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Pierce College
Putman/Biol 241
Lecture Unit 07 Notes: Muscle Physiology
FUNCTIONS OF THE MUSCULAR SYSTEM
1.
2.
3.
4.
Movement of body
Maintenance of body position.
Heat generation.
Movement of materials.
a. Gut. Through gut, etc. via peristalsis.
b. Lymphatic circulation. The contraction of skeletal muscles moves lymph through lymph vessels.
c. Blood circulation. Myocardium of heart contracts, moves blood through cardiovascular system.
5. Regulation of material flow via sphincters.
6. Regulation of blood flow/pressure.
a. Vasoconstriction of tunica muscular (media) in walls of arteries & veins constrict decreases flood
flow, increases BP
b. Vasodilation increases blood flow, decreases BP.
7. Protects/supports soft tissues.
MUSCLE TISSUE TYPES & CHARACTERISTICS
1. Skeletal Muscle
a. Attached to skeleton either directly or indirectly
b. Voluntary; quick to act, quick to fatigue
c. Not autorhythmic; no internal contraction control; generally controlled more by nervous system
than hormones
d. Long (~30-40 cm!), cylindrical, unbranched cells.
e. Striated—sarcomeres regularly placed
f. Multinucleated; nuclei peripheral.
1) Genetic information needed to make proteins; multiple nuclei optimizes this.
g. Low regeneration capability.
2. Cardiac Muscle
a. In heart only
b. Involuntary; quick response time; does not fatigue
c. Autorhythmic; heart beat propagation is intrinsic; heart rate control is extrinsic (nervous +
endocrine)
d. Normal length (~ 50-100 um), cylindrical, branched cells; intercalated discs join cells end-to-end.
e. Striated—sarcomeres regularly placed
f. Uninucleated; nucleus central.
g. Low regeneration capability.
3. Smooth Muscle
a. Found in/as
1) Tunica muscularis (media) layer of walls of hollow organs (gut, bladders), blood vessels,
ducts & tubes.
2) Sphincters in the same mentioned areas
3) Arrector pili muscle of hair follicles.
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b. Involuntary; slow response time; slow to fatigue
c. Some smooth muscle is autorhythmic, such as tunica muscularis of gut; generally controlled more
by hormones than nervous system.
d. Short (20-50 um), spindle-shaped cells, unbranched.
e. Not striated—contractile elements not regularly placed.
f. Uninucleate; nucleus central.
g. Good regeneration capability.
SKELETAL MUSCLE STRUCTURE: GROSS ANATOMY
--Note: Fascia is any fibrous connective tissue (CT) sheet that covers & supports internal structures!
1. Superficial Fascia.
a. Immediately deep to skin, superficial to deep fascia.
b. Composed of areolar CT (collagen & elastin) + adipose, so it pads/cushions muscles, as well as
securely connects the cutaneous membrane to deep fascia.
c. Contains/supplies blood vessels, lymphatic vessels & nerves to/from muscles.
2. Deep Fascia.
a. Surrounds muscle groups (muscles with same function).
b. Composed of dense irregular CT (rich in collagen).
c. Confluent with tendons (which are confluent with periosteum) and epimysium, and/or
aponeuroses (sheets of deep fascia that connect muscles to muscles).
3. Epimysium.
a. Surrounds individual muscles.
b. Composed of dense irregular CT.
c. Confluent with deep fascia & perimysium.
4. Perimysium.
a. Surrounds muscle fascicles forming bundles of myofibers.
b. Composed of dense irregular CT.
c. Confluent with epimysium & endomysium.
5. Endomyusium.
a. Surrounds individual myofibers.
b. Composed of areolar CT (thin layer).
--General functions of muscle CT (fascia) sheaths:
1. Bundles myofibers together, thus focuses and optimizes force of muscle.
2. Attaches muscles to bone (tendons) or muscles to muscle (aponeuroses)
3. Support/conduit for blood vessels (providing nutrient/waste & respiratory gas exchange, plus
transportation to and from of other substances such as hormones), lymphatic vessels (fluid drainage)
and nerves (rapid control).
MYOFIBER FORMATION, GROWTH & REPAIR
1. Formation & Growth
a. Embryonic Development. Mesenchyme differentiates into myoblasts.
1) Myoblasts have single nuclei, are mature and amitotic; fuse into syncytial skeletal muscle
tissue.
b. Satellite cells: Myoblasts that persist and do not fuse.
c. Post partum.
1) Hypertrophy of muscle fibers causes growth
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a) Stimulated by HGH and testosterone.
