Chapter 11 Flashcards
three types of muscles in the body are
skeletal, cardiac, smooth
skeletal muscle
- striated
- voluntary
- attached to bone
cardiac muscle
- striated
- involuntary
- heart
smooth muscle
- not striated
- involuntary
- hollow organs
the four muscle functions
- producing body movements
- stabilizing body positions
- storing and moving substances within the body
- generating heat
muscle function: producing body movements
walking and running, localized movementsm
muscle functions: stabilizing body positions
skeletal muscle contractions and postural muscle contractions
skeletal muscle contractions
- stabilizing joints
- maintain body positions, such as standing or sitting
postural muscle contactions
- continuously when you are awake
- sustained contractions of your neck muscles hold your head up
muscle function: storing and moving substances within the body
storage is accomplished by sustained contractions of ring-like bands of smooth muscle called sphincters
- prevent outflow of the contents of a hollow organ
- temporary storage of food in the stomach or urine in the urinary bladder
- cardiac muscle contractions of the heart pump blood through the blood vessels of the body
muscle function: generating heat
as muscle contracts, it produces heat
- this process is known as thermogenesis
the three muscle properties
electrical excitability, contractility, extensibility
electrical excitability
a property of both neurons and muscle cells
- ability to respond to certain stimuli by producing action potentials
contractility
ability of muscle to contract forcefully when adequately stimulated
- when a muscle contracts, it generates tension, and possibly movement
extensibility
ability of muscle to stretch without being damaged
thousands of muscle cells =
muscle fibers
fascicles
bundles of 10-100 or more muscle fibers covered in connective tissue
tendon
connective tissue that connects muscle to bone
ligament
connective tissue that connects bone to bone
muscular dystrophy
inherited muscle-destroying diseases, characterized by degeneration of muscle fibers (cells) that causes progressive atrophy of the skeletal muscle
Duchenne muscular dystrophy is the most common form
muscle fiber degeneration and necrosis, variation in fiber size, internal nuclei, increased connective tissue, etc.
myoblasts
small, undifferentiated cells, progenitor cells for mature skeletal muscle fibers
satellite cells
resident stem cells located in skeletal muscles, a few myoblasts do persist in mature skeletal muscles as satellite cells
stem cells self-renew and give rise to satellite cells and these mature in
myoblasts then fuse into a myotube (muscle cell = muscle fiber = myocyte)
sarcolemma
the cell membrane of a muscle fiber (cell), especially of a skeletal muscle fiber
transverse (T) tubules
small, cylinder invaginations of the sarcolemma of striated muscle fibers (cells) that conduct muscle action potentials toward the center of the muscle fiber
sarcoplasm
the cytoplasm of a muscle fiber (cell)
myoglobin
the oxygen-binding, iron-containing protein present in the sarcoplasm of the muscle fiber (cells); contributes the red color to muscle
myofibrils
the contractile elements of the skeletal muscle fiber that extends throughout the sarcoplasm
filaments
smaller structures within myofibrils, can have thick or thin diameters
thin filament
8nm in diameter and 1-2 um long
thick filaments
16nm in diameter and 1-2 um long
sarcoplasmic reticulum (SR)
a network of sacs and tubes surrounding myofibrils of muscle fiber (cell), comparable to endoplasmic reticulum; functions to reabsorb calcium ions during relaxation and to release them to cause contraction
terminal cisternae (lateral sacs)
dilated end sacs of the sarcoplasmic reticulum that butt against a T tubule from both sides
triad
a complex of three units in a muscle fiber composed of a transverse tubule and the sarcoplasmic reticulum terminal cisternae on both sides of it
triggers muscle contraction
release of Ca2+ from the terminal cisternae of the sarcoplasmic reticulum
sarcomeres
a contractile unit in a striated muscle fiber (cell) extending from one z disc to the next z disc
Z disc
narrow, plate-shaped regions of dense protein material that separate one sarcomere from the next
A band
the dark, middle part of the sarcomere that extends the entire length of the thick filaments and also includes those parts of the thin filaments that overlap with the thick filaments
zone of overlap
cross section toward the end of the A band where the thick and thin filaments overlap; reveals that each thick filament is surrounded by a hexagonal arrangement of six thin filaments, and each thin filament is surrounded by a triangular arrangement of three thick filaments
I band
