Upload
adela-riley
View
214
Download
0
Embed Size (px)
Citation preview
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
fatigue
11-1
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-bridge11-25
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