2) Myofibers are amitotic; growth of muscle occurs by hypertrophy, NOT by hyperplasia.
2. Repair
a. Satellite cells.
1) Persistent myoblasts
2) Fuse with damaged myofibers or with other satellite cells, replacing damaged muscle tissue.
3) Few satellite cells, thus skeletal muscle regeneration limited.
b. Fibrosis.
1) Damaged muscle tissue that is not replaced by muscle replaced with fibrous CT, which forms
scars.
2) Scars less elastic than muscle and do not have contraction ability!
MICROSTRUCTURE OF MYOFIBERS (= MUSCLE CELLS)
1. Sarcolemma.
a. Cell membrane of myofiber; T- (transverse) tubules are extensions or invaginations of the
sarcolemma that run deep into the sarcoplasm, intimately contacting areas of the sarcoplasmic
reticulum (SR) called cisternae.
2. Nucleus. Just under the sarcolemma.
3. Sarcoplasm.
a. Cytoplasm of myofiber
b. Contains
1) Glycogen (glucose storage, needed to make ATP anaerobically)
2) Myoglobin (oxygen storage, needed to make ATP aerobically)
3) Mitochondria (site of aerobic ATP synthesis)
4) Ribosomes (free—not attached to SR; site of polypeptide synthesis)
4. Sarcoplasmic Reticulum (SR).
a. Smooth ER
b. Surrounds myofibrils
c. Stores calcium ions in cisternae.
1) Cisternae in intimate association with T-tubules so that one T-tubule ending is sandwiched
between adjacent cisternae.
5. Sarcomere.
a. Z discs. Structural proteins (SP) that serve as attachment for
1) Thin filaments:
a) Actin (functional protein, FP)
b) Tropomyosin (FP)
c) Troponin (FP)
2) Nebulin (SP), runs from Z disc to end of individual actin filament and helps support it
3) Titin (SP), extends from Z disc to M line and attaches to both ends of myosin.
a) An elastic protein, helps sarcomere return to original shape after contraction or being
stretched.
b. A band. Corresponds to length of thick filament.
c. I band. Corresponds to length of thin filament in area where thick filament does not overlap.
1) Narrows & mostly disappears during contraction.
d. H zone. Corresponds to thick filament without thin filament overlap.
1) Narrows & disappears during contraction.
e. M line. Central attachment site for thick filaments and titin.
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SARCOMERE CONTRACTION: NEUROMUSCULAR JUNCTION
1. Motor neurons innervate myofibers.
a. Axon endings terminate in swellings called synaptic end bulbs (or motor end plates).
b. Synaptic end bulbs fit into depressions in the sarcolemma, but don’t actually touch the
sarcolemma.
c. Synapse is space between synaptic end bulbs and sarcolemma.
2. Motor unit: One motor neuron innervating many myofibers.
3. When action potential (nerve impulse) reaches synaptic end bulb:
a. Ca++ channels open.
b. Ca++ entering synaptic end bulb causes acetylcholine (Ach) vesicles to fuse with the presynaptic
membrane.
c. Ach diffuses across synapse;
d. Binding of two Ach to receptors opens ion channels
e. Na+ diffuses quickly into sarcoplasm, K+ diffuses out;
1) Na+ influx initiates action potential in the sarcolemma.
SARCOMERE CONTRACTION: SLIDING FILAMENT MECHANISM
1. Action potential down T-tubules opens Ca++ channels in cisternae of SR;
a. Ca++ floods out through calcium channels (facilitated transport).
2. Ca++ bonds to troponin.
a. Conformational change pulls tropomyosin off myosin binding sites on actin.
3. Myosin heads attach to myosin binding sites on actin.
4. Myosin head bonding releases phosphate from myosin head.
5. Myosin heads move forward
a. = power stroke of myofibril contraction.
6. Myosin head movement releases ADP from myosin.
7. ATP binds to myosin;
a. Conformational change releases myosin from actin.
8. Myosin hydrolyses ATP to ADP + P,
a. Recocks myosin head.
9. Cycle repeated until full sarcomere contraction has occurred.
Note: One ATP molecule is needed for each power stroke!
CONTINUED FILAMENT CONTRACTION REQUIRES
1. Repeated action potentials from nervous system.
a. Calcium is constantly being removed from sarcoplasm by calcium active transport pumps, which
use ATP to pump calcium into the cisternae of the SR against a gradient; they are located on the
cisternae membrane.
b. Inside cisternae, calsequestrin (a protein) binds calcium, reducing the negative gradient, making it
easier for the Ca++ active transport pumps to restore calcium.
c. Lowering Ca++ levels beyond threshold needed to remove tropomyosin from actin causes actin &
myosin to relax in releationship to each other.