the lighter, less dense area of the sarcomere that contains the rest of the thin filaments but no thick filaments. A Z disc passes through the center of each I band
H zone
a narrow region in the center of each A band that contains thick filaments but no thin filaments
M line
a region in the center of the H zone that contains proteins that hold the thick filaments together at the center of the sarcomere
there are three types of muscle proteins
contractile proteins, regulatory proteins, structual proteins
contractile proteins
actin and myosin
regulatory proteins
tropomyosin and troponin
structural proteins
titin, alpha-actinin, myomesin, nebulin, and dystrophin
the sarcomere has two contractile proteins
myosin: thick and actin: thin
myosin heads
contain actin-binding sites and ATP-binding sites, essential for muscle contraction
heavy chains and light chains
structural components of the myosin molecule
hinge region
provides flexibility, allowing the myosin head to move
myosin tail
forms the backbone of the thick filament
two regulatory proteins that are part of the thin filament
tropomyosin and troponin
tropomyosin
a rod-shaped protein that joins with other tropomyosin molecules to form long strands that wrap around the F actin double helix; covers myosin binding sites on the actin
troponin
a protein that consists of three globular subunits - one that binds to tropomyosin, on that binds to actin, and one that had binding sites for calcium ions (Ca2+)
in the presence of Ca2+, myosin can
bind actin
several key structural proteins that contribute to the alignment, stability, extensibility, and elasticity
tinin, alpha-actinin, myomesin, nebulin, dystrophin
tinin
a structural protein that connects a Z disc to the M line of the sarcomere, helping to stabilize the position of the thick filament; because it can stretch and then spring back unharmed, titin accounts for much of the elasticity and extensibility of myofibrils
alpha-actinin
a structural protein of the Z discs that attaches to actin molecules of thin filaments and to titin molecules
myomesin
a structural protein that forms the M line of the sarcomere; it binds to titin molecules and connects adjacent thick filaments to one another
nebulin
a structural protein that wraps around the entire length of each thin filament; it helps anchor the thin filaments to the Z discs and regulates the length of the thin filaments during development
dystrophin
a structural protein that links the thin filaments of the sarcomere to integral membrane proteins in the sarcolemma, which are attached in turn to proteins in the connective tissue matrix that surrounds muscle fibers; it is thought that dystrophin helps reinforce the sarcolemma and helps transmit tension generated by sarcomeres to tendons
sliding filament mechanism
explains the mechanism of muscle contraction at the molecular level
relaxed muscle
- sarcomere is at its longest
- H zone and I band are wide
- actin and myosin only partially overlap
partially contracted muscle
- sarcomere shortens
- H zone narrows
- I band decreases in size
- actin slides past myosin, increasing overlap
maximally contracted muscle
- sarcomere is at its shortest
- H zone disappears
- I band is almost gone
- actin and myosin fully overlap
In skeletal muscle, which of the following is not found in a thin myofilament?
A. Troponin
B. Calcium receptors
C. Tropomyosin
D. F actin
E. Titin
E. Tinin
Which incorrectly describes what happens during skeletal muscle contraction?
A. The I bands narrow.
B. The width of the A band remains constant.
C. The width of the A band decreases.
D. The H zone gets smaller.
E. The sarcomere narrows.
C. The width of the A band decreases
Which of the following contains overlapping thick and thin myofilaments?
A. H band
B. A band
C. Z discs
D. M line
E. I band
B. A band
Where in a sarcomere do actin and myosin overlap?
A. The M line
B. The H band
C. The I band
D. The Z disc
E. The A band
E. The A band
contraction cycle four major steps
- ATP hydrolysis
- attachment of myosin to actin (cross-bridge formation)
- power stroke
- detachment of myosin from actin
contraction cycle in depth
a. ATP hydrolysis. As mentioned earlier, a myosin head includes an ATP-binding site that functions as an ATPase—an enzyme that hydrolyzes ATP into ADP (adenosine diphosphate) and a phosphate group. The energy generated from this hydrolysis reaction is stored in the myosin head for later use during the contraction cycle. The myosin head is said to be energized when it contains stored energy. The energized myosin head assumes a “cocked” position, like a stretched spring. In this position, the myosin head is perpendicular (at a 90° angle) relative to the thick and thin filaments and has the proper orientation to bind to an actin molecule. Notice that the products of ATP hydrolysis—ADP and a phosphate group—are still attached to the myosin head.
