muscle physiology

muscle physiology

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functions of muscle tissue

-produce body movements
-stabilize body positions
-regulate organ volumes (bands of smooth muscle called sphincters)
-movement of substances w/in the body (blood, lymph, urine, air, food and fluids, sperm)
-produce heat (involuntary contractions of skeletal/voluntary muscle)

excitability

property of muscle tissue

ability to respond to stimuli and produce electrical signals

contractability

property of muscle tissue

ability to shorten and generate force once excited

extensibility

property of muscle tissue

ability to stretch w/out damaging the tissue

elasticity

property of muscle tissue

ability to return to normal length after being extended

thermal

property of muscle tissue

ability to produce heat energy

Skeletal muscle tissue

attaches to bone, skin or fascia (connective tissue)

striated w/ light and dark bands

voluntary control of contraction & relaxation

multi-nucleated

epimysium

connective tissue layer that surrounds the whole muscle

perimysium

connective tissue that surrounds the fascicles/bundles of 10-100 muscle cells/fibers

endomysium

connective tissue that separates individual muscle cells/fibers

sarcoplasma

name for the cytoplasm in a muscle

contains lots of glycogen for energy production and myoglobin for oxygen storage

sarcolemma

cell membrane in a muscle

sarcoplasmic reticulum (SR)

storage network of calcium

system of tubular sacs

stores Ca2+ in relaxed muscle, release of Ca2+ triggers muscle contraction

transverse (t) tubule

brings electrical signal into the muscle cell

tiny invaginations of the sarcolemma

filled with ECF and quickly spread the muscle action potential to all pts of the fiber

myofibrils have 3 kinds of protein

1. contractile proteins
2. regulatory proteins (turn contraction on and off)
3. structural proteins

contractile proteins

myosin and actin

regulatory proteins

troponin and tropomyosin

structural proteins

titin, myomesin, nebulin, dystrophin

provide proper alignment, elasticity and extensibility; link myofibrils to sarcolemma and extracellular matrix

sarcomere

functional unit of muscle contraction

one Z disc/line to the next

thick filaments

myosin

each molecule resembles 2 golf clubs twisted 2gether

myosin heads (cross bridges) extend toward the thin filaments

held in place by the M line proteins

thin filaments

made up of actin, troponin & tropomyosin

at rest, want myosin binding sights on actin covered by tropomyosin

troponin

tells tropomyosin when to cover/expose binding sites on actin

Z disc

thin filaments are held in place by this disc

H zone

only myosin

almost disappears during contraction

A band

"all" actin & myosin

doesn't change length during contraction

I band

actin only

almost disappears during muscle contraction

contraction

when myosin pulls actin inward

motor unit

one motor neuron (nerve) & all the skeletal muscle cells/fibers it innervates (10-2,000 cells)

why so many?
precise movements; call on bigger motor units (i.e. to punch) or call on more; allow us to grade our contraction, meed the needs of our skill

one; multiple

each muscle cell is supplied by ____ motor neuron terminal branch

each motor neuron supplies _______ muscle cells

motor unit recruitment

increasing the # of active motor units

motor units in a whole muscle fire asynchronously

-some fibers are active others are relaxed
-delays fatigue
-produces smooth muscular contraction rather than a series of jerky movements

precise mvmts require smaller contractions/smaller motor units (less fibers/nerve)

the all-or-none response

for a motor unit to be recruited into activity the motor nerve impulse must meet or exceed the threshold

if the threshold is not met no fibers in that unit act

muscle tone

involuntary contraction of a small # of motor units (alternately active and inactive in a constantly shifting pater)

keeps muscles firm even though relaxed (always keep some level of overlap)

doesn't produce movement

essential for maintaining head posture; important in maintaining BP*
-tone of smooth muscles in walls of blood vessels

how muscle contraction begins

1. nerve impulse arrives at axon terminal & synaptic vesicles release ACh
2. ACh binds to receptors on the muscle motor end plate; this opens Na+ channels and Na+ rushes into the cell
3. Inside of the muscle cell becomes more positive, triggers muscle action potential that spreads over sarcolemma and down into the t tubules
4. the release of Ca2+ from the SR is triggered and the muscle cell will shorten & generate force
5. Ca2+ binds to troponin & causes troponin-tropomyosin complex to move & reveal myosin binding sites on actin
6. the contraction cycle begins

steps in the contraction cycle

1. myosin heads hydrolyze ATP and become reoriented and energized (ready to bind)
2. myosin heads bind to actin, forming crossbridges
3.myosin crossbridges rotate toward center of the sarcomere (power stroke)
4. As myosin heads bind ATP, the crossbridges detach from actin (need ATP to break the crossbridge)

the contraction cycle keeps repeating as long as there is...