2. When Ach is secreted and diffuses across the synapse, acetylcholinesterase immediately starts to
digest it into acetate and choline.
a. Choline transporters pump it back into the neuron
1) Recombines with acetate inside neuron into Ach and is packaged into Ach vesicles.
2) Acetate released into interstitial fluid is picked up by other cells and metabolized.
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3. ATP required! Needed to cause conformational change removing myosin head from actin!
RIGOR MORTIS
1. Observations:
a. A few hours after death, muscles stiffen
b. About a half a day after death, muscles reach their maximum stiffness
c. Muscle stiffness subsides two to three days after death.
2. Physiology:
a. No O2, no ATP made.
1) Ca++ can’t be pumped back into cisternae from sarcoplasm.
2) High Ca++ levels keep myosin binding sites exposed
a) Myosin become irreversibly fused to actin! (Rigor)
b. Lysosomes eventually break down muscle proteins
1) After about 12 hours, effects of protein degradation detected
TO RETURN MUSCLES TO ORIGINAL LENGTH AFTER CONTRACTION you need:
1. Relaxation of muscle fibers!
a. Stop action potentials!
b. Break down Ach!
c. Removal of Ca++ from sarcoplasm!
2. Titin: Pushes filaments back out!
3. Antagonistic muscles pull relaxed muscles out!
4. Gravity (sometimes)!
SKELETAL MUSCLE FIBERS: GENERAL COMMENTS
1. Muscle fibers classified by
a. Quickness of action,
b. ATP source
c. Quickness to fatigue.
2. Motor units consist of only one type of fiber.
3. Muscles consist of combinations of all three types of fibers.
a. Combination depends on function of the muscle
b. Genetically determined
1) Cannot change proportions
2) Can increase the size and efficiency of muscle fibers.
SKELETAL MUSCLE FIBERS: CLASSIFICATION
1. Slow Oxidative Fibers
a. Myosin heads split ATP slowly
b. ATP produced by aerobic respiration, thus it’s oxidative (needs O2)
1) Lots of mitochondria,
2) Lots of myoglobin;
3) High vascularization (provides needed O2)
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4) Fibers thinnest of the three types,
a) Reduces diffusion distances for respiratory gases.
c. Slow to tire because of high availability of oxygen to produce ATP and metabolize lactate; thus
time to fatigue is low.
d. Found in high proportion where you need/have
1) Prolonged contraction (postural muscles of back and neck)
2) Aerobic endurance (leg muscles)
2. Fast Oxidative-Glycolytic Fibers
a. Myosin heads split ATP quickly, thus contraction is fast.
b. ATP produced by both aerobic respiration and anaerobic respiration (glycolysis).
1) Anaerobic respiration necessitates high glycogen stores, which these fibers have.
2) Aerobic respiration necessitates the presence of some myoglobin (not as much as in slow
oxidatives), vascularization (not as much as in slow oxidatives) and mitochondria (not as
many as in slow oxidatives).
3) Muscle diameter is midway between slow oxidatives and fast glycolytics.
c. Intermediate to tire since there is some vascularization, so fatigue is reduced, but not as much as
in slow oxidatives.
d. These fibers are found in high proportion where you need intermediate-level muscle activity, as
in walking or short-distance jogging (leg muscles).
3. Fast Glycolytic Fibers
a. Myosin heads split ATP fast, so contraction is fast.
b. ATP produced by anaerobic respiration (glycolysis—thus glycolytic; don’t require O2):
1) High glycogen stores (needed to provide glucose for glycolysis)
2) Low myoglobin (stored O2 not needed)
3) Low vascularization
4) Thickest of the three muscle fibers, and have low numbers of mitochondria.
c. Low levels of oxygen mean lactate builds up rapidly,
1) Thus fatigue quickly.
d. Thickest of muscle fibers,
1) So are the most powerful of muscle fibers.
e. Found in high proportion where
Quick, strength-dependent activities are performed (arm muscles).
f. Fatigue-resistant fast glycolytic fibers can be developed through exercise
1) This increases vascularization and numbers of mitochondria in fibers.