2. Attachment of myosin to actin. The energized myosin head attaches to the myosin-binding site on actin and releases the previously hydrolyzed phosphate group. When a myosin head attaches to actin during the contraction cycle, the myosin head is referred to as a crossbridge. Although a single myosin molecule has a double head, only one head binds to actin at a time.
3. Power stroke. After a crossbridge forms, the myosin head pivots, changing its position from a 90° angle to a 45° angle relative to the thick and thin filaments. As the myosin head changes to its new position, it pulls the thin filament past the thick filament toward the center of the sarcomere, generating tension (force) in the process. This event is known as the power stroke. The energy required for the power stroke is derived from the energy stored in the myosin head from the hydrolysis of ATP (see step 1). Once the power stroke occurs, ADP is released from the myosin head.
4. Detachment of myosin from actin. At the end of the power stroke, the crossbridge remains firmly attached to actin until it binds another molecule of ATP. As ATP binds to the ATP-binding site on the myosin head, the myosin head detaches from actin.
contration cycle key words from the slides
- load the spring
- attach = crossbridge
- ADP/pi –> pivot = power stroke
- ATP –> detach
the neuromuscular junction (NMJ)
synapse between a somatic motor neuron and a skeletal muscle fiber
- motor end plate (muscle membrane)
- end plate potential
end plate potential (EPP)
action potential generated at the muscle membrane
skeletal muscle action potential
depolarizing phase and repolarizing phase
depolarizing phase
- the membrane potential rapidly rises (-90mV to +30mV)
- voltage-gated Na+ channels open, allowing Na+ to enter the cel
- this influx of Na+ makes the inside of the cell more positive
repolarizing phase
- the membrane potential returns or falls (+30mv to -90mV)
- voltage-gated K+ channels open, allowing K+ to leave the cell
- this efflux of K+ restores the negative resting membrane potentials
electromyography (EMG)
test that measures the electrical activity (muscle action potential) in resting and contracting muscles
- normally, resting muscle produces no electrical activity, a slight contraction produces some electrical activity
excitation-contraction coupling (relaxed)
calcium sequestration: Ca2+ ions are stored in the sarcoplasmic reticulum
blocked myosin-binding sites: tropomyosin, held in place by troponin, covers the myosin-binding sites on actin
no cross-bridge formation: since myosin cannot bind to actin, no contraction occurs
excitation-contraction coupling (contraction)
muscle action potential: a nerve impulse triggers depolarization of the sarcolemma and transverse tubules
calcium release: voltage-gated Ca2+ channels open, releasing Ca2+ from the sarcoplasmic reticulum
binding to troponin: Ca2+ binds to troponin, causing a conformational change that moves tropomyosin away from myosin-binding sites on actin
cross-bridge formation: myosin binds to actin, allowing the contraction cycle to proceed
skeletal muscle contraction summary
- a nerve action potential in a somatic motor neuron triggers the release of acetylcholine (ACh)
- ACh binds to receptors in the motor end plate, triggering an end plate potential, which in turn generates a muscle action potential
- Acetylcholinesterase destroys ACh so another muscle action potential does not arise unless more ACh is released from the somatic motor neuron
- a muscle action potential traveling along a transverse tubule triggers a change in the dihydropyridine receptors that causes the Ca2+ release channels to open, allowing the release of calcium ions into the sarcoplasm
- Ca2+ binds to troponin on the thin filament, exposing the myosin-binding sites on actin
- contraction: myosin heads bind to actin, undergo power strokes, and release; thin filaments are pulled toward center of sarcomere
- Ca2+ release channels close and Ca2+ ATPase pumps use ATP to restore low level of Ca2+ in the sarcoplasm
- tropomyosin slides back into position where it blocks the myosin-binding sites on actin
- muscle relaxes
ATP production in skeletal muscle overview
ATP is produced through various metabolic pathways: glycolysis, aerobic respiration, creatine phosphate, fatty acids and amino acids
glycolysis ATP production
Glucose (from blood or muscle glycogen) is broken down into 2 pyruvic acid molecules, generating ATP. If oxygen (O₂) is insufficient, this leads to the production of 2 lactic acid molecules, which can accumulate and cause muscle fatigue.
aerobic respiration (with sufficient O2) ATP production
When oxygen is available, pyruvic acid enters the mitochondria and undergoes aerobic respiration. This includes the Krebs cycle and the electron transport chain, producing ATP, CO₂, and H₂O as byproducts.
