in this process excitation = nerve action potentials lead

to action potentials in muscle fiber excitation-contraction coupling = action

potentials on the sarcolemma activate myofilaments

contraction = shortening of muscle fiber relaxation = return to resting length

Images will be used to demonstrate the steps of each of these actions

11-19

EXCITATION (STEPS 1 AND 2)

Nerve signal opens voltage-gated calcium channels. Calcium stimulates exocytosis of synaptic vesicles containing ACh = ACh release into synaptic cleft.

11-20

EXCITATION (STEPS 3 AND 4)

11-21

Binding of ACh to receptor proteins opens Na+ and K+ channels resulting in jump in RMP from -90mV to +75mV forming an end-plate potential (EPP).

EXCITATION (STEP 5)

11-22

Voltage change in end-plate region (EPP) opens nearby voltage-gated channels producing an action potential

EXCITATION-CONTRACTION COUPLING (STEPS 6 AND 7)

Action potential spreading over sarcolemma enters T tubules -- voltage-gated channels open in T tubules causing calcium gates to open in SR

11-23

EXCITATION-CONTRACTION COUPLING (STEPS 8 AND 9)

Calcium released by SR binds to troponin Troponin-tropomyosin complex changes

shape and exposes active sites on actin 11-24

CONTRACTION (STEPS 10 AND 11)

Myosin ATPase in myosin head hydrolyzes an ATP molecule, activating the head and “cocking” it in an extended position

It binds to actin active site forming a cross-bridge 11-25

CONTRACTION (STEPS 12 AND 13)

Power stroke = myosin head releases ADP and phosphate as it flexes pulling the thin filament past the thick

With the binding of more ATP, the myosin head extends to attach to a new active sitehalf of the heads are bound

to a thin filament at one time preventing slippage

thin and thick filaments do not become shorter, just slide past each other (sliding filament theory)

11-26Animation

RELAXATION (STEPS 14 AND 15)

Nerve stimulation ceases and acetylcholinesterase removes ACh from receptors. Stimulation of the muscle cell ceases.

11-27

RELAXATION (STEP 16) Active transport needed

to pump calcium back into SR to bind to calsequestrin

ATP is needed for muscle relaxation as well as muscle contraction

11-28

RELAXATION (STEPS 17 AND 18) Loss of calcium from

sarcoplasm moves troponin-tropomyosin complex over active sites stops the production or

maintenance of tension Muscle fiber returns to

its resting length due to recoil of series-elastic components and contraction of antagonistic muscles

11-29

RIGOR MORTIS

Stiffening of the body beginning 3 to 4 hours after death

Deteriorating sarcoplasmic reticulum releases calcium

Calcium activates myosin-actin cross-bridging and muscle contracts, but can not relax.

Muscle relaxation requires ATP and ATP production is no longer produced after death

Fibers remain contracted until myofilaments decay

11-30

NEUROMUSCULAR TOXINS Pesticides (cholinesterase inhibitors)

bind to acetylcholinesterase and prevent it from degrading ACh

spastic paralysis and possible suffocation Flaccid paralysis (limp muscles) due to

curare that competes with ACh respiratory arrest

11-31

NERVE-MUSCLE RELATIONSHIPS

Skeletal muscle must be stimulated by a nerve or it will not contract

Axons of somatic motor neurons = somatic motor fibers terminal branches supply one muscle

fiber Each motor neuron and all the

muscle fibers it innervates = motor unit

11-32

MOTOR UNITS A motor neuron and the muscle fibers it

innervates dispersed throughout the muscle when contract together causes weak

contraction over wide area provides ability to sustain long-term

contraction as motor units take turns resting (postural control)

Fine control small motor units contain as few as

20 muscle fibers per nerve fiber eye muscles

Strength control gastrocnemius muscle has 1000

fibers per nerve fiber

11-33

LENGTH-TENSION RELATIONSHIP Amount of tension generated

depends on length of muscle before it was stimulated length-tension relationship

Overly contracted (weak contraction results) thick filaments too close to Z

discs and can’t slide Too stretched (weak contraction

results) little overlap of thin and thick

does not allow for very many cross bridges too form

Optimum resting length produces greatest force when muscle contracts central nervous system

maintains optimal length producing muscle tone or partial contraction

11-34

MUSCLE TWITCH IN FROG Threshold = voltage producing an action

potential a single brief stimulus at that voltage produces a quick cycle

of contraction and relaxation called a twitch (lasting less than 1/10 second)

A single twitch contraction is not strong enough to do any useful work

11-35

MUSCLE TWITCH IN FROG 2 Phases of a twitch contraction

latent period (2 msec delay) only internal tension is generated no visible contraction occurs – elastic components are

being stretched contraction phase

external tension develops as muscle shortens relaxation phase

loss of tension and return to resting length as calcium returns to SR

11-36

CONTRACTION STRENGTH OF TWITCHES

Threshold stimuli produces twitches Twitches unchanged despite increased

voltage “Muscle fiber obeys an all-or-none law”

contracting to its maximum or not at all not a true statement since twitches vary in

strength depending upon, Ca2+ concentration, previous stretch of

the muscle, temperature, pH and hydration Closer stimuli produce stronger twitches