CARDIAC MUSCLE
1. Intercalated Discs.
a. Microvilli-like modifications of myofiber ends—increases surface area!
b. Desmosomes provide secure connections between adjacent sarcolemma. (More surface area
increases secure connections)
c. Gap junctions connect adjacent myofibers so action potentials can spread flawlessly between
cells. (More surface area increases numbers of gap junctions, which increases action potential
conduction.)
2. Myofibrils. Similar to those in skeletal muscle.
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3. Sarcoplasmic Reticulum. Less developed as in skeletal muscle, thus fewer cisternae and fewer Ca++
channels and fewer Ca++ Active Transport Pumps. [Ca++] build up in and decrease from sarcoplasm
much slower than in skeletal muscle. So, contraction is 10-15 x longer than in skeletal muscle!
4. Ca++ Source for Contraction.
a. Cisternae of SR (reduced availability)
b. Interstitial fluid surrounding cells. Sarcolemma has Ca++ channels, unlike skeletal muscle.
5. T-tubules. Fewer in number than in skeletal muscle.
6. Autorhythmic cells oscillate Na+/K+ concentrations; resultant action potential sent across sarcolemma
and to adjacent myofibers.
7. Mitochondria.
a. More and larger than in skeletal muscle, high myoglobin and high vascularization.
1) Provides sufficient gas exchange allowing for ATP to be produced through aerobic
respiration.
b. Source of energy to make ATP is glucose and lactate
1) Cardiac muscle regularly and efficiently metabolizes lactate taking in from blood (from other
muscle cells) and turns it into pyruvate—helping to remove lactic acid from the blood. This
helps other muscles to work more efficiently and provides energy for the heart!
SMOOTH MUSCLE
1. Not striated because myosin and actin filaments are not arranged so that the various bands, zones,
lines (etc) line up. Intermediate filaments stabilize the thick & thin filaments. Contractile filaments
connect to intermediate filaments at the dense bodies. The orientation of the intermediate filaments
cause smooth muscle to contract in a spiral fashion.
2. No T-tubules, but caveolae present. SR & cisternae are sparse. Thus is takes longest of the three
muscle fibers for Ca++ to be released to or restored from the sarcoplasm. Besides from cisternae,
Ca++ is also released from the interstitial fluid.
3. Contraction physiology is different from striated muscles.
a. No troponin present; instead, Ca++ binds to calmodulin.
b. The Ca++-calmodulin complex activates myosin kinase.
c. Myosin kinase phosphorylates myosin head.
d. Phosphorylated myosin head
1) Cocks,
2) Connects to actin binding site
3) Pushes against actin.
e. Myosin phosphatase then removes phosphate from myosin head.
f. Dephosphorylated myosin head detaches from actin, but it does it really slow;
1) Helps maintain smooth muscle contraction without the use of ATP. (important!)
4. Two Types of Smooth Muscle:
a. Single Unit
1) Most common type of smooth muscle, found in the TM layer of blood vessels (small to
medium), gut, uterus and urinary bladder.
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2) Autorhythmic. Gap junctions connect adjacent cells. This allows for a single action potential
to spread through the entire unit; thus, a single point of stimulation is required.
b. Multiple Unit
1) Least common type of smooth muscle, found in TM of major arteries and the respiratory tree,
and is the smooth muscle type that makes up the arrector pili muscles.
2) Not autorhythmic. Gap junctions not present between adjacent cells. Innervated as motor
units.
ENERGY FOR MUSCLE CONTRACTION: ATP SOURCES
--Need ATP for
a. Detachment of myosin heads
b. Ca++ Active Transport Pumps
1. Sarcoplasmic ATP Stores: Last 1 to 3 seconds.
2. Creatin Phosphate: ~ 8 to 12 seconds; fast glycolytics have the most, slow oxidatives the least.
a. Produced from excess ATP during muscle relaxation
b. Phosphorylates ADP to ATP when ATP stores are gone.
3. Glycolysis (Anaerobic Respiration)
a. Glucose turned into 2 pyruvates, yielding 2 ATP net.
b. Glucose from stored glycogen granules or from glucose taken from blood;
1) If blood levels decrease, liver glycogen yields glucose that is put into blood, restoring blood
glucose levels.
c. If there is insufficient oxygen available (see below), pyruvate is converted into lactate,
1) Stored in liver and muscles
2) Creates hypertonic environment,
a) Water enters hepatocytes and muscles by osmosis.
b) Muscles swell, causing pain; i
c) Muscles stiffen, making it harder for muscles to work, thus contributing to fatigue.
d. If there is sufficient oxygen available, pyruvate goes into aerobic respiration (see next).