creatine phosphate ATP production
In addition to glucose and fatty acids, creatine phosphate helps regenerate ATP rapidly in the muscle. Creatine phosphate donates a phosphate group to ADP, forming ATP quickly during short bursts of intense activity.
fatty acids and amino acids ATP production
These can also be used for ATP production when glucose is scarce, contributing to energy production through aerobic respiration in the mitochondria.
creatine phosphate
energy-rich molecule found in myofibers made by Creatine Kinase
creatine phosphate is the first source of
ATP during muscle contraction
creatine + ATP <–CK–> creatine phosphate + ADP
extra creatine is lost through
urine
creatine is still not super well studied long term
- safety and efficacy still not known
- kidney dysfunction is caused by long term use
anaerobic glycolysis produces
ATP when oxygen levels are low
anaerobic glycolysis can rapidly provide
about 2 minutes of energy when ATP levels become low in maximal muscle activity
accumulate in anaerobic glycolysis
lactic acid
aerobic respiration generates
ATP when sufficient oxygen is available
pyruvic acid enters the mitochondria and with O2,
aerobic respiration via the Krebs cycle
aerobic respiration is slower than
glycolysis but yields more ATP
time of aerobic respiration is
several minutes to an hour or more
myoglobin serves as
muscle oxygen reservoir
muscle myoglobin binds
oxygen reversibly
muscle fatigue
the inability of a muscle to maintain force of contraction after a prolonged activity
central fatigue
associated with the CNS
muscle fatigue
- energy availability
- calcium cytoplasmic decline
- oxygen, glycogen, and ACh depletion
- lactic acid build up
oxygen consumption will increase for a while after exercise
- initially muscle is in an oxygen debt
- but additional O2 allows it to recover in minutes to hours
- extra O2 is important for: converting lactic acid to glycogen, tissue repair, resynthesizing creatine phosphate
- a better term is recovery O2 uptake
a motor unit
- comprised of a somatic motor neuron and its muscle fibers
- myofiber number ranges from 3 in the eye muscles to 1000 in the gastrocnemius
motor unit recruitment
the process of increasing the number of active motor units
a muscle twitch
- the brief contraction of a group of muscle fibers within a muscle in response to a single action potential
- consists of latent, contraction, and relaxation periods
latent period
a brief delay that occurs between application of the stimulus and the beginning of contraction, lasts about 2msec
contraction period
Ca2+ binds to troponin, myosin-binding sites on actin are exposed, and myosin cross bridges for, lasts 10-100 msec
relaxation period
Ca2+ is actively transported back into the sarcoplasmic reticulum, myosin binding sites are covered by tropomyosin, myosin heads detach from actin, and tension in the muscle fiber decreases, also about 10-100 msec
graded contractions can occur in skeletal muscles and numerous factors affect muscle tension
- action potential frequency
- muscle fiber length
- muscle fiber diameter
- motor unit size
- motor unit recruitment (progression of adding numbers to the motors units engaged)
effect of increased frequency of action potentials: single twitch
a single action potential leads to a brief contraction (small peak in muscle tension)
effect of increased frequency of action potentials: wave summation
multiple stimuli occur before the muscle fully relaxes, leading to an increase force due to the additive effect on contraction
effect of increased frequency of action potentials: unfused tetanus
rapid, repeated stimulation leads to a fluctuating but sustained increase in muscle tension
effect of increased frequency of action potentials: fused tetanus
very high-frequency stimulation results in a smooth and sustained contraction with maximum tension
length-tension relationship: understretched
- ~1.8 um
- filaments overlap excessively, reducing cross bridge formation resulting in lower tension
- when the sarcomere is too short (under 60% of the optimum length), the filaments are overly compressed, and tension decreases
length-tension relationship: optimal length
- ~2.2 um
- maximum overlap between thick and thin filaments, allowing optimal cross bridge formation and the highest tension
- the optimal range for the sarcomere length where maximum force is produced (around 80-120% of the optimum)
- at this length, the thin and thick filaments (actin and myosin) overlap the best to generate maximum tension
length-tension relationship: overstretched
- ~3.8 um
- minimal or no filament overlap, reducing cross bridge interactions, leading to little or no tension development
- when the sarcomere is stretched beyond the optimal length (above 120%), the overlap between the filaments is reduced, leading to a decrease in the generated tension
muscle tone