calcium, ATP, and the signal/theAP/stimulus

leaky SRs

theory that muscle fatigue may be the result of calcium leaking out of the SR (then calcium isnt there for contraction)

Relaxation

Acetylcholinesterase (AChE) breaks down ACh within the synaptic cleft [neurotransmitter can't go across]

Muscle AP ceases

Ca2+ release channels are closed

Active transport pumps Ca2+ back into SR

Troponin holds tropomyosin in position to block myosin-binding sites on actin

Contraction

Ca2+ release channels are open

Ca2+ binds to tropinin, which changes the shape of the troponin-tropomyosin complex & uncovers the myosin-binding sites on actin

sarcomeres, muscle fiber and muscle shorten
*thick and thin filaments do not change in length

*can't generate anymore force or tension in full contraction

acetylcholinesterase (AChE)

enzyme that breaks down ACh within the synaptic cleft in order to relax muscle

rigor mortis

state of muscular rigidity that begins 3-4 hrs after death and lasts ab 1day

After death, Ca2+ ions leak out of the SR and allow myosin heads to bind to actin

since ATP synthesis has ceased, crossbridges cannot detach from actin until enzymes start to digest decomposing cells

types of skeletal muscle fibers

1) Type I, slow oxidative, slow-twitch
2)Type IIa, fast oxidative-glycolytic, (FOG)
3)Type IIb, fast glycolytic fibers, fast-twitch

Type I

aka slow oxidative, slow-twitch

red in color (lots of mitochondria, myoglobin & blood vessels)

prolonged, sustained contractions for maintaining posture

great ability to make energy

fatigue resistant, bc have lots of mitochondria, blood & oxygen (aerobic fuels)

small fiber size, small motor unit, slow twitch speed, highest capillary density, low glycogen content, slow fatigability rate

Type IIa

aka fast oxidative-glycolytic (FOG)

pinkish in color (lots of mitochondria, myoglobin & bvs) -not as much as Type I

split ATP at very fast rate; used for walking & sprinting

Fast twitch speed, high capillary density, aerobic & anaerobic, intermediate glycogen content, fatigability rate, fiber size, and motor unit size

Type IIb

aka fast glycolytic, fast-twitch

white in color (few mitochondria & BV, low myoglobin)

anaerobic movements for short duration; used for weight lifting

respond quickly, fatigue quickly

large fiber size, large motor unit & NMJ size, fast twitch speed, low capillary density, anaerobic , high glycogen content

shoulder & arm muscles have a higher proportion of... ____ fibers

fast glycolytic (Type II)

neck, back and leg muscles have a higher portion of _____ fibers

postural, slow oxidative (Type I)

distribution & recruitment of dif types of fibers

# of muscle fibers doesn't change

growth is enlargement of existing cells (hypertrophy)

characteristics can be altered (takes a while)

atrophy

wasting away of muscles

caused by disuse (castin, space travel) or severing of the nerve supply

the transition to connective tissue can't be reversed

hypertrophy

inc in the diameter of muscle fibers

resulting from very forceful, repetitive muscular activity and an inc in myofibrils, SR & mitochondria

anabolic steroids

similar to testosterone

increases muscle size, strength & endurance

side effects:
liver cancer, kidney damage, <3 disease, mood swings, facial hair and voice deepening in females, atrophy of testicles & baldness in males

aging & muscle tissue

skeletal muscle starts to be replaced by fat beginning @ 30
-body goes into conservation mode
-slowing of reflexes & dec in maximal strength
-change in fiber type to slow oxidative fibers may be due to lack of use or may be result of aging

aging & muscle tissue

skeletal muscle starts to be replaced by fat beginning @ 30
-body goes into conservation mode
-slowing of reflexes & dec in maximal strength
-change in fiber type to slow oxidative fibers may be due to lack of use or may be result of aging

types of contractions

1)concentric
2)eccentric
3)isometric

concentric contractions

muscle shortens to produce force & movement, like biceps curl upward

eccentric contractions

muscle lengthens while maintaining force & movement

isometric contractions

tension generated, no muscle shortening, no movement

maintaining posture & supports objects in a fixed position

increased force

increased motor units activated

increased force

increased # of fast-twitch motor neurons activated

increased force

inc'd muscle fiber size

more interaction of cross bridge b/w actin & myosin

equals more force (cross bridge)

length tension curve

at rest we develop the most tension, at about 80-120% of the optimum length

joint angle

optimal joint angle maximizes the force transmitted to the bone (via # of crossbridges)
90 degrees optimal

speed of reaction in relation to force production

decrease force, increase velocity (the lighter the load, the quicker we can shorten the muscle)

increase load, decrease velocity (the heavier the load, the slower we can shorten the muscle)