4. Aerobic Respiration.
a. If there is sufficient oxygen available, pyruvate enters mitochondria where aerobic respiration
takes place.
b. The energy from two pyruvates from glycolysis is used to phosphorylate 34 ADPs to 34 ATPs.
What’s left is 6 carbon dioxide molecules, some electrons and some hydrogens. At the very end
of this process, BEFORE the ATP is produces, oxygens take up the excess hydrogens and
electrons, forming water. If there is insufficient oxygen present, the hydrogens and electrons from
the catabolism of pyruvate can’t be removed and NO ATP is produced! This is why you (and
other organisms) need to breathe in oxygen!
c. To optimize aerobic respiration, myofibers need a good source of glucose and oxygen. Thus cells
that use this process optimally to obtain their ATP have, besides lots of mitochondria, lots of
myoglobin and high vascularization—which provides for high levels of respiratory gas exchange.
These cells are also thin cells, increasing the ability of respiratory gases to diffuse in and out of
the cells—it take much longer for respiratory gases to diffuse in and out of thick cells!
d. Note that glycerol, fatty acids and amino acids can enter anaerobic respiration-aerobic respiration
at various points, providing energy for ATP production!
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WHOLE MUSCLE PHYSIOLOGY
1. Muscles are made of muscle units, which is one motor neuron + associated myofibers.
a. Motor units with fewer myofibers allow for increased control over entire muscle.
b. Strength of whole muscle contraction depends on how many motor units are triggered at a time.
c. Contraction of motor units is all-or-nothing; if threshold is reached, complete contraction occurs.
2. Twitch.
a. Single single to muscle
b. Latent Period.
1) Lasts a few milliseconds.
2) Action potential propagates across sarcolemma & down T-tubules; Ca++ floods into
sarcoplasm.
c. Period of Contraction.
1) Lasts 10 to 100 milliseconds.
2) Myosin crossbridges active.
d. Period of Relaxation.
1) Lasts 10 to 100 milliseconds.
2) Ca++ Active Transport Pumps have reduced [Ca++] levels; Ca++ leaves troponin and myosin
heads can’t attach; muscle relaxes.
3. Summation. Two or more signals close enough together so that motor unit(s) can’t fully relax & more
motor units are recruited
4. Tetanus. Multiple signals so close together that [Ca++] in myofibers is kept at maximum & all
myfibers in muscle contract; no relaxation between signals is possible.
5. Fatigue. Causes not entirely known; probably involves lactic acid buildup due to insufficient oxygen
& glycogen depletion, which decreases ATP production. You see fatigue on a myogram when
continue to stimulate muscle with action potentials but muscle stops contracting.
6. Contracture. The “lockup” of muscles caused by a lack of ATP resulting from heavy activity.
7. Muscle Tone. Maintained by some motor units in muscle always being contracted at any one time.
Conditioned muscles exhibit higher muscle tone because more motor units are active per unit time
than in “couch potato” muscles.
8. Types of Contractions:
a. Isotonic Contractions. Muscle changes length during tension.
1) Concentric Isotonic Contractions. Muscle shortens.
2) Eccentric Isotonic Contractions. Muscle lengthens during tension; damages muscles, making
muscles sore.
b. Isometric Contractions. Muscles do not change length during tension.
1) Body coordinates both isotonic & isometric contractions during normal activities.
MUSCULAR SYSTEM PATHOLOGIES
1. Contracture.
2. Cramps. Occur when sarcoplasmic [Ca++] remain high.
3. Strain. Tearing of muscle resulting in inflammation.
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4. Muscular Dystrophy.
a. Several related pathologies, all characterized by gradual weakening & degeneration of muscle
tissue. Death by age 20 due to heart & diaphragm failure.
b. Duchenne Muscular Dystrophy.
1) Most common form of muscular dystrophy.
2) Genetic; recessive mutation on X chromosome; dystrophin not produced.
3) Lack of dystrophin activates enzyme that destroys muscles.
4) Satellite cell injection helps as they produce dystrophin.
5. Myasthenia Gravis.
a. Autoimmune disease; antibodies against acetylcholine receptors produced.
b. Impared muscle contraction, esp. in head region & limbs
c. Mostly in women, 20-40 years old.
d. Pulmonary failure in 10%.
e. Drug treatments available, but intensive monitoring necessary.
6. Tetanus.
a. Bacterium produces tetanus toxin.
b. Toxin interferes with Ach-Ache, thus muscles fail to relax.
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