a small amount of tautness or tension in the muscle due to weak, involuntary contractions of its motor units
muscle tone is established by
different motor units alternately active anfd inactive
tone helps to maintain
posture
smooth muscle tone helps maintain
blood pressure
muscle attachment sites
origin and insertion
origin
the attachment of a muscle’s tendon to the more stationary bone; stable portion
insertion
the attachment of the muscle’s other tendon to the more moveable bone; moveable portion
muscle action
the type of movement that occurs when a muscle contracts; when the insertion pulls toward the origin and creates movement
agonist muscle
makes the movement
antagonist muscle
opposite action at the same joint; ex: bicep and tricep
example movement
increasing joint angle or decreasing it away from the midline or towards it
movement of the forearm can be illustrated by the
lever-fulcrum principle
lever
- a rigid structure that can move around a fixed point called a fulcrum
a lever is acted on at two different points by two different forces:
the effort (E), which causes movement, and the load or resistance, which opposes movement
in the example of the forearm what is what in the lever system
lever = rigid bone structure
effort = contraction of the bicep
fulcrum = elbow joint
load = weight of object plus forearm in hand
mechanical advantage in a lever system
the load is closer to the fulcrum than the effort
ex: wheelbarrow (fulcrum = wheel, load = the contents being moved, effort = the handles being kept up to move the wheelbarrow)
in the leg (fulcrum = the ball of your foot, load = the weight of your body on the arch of your foot, effort = calf muscle to manage weight and move body)
- SECOND CLASS LEVER
mechanical disadvantage in a lever system
the load is farther from the fulcrum than the effort
ex: shovel (fulcrum = handle end, effort = middle where you hold, load = contents being shoveled)
the forearm example too
- THIRD CLASS LEVER
first class lever
seesaw, jaw
two major categories of muscle contractions are
isotonic and isometric
isotonic = same tension
- movement is created
- muscle changes length
- subtypes are eccentric and concentric
isomeric = same length
- no movement is created
- muscle length does not change
- muscle proteins are engaged but there is no change in length
concentric contraction (book)
picking up the book
eccentric contraction (book)
lowering the book
isomeric contraction (book)
holding the book steady
the three muscle fiber types are
slow oxidative, fast oxidative-glycolytic, and fast glycolytic
slow oxidative
- have a high resistance to fatigue
- ATP hydrolysis by myosin head is slow
- contraction relatively slow and takes longer to reach peak tension (ex: marathon running muscles and posture maintenance muscles)
fast oxidative-glycolytic
- moderate resistance to fatigue
- muscle fibers are often 50% larger than in an endurance athlete due to fiber hypertrophy
- fibers are intermediate in diameter (ex: walking and sprinting)
fast glycolytic
- low resistance to fatigue (ex: rapid, intense such as snatch weight lifting)
muscle fibers: muscle fiber diameter
SO = smallest
FOG = intermediate
FG = largest
muscle fibers: myoglobin content
SO = large amount
FOG = large amount
FG = small amount
muscle fibers: mitochondria
SO = many
FOG = many
FG = few
muscle fibers: capillaries
SO = many
FOG = many
FG = few
muscle fibers: color
SO = red
FOG = red-pink
FG = white (pale)
muscle fibers: capacity for generating ATP and method used
SO = high capacity, by aerobic respiration
FOG = intermediate capacity, by both aerobic respiration and anaerobic glycolysis
FG = low capacity, by anaerobic glycolysis
muscle fibers: rate of ATP hydrolysis by myosin ATPase
SO = slow
FOG = fast
FG = fast
muscle fibers: contraction velocity
SO = slow twitch
FOG = fast twitch
FG = fast twitch
muscle fibers: fatigue resistance
SO = high
FOG = intermediate
FG = low
muscle fibers: creatine kinase
SO = lowest amount
FOG = intermediate amount
FG = highest amount
muscle fibers: glycogen stores
SO = low
FOG = intermediate
FG = high
muscle fibers: order of recruitment
SO = first
FOG = second
FG = third
muscle fiber: location where fibers are abundant
SO = postural muscles such as those of the neck
FOG = lower limb muscles
FG = upper limb muscles
muscle fibers: primary function of fibers
SO = maintaining posture and aerobic endurance activities; marathon running
FOG = walking, sprinting, or running fast
FG = rapid, intense movements of short duration; weight lifting
research shows that fiber types shift with
change in training regimen
gene responsible for Duchenne muscular dystrophy
- has a local connection
- dystrophin
dystrophin was first sequenced, and its loss linked to Duchenne by
Eric Hoffman, then at the University of Pittsburgh
- subsequently sequenced and a huge body of research done on it
- more than 45 years, still no cure
why is there still no cure for Duchenne muscular dystrophy
huge gene!