parts of a twitch contraction

1. Latent Period (2msec)
--Ca2+ is released from SR
--slack is being removed from elastic components
2) Contraction Period (10-100 msec) filaments slide past each other
3) Relaxation Period (10-100 msec) active transport of Ca2+ back into SR
4) Refractory Period (5msec in skeleta, 300 in cardiac)
--muscle can't respond and has lost its excitability

wave summation

second stimulus applied before muscle has completely relaxed after theprevious stimulus; results in increased strength of contraction

incomplete/unfused tetanus

sustained muscle contraction that permits partial relaxation b/w stimuli (several APs)

complete/fused tetanus

sustained contraction w/ NO relaxation b/w stimuli (just applies to skeletal muscle)

muscle gets stuck/stays stimulated @ highest pt

3 sources of ATP production w/in muscle

1) Creatine Phosphate (CP)
2) Anaerobic Cellular Respiration/ Glycolysis
3) Aerobic Cellular Respiraton (reqs O2)

creatine phosphate

source of ATP production in muscle

excess ATP w/in resting muscle used to form creatine phosphate

CP 3-6x more plentiful than ATP w/in muscle

empties quickly (~15 sec); quick breakdown

1 P from ATP goes to creatine phosphate (waiting to b released quickly); creatine P drops P to produce ATP for contraction

during relaxation-build more creatine p stores

anaerobic cellular respiration

aka glycolysis

ATP produced from glucose brkdwn into pyruvic acid during glycolysis

If no O2 present, pyruvic acid converted to lactic acid, which diffuses into the blood

30-40 seconds of maximal activity (200 m run)

aerobic cellular respiration

source of ATP production in muscle

reqs O2
ATP for activities >30 sec
Provides 90% of ATP energy if activity lasts more than 10 minutes

fats, carbs, proteins brk down aerobically through cellular respiration in mitochondria

factors that contribute to muscle fatigue

-feeling of tiredness & desire to stop (protective mechanism)
-insufficient release of ACh from motor neurons
-depletion of Creatine Phosphate (short term fatigue)
-decline of Ca2+ w/in sarcoplasm/ Ca2+ leaking ou of SR
-insufficient oxygen or glycogen
-buildup of lactic acid and ADP

muscle cramps

cause not known
possible causes:
-feed forward loop b/w muscle and spinal cord
-pain or sensory impulses to the spinal cord generates feedback response= muscle contraction
--over-exercised muscle or lack of blood to muscle
--electrolyte imbalance (K, Na, Ca) if not enough K, can't repolarize
--poor biomechanics (i e you're off balance...)

cardiac muscle

-striated
-involuntary control
-autorhythmic bc of built in pacemaker
-similar arrangement of thick and thin filaments
-found only in the heart wall
-striated, short, quadrangular-shaped, branching fibers
-single centrally located nucleus
- cells connected by intercalated discs w/ gap junctions (electrical synapse)

lots of mitochondria (larger than skeletal, thus req more O2)
longer contractions than skeletal

cardiac muscle

-striated
-involuntary control
-autorhythmic bc of built in pacemaker
-similar arrangement of thick and thin filaments
-found only in the heart wall
-striated, short, quadrangular-shaped, branching fibers
-single centrally located nucleus
- cells connected by intercalated discs w/ gap junctions (electrical synapse)

smooth muscle

-attached to hair follicles in skin
-in walls of hollow organs (BVs and GI tract)
-nonstriated in appearance
-small, involuntary cells; tapering @ ends
-single, oval-shaped, centrally located nucleus

contraction of smooth muscle

-no sarcomeres
-sliding of thick & thin generates tension
-transferred to intermediate filaments & dense bodies attached to sarcolemma
-contracts: twists into a helix as it shortens, relaxes by untwisting
-intermediate filaments and dense bodies; generate tension to pull on dense bodies

multiunit smooth muscle

individual fibers with OWN motor neuron ending, fibers operate individually (no gap junctions; not as a unit)

found in large arteries, large airways, arrector pili, iris & ciliary muscles

visceral (single-unit) smooth muscle

in the walls of hollow viscera and small BV

autorhythmic; fibers contract in unison (gap junctions)

all fibers act 2gether in a single unit

physiology of smooth muscle

-contraction starts slowly and lasts longer
--no transverse tubules and very little SR
--Ca2+ must flow in from outside
-regulator protein:calmodulin= binds calcium ions in the cytosol

calmodulin

in smooth muscle; activates the enzyme myosin light chain kinase, which facilitates myosin-actin binding and allows contraction to work at a relatively slow rate

smooth muscle tone

•Prolonged presence of calcium in the cytosol leads to
smooth muscle tone, a state of continued partial
contraction
• Stress-Relaxation Response: smooth muscle fibers can
stretch considerably without developing tension
• Useful for maintaining blood pressure or a steady
pressure on the contents of GI tract


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