11-37

RECRUITMENT AND STIMULUS INTENSITY

Stimulating the whole nerve with higher and higher voltage produces stronger contractions

More motor units are being recruited called multiple motor unit summation lift a glass of milk versus a whole gallon of milk 11-38

TWITCH AND TREPPE CONTRACTIONS

Muscle stimulation at variable frequencies low frequency (up to 10 stimuli/sec)

each stimulus produces an identical twitch response moderate frequency (between 10-20

stimuli/sec) each twitch has time to recover but develops more

tension than the one before (treppe phenomenon) calcium was not completely put back into SR heat of tissue increases myosin ATPase efficiency

11-39

INCOMPLETE AND COMPLETE TETANUS

Higher frequency stimulation (20-40 stimuli/second) generates gradually more strength of contraction each stimuli arrives before last one recovers

temporal summation or wave summation incomplete tetanus = sustained fluttering contractions

Maximum frequency stimulation (40-50 stimuli/second) muscle has no time to relax at all twitches fuse into smooth, prolonged contraction called

complete tetanus rarely occurs in the body

11-40

ISOMETRIC AND ISOTONIC CONTRACTIONS

Isometric muscle contraction develops tension without changing length important in postural muscle function and

antagonistic muscle joint stabilization Isotonic muscle contraction

tension while shortening = concentric tension while lengthening = eccentric 11-41

ATP SOURCES

All muscle contraction depends on ATP Pathways of ATP synthesis

anaerobic fermentation (ATP production limited)

without oxygen, produces toxic lactic acid aerobic respiration (more ATP produced)

requires continuous oxygen supply, produces H2O and CO2

11-42

IMMEDIATE ENERGY NEEDS Short, intense exercise (100 m

dash) oxygen need is supplied by

myoglobin Phosphagen system

myokinase transfers Pi groups from one ADP to another forming ATP

creatine kinase transfers Pi groups from creatine phosphate to make ATP

Result is power enough for 1 minute brisk walk or 6 seconds of sprinting

11-43

SHORT-TERM ENERGY NEEDS

Glycogen-lactic acid system takes over produces ATP for 30-40 seconds of maximum

activity playing basketball or running around baseball

diamonds muscles obtain glucose from blood and stored

glycogen

11-44

LONG-TERM ENERGY NEEDS

Aerobic respiration needed for prolonged exercise Produces 36 ATPs/glucose molecule

After 40 seconds of exercise, respiratory and cardiovascular systems must deliver enough oxygen for aerobic respiration oxygen consumption rate increases for first

3-4 minutes and then levels off to a steady state

Limits are set by depletion of glycogen and blood glucose, loss of fluid and electrolytes11-45

FATIGUE

Progressive weakness from use ATP synthesis declines as glycogen is

consumed sodium-potassium pumps fail to maintain

membrane potential and excitability lactic acid inhibits enzyme function accumulation of extracellular K+

hyperpolarizes the cell motor nerve fibers use up their acetylcholine

11-46

ENDURANCE Ability to maintain high-intensity

exercise for >5 minutes determined by maximum oxygen uptake

VO2 max is proportional to body size, peaks at age 20, is larger in trained athlete and males

nutrient availability carbohydrate loading used by some athletes

packs glycogen into muscle cells adds water at same time (2.7 g water with each

gram/glycogen) side effects include “heaviness” feeling

11-47

OXYGEN DEBT Heavy breathing after strenuous exercise

known as excess postexercise oxygen consumption (EPOC)

typically about 11 liters extra is consumed Purposes for extra oxygen

replace oxygen reserves (myoglobin, blood hemoglobin, in air in the lungs and dissolved in plasma)

replenishing the phosphagen system reconverting lactic acid to glucose in kidneys

and liver serving the elevated metabolic rate that occurs

as long as the body temperature remains elevated by exercise

11-48

SLOW- AND FAST-TWITCH FIBERS

Slow oxidative, slow-twitch fibers more mitochondria, myoglobin and capillaries adapted for aerobic respiration and resistant

to fatigue soleus and postural muscles of the back

(100msec/twitch)

11-49

SLOW AND FAST-TWITCH FIBERS Fast glycolytic, fast-twitch fibers

rich in enzymes for phosphagen and glycogen-lactic acid systems

sarcoplasmic reticulum releases calcium quickly so contractions are quicker (7.5 msec/twitch)

extraocular eye muscles, gastrocnemius and biceps brachii

Proportions genetically determined

11-50

MUSCULAR DYSTROPHY Hereditary diseases - skeletal muscles

degenerate and are replaced with adipose Disease of males

appears as child begins to walk rarely live past 20 years of age

Dystrophin links actin filaments to cell membrane leads to torn cell membranes and necrosis

Fascioscapulohumeral MD -- facial and shoulder muscle only

11-51

MYASTHENIA GRAVIS Autoimmune disease - antibodies attack NMJ

and bind ACh receptors in clusters receptors removed less and less sensitive to ACh

drooping eyelids and double vision, difficulty swallowing, weakness of the limbs, respiratory failure

Disease of women between 20 and 40 Treated with cholinesterase inhibitors, thymus

removal or immunosuppressive agents

11-52

MYASTHENIA GRAVIS

11-53

Drooping eyelids and weakness of muscles of eye movement