sinus node (SA node)
the natural pacemaker of the heart, located in the right atrium
atrioventricular (AV) node
receives impulses from the SA node and transmits them to the ventricles
bundle of His
conducts impulses from the AV node to the ventricles
right and left bundle branches
further conduct impulses to the right and left ventricles
Purkinje fibers
specialized fibers that distribute the action potential throughout the ventricles, facilitating coordinated contraction
atrial syncytium
comprised of autorhythmic and contractile fibers, allowing for efficient contraction of the atria
ventricular syncytium
similarly composed of autorhythmic and contractile fibers, ensuring effective ventricular contraction
gap junctions
facilitate communication between cardiac cells, allowing action potentials to propagate smoothly
action potential
refers to the electrical signal that triggers cardiac muscle contraction
nucleus in cardiac muscles
each cardiac muscle cell (fiber) contains one or two centrally located nuclei
striations
- visible alternating light and dark bands due to the arrangement of actin and myosin filaments, similar to skeletal muscle
intercalated discs in cardiac muscle
- dark-staining junctions between cells that contain gap junctions and desmosomes
- they allow rapid electrical and mechanical coupling, ensuring synchronized contraction of the heart
cardia muscle fibers (cells)
branched, striated, and involuntary muscle fibers that are specialized for continuous rhythmic contractions
heart muscle has high demand for
oxygen
in cardiac muscle, the number of mitochondria is
very high
70 contractions/min for life =
a lot of work
intercalated discs (cardiac muscle)
found at the junction between two muscle cells
functional syncytium (cardiac muscle)
all cells work together as a single unit
autorhythmicity (cardiac muscle)
electrical potentials are created within cardiac cells
- does not require nervous stimulation
- maintenance of HR is done by ANS
excitation-contraction coupling in cardiac muscle
- muscle action potential propagation: an electrical signal travels along the sarcolemma and enters the transverse (T) tubules
- activation of L-type voltage-gated Ca2+ channels (dihydropyridine receptors - DHPRs): these channels, located in the T-tubule membrane, open in response to the action potential; this allows Ca2+ influx into the sarcoplasm
- triggering Ca2+ release from sarcoplasmic reticulum (SR): the small influx of Ca2+ from the T-tubule binds to and activates the ryanodine receptors (Ca2+ release channels) on the sarcoplasmic reticulum; this leads to a massive release of stored Ca2+ from the SR into the sarcoplasm
- muscle contraction initiation: increased Ca2+ concentration in the sarcoplasm binds to troponin, initiating muscle contraction
refractory period
the period of time after an action potential begins when an excitable cell temporarily loses its excitability
in cardiac muscle, there is a relationship between
action potential and refractory period
in cardiac muscle, refractory is long enough that
tetanus doesn’t happen
depolarizing phase in cardiac muscle
- fast voltage-gated Na+ channels open, causing a rapid influx of Na+, leading to depolarization
initial repolarizing phase in cardiac muscle
- fast voltage-gated Na+ channels close
- fast voltage-gated K+ channels open, leading to a small drop in membrane potential
plateau phase in cardiac muscle
- L-type voltage-gated Ca2+ channels open, allowing Ca2+ influx, which sustains depolarization
- fast voltage-gated K+ channels close, while slow voltage-gated K+ channels partially open, maintaining a steady potential
final repolarizing phase in cardiac muscle
- L-type voltage-gated Ca2+ channels close
- slow voltage-gated K+ channels fully open, leading to K+ efflux and restoration of the resting membrane potential
after skeletal muscle trauma, what proteins may appear in blood or urine test? What about the cardiac muscle?
after skeletal muscle trauma, myoglobin is a key protein that may appear in the blood or urine
after cardiac muscle trauma, troponin is the primary protein that appears in the blood
cardiac troponin T test
done to rule out damage to the heart muscle
smooth muscle fibers have
thick and thin filaments
in smooth muscle calmodulin binds
Ca2+
smooth muscle contains myosin, actin, and tropomyosin but no
troponin
smooth muscle: only a small amount of
sarcoplasmic reticulum
smooth muscle: caveolae
small pouch-like invaginations of the plasma membrane, release extracellular Ca2+
smooth muscle: dense bodies
functionally similar to Z discs in striated muscle fibers
contraction and relaxation in smooth muscle occurs more slowly than in
striated muscle
contraction is smooth muscle Ca2+ driven change in
myosin
contraction of smooth muscle
- Ca2+ binds to calmodulin, a regulatory protein in the sarcoplasm that is similar in structure to troponin.
- The Ca2+–calmodulin complex activates an enzyme called myosin light chain kinase (MLCK), which is also present in the sarcoplasm.
- Activated MLCK in turn phosphorylates (adds a phosphate group to) light chains in the myosin heads.
- The phosphorylated myosin heads bind to actin, and muscle contraction begins.
tropomyosin does not cover the
myosin-binding sites on actin
myosin molecule can bind to actin only aftern
phosphate groups are added to light chains in the myosin heads
signal transduction of nitric oxide abrogates
the work of Ca2+/calmodulin
MLCK =
myosin light chain kinase, a protein that promotes the interaction of myosin and actin
smooth muscle
autonomic nervous system regulate smooth muscle contraction
varicosities
points of release of neurotransmitters
receptors are not confined to motor end plate, but on
the entire surface on the cell
two forms of smooth muscle
single unit and multi unit
single-unit smooth muscle
- small number of specialized smooth muscle autorhythmic fibers (pacemaker cells)
- fibers contract together as one
- ex: visceral muscle, intestine, uterus, urinary bladder, and blood vessels
multi-unit smooth muscle
- fibers act independently of each other
- ex: pupillary muscle, airways, iris, ciliary body, hair, arrector pili
hair moving muscles =
arrector pili
arrector pili function
thermoregulation: muscles contract and create an insulating layer of air by raising the hair to maintain body heat, limited in humans but common in felines
because contractile single-smooth muscle fibers cannot initiate action potentials, they are excited and then contracted in response to
action potentials conducted to them by autorhythmic single-unit smooth muscle fibers
single unit smooth muscle exhibti
autorhythmicity
two types of spontaneous potentials exist in smooth muscle cells
pacemaker potentials and slow wave potential
pacemaker potentials in smooth muscle
- spontaneous potentials that always reach threshold
- Ca++ and K+ movements
slow wave potentials in smooth muscle
- cycles of depolarizations and repolarizations that do not necessarily reach threshold
- fluctuations in Na+ due to periodic activity of Na+/K+ ATP pumps
two types of spontaneous depolarizations can occur in autorhythmic smooth muscle fibers
pacemaker and slow wave potentials
pacemaker potential in smooth muscle
- gradual depolarization occurs due to increased Ca2+ influx or decreased K+ efflux
- brings the membrane potential to the threshold, triggering an action potential
significance of pacemaker potential
- found in autorhythmic smooth muscles, such as those in the gastrointestinal tract
- responsible for spontaneous contractions without requiring external stimuli
- maintains rhythmic activity in organs like the intestines and uterus
slow-wave potential in smooth muscle
- represents rhythmic fluctuations in membrane potential due to periodic changes in Na+/K+ pump activity
- does not always lead to an action potential unless it reaches the threshold
significance of slow-wave potentials
- found in autorhythmic smooth muscles, such as in the digestive system
- helps regulate rhythmic contractions, such as peristalsis
- not every slow wave reaches the threshold, so contraction frequency is modulated by external stimuli (e.g. neurotransmitters, hormones)
in contractile smooth muscle fibers that are capable of producing action potentials, the AP can be either
a spike potential or an action potential with a plateau
spike potential time
50msec
action potential with a plateau time
200msec
smooth muscle contractile cells
can contract via autorhythmicity or other stimuli
spike potential in smooth muscle: repolarization phase
L-type voltage-gated Ca2+ channels close, and voltage -gated K+ channels open, restoring the resting membrane potential
spike potential in smooth muscle: depolarizing phase
L-type voltage-gated Ca2+ channels open, causing a rapid increase in membrane potential
action potential with a plateau: depolarization phase
L-type voltage-gates Ca2+ channels open
action potential with a plateau: plateau phase
L-type voltage-gated Ca2+channels remain open, and voltage-gated K+ channels partially open, leading prolonged depolarization
action potential with a plateau: repolarizing phase
L-type voltage-gated Ca2+ channels close, and voltage-gated K+ channels fully open, leading to repolarization
significance of the plateau phase
- prolongs contraction in certain smooth muscle types (e.g., vascular or uterine smooth muscle)
- allows sustained calcium entry, which enhances contractile force
the increase in sarcoplasmic Ca2+ concentration that triggers contraction of a smooth muscle fiber can be caused by the opening of one or more of the following types of channels:
voltage-gated, Ca2+ release, receptor-activated, IP3-gated, store-operated, and mechanically-gated
excitation-contraction coupling in smooth muscle: voltage-gated channels
The sarcolemma of a smooth muscle fiber contains L-type voltage-gated Ca2+ channels that open in response to membrane depolarization, allowing Ca2+ to move from extracellular fluid into the sarcoplasm. The L-type voltage-gated Ca2+ channels in smooth muscle open in a graded fashion: As the strength of the depolarization increases, more channels open. In smooth muscle fibers that produce action potentials, the strong depolarization associated with the initial phase of the action potential opens a large number of L-type voltage-gated Ca2+ channels. This allows a large amount of Ca2+ to enter the sarcoplasm, which in turn causes a strong contraction. In smooth muscle fibers that produce only subthreshold depolarizations, only a few L-type voltage-gated Ca2+ channels open. This allows just a small amount of Ca2+ to enter the sarcoplasm, resulting in a weak contraction.
excitation-contraction coupling in smooth muscle: Ca2+ release channels
The Ca2+ that enters a smooth muscle fiber through L-type voltage-gated Ca2+ channels also serves as trigger Ca2+ that binds to and opens Ca2+ release channels in the membrane of the sarcoplasmic reticulum (SR). As a result, more Ca2+ is released into the sarcoplasm from the SR. Recall that the process by which extracellular Ca2+ triggers the release of additional Ca2+ from the SR is called Ca2+-induced Ca2+ release (CICR). You first learned about CICR in cardiac muscle, where it provides the majority of the Ca2+ needed for contraction since cardiac muscle fibers have a moderately extensive SR with a large intracellular reserve of Ca2+. In smooth muscle, however, CICR provides only a small amount of the Ca2+ required for contraction because the SR is present in small amounts and therefore has only a small intracellular Ca2+ reserve. Most of the Ca2+ needed for contraction in smooth muscle comes from extracellular fluid.
excitation-contraction coupling in smooth muscle: receptor-activated channels
Some neurotransmitters and hormones open receptor-activated channels in the sarcolemma of a smooth muscle fiber. Examples include ligand-gated channels and channels associated with G protein-coupled receptors. When these channels open, Ca2+ moves into the sarcoplasm from extracellular fluid.
excitation-contraction coupling in smooth muscle: inositol triphosphate (IP3)-gated channels
Although some neurotransmitters and hormones increase the sarcoplasmic Ca2+ concentration in smooth muscle by opening receptor-activated channels, others can increase the sarcoplasmic Ca2+ concentration by activating a second messenger pathway that opens inositol trisphosphate (IP3)–gated channels. During this process, the neurotransmitter or hormone binds to a G protein-coupled receptor that activates the enzyme phospholipase C, which in turn causes the production of the second messengers, inositol trisphosphate (IP3) and diacylglycerol (DAG). Once IP3 is generated, it binds to and opens IP3–gated Ca2+ channels in the SR membrane, causing the release of Ca2+ ions from the SR into the sarcoplasm.
excitation-contraction coupling in smooth muscle: store-operated channels
When the intracellular reserves of Ca2+ in the SR are depleted, a signal is relayed from the SR to the sarcolemma, where it causes store-operated channels to open. Opening these channels allows Ca2+ to enter the sarcoplasm from extracellular fluid. The entering Ca2+ can be used for contraction or to replenish the depleted Ca2+ stores in the SR.
excitation-contraction coupling in smooth muscle: mechanically-gated channels
The sarcolemma of a smooth muscle fiber contains mechanically-gated channels that are sensitive to stretch. Therefore, when a smooth muscle fiber is stretched, the mechanically-gated channels open, allowing extracellular Ca2+ to move into the sarcoplasm.
smooth muscle activity
- regulated by a lot of factors
- stress relaxation response allows increase in length without affecting ability to contract
- ATP
the activity is regulated by a lot of factors
- excitatory and inhibitory neurotransmitters (ANS)
- pH, local factors, CO2, temperature, ion concentrations, other
stress-relaxation response allows increase in length without affecting ability to contract
- smooth muscle increase tension initially when stretched but then after a minute or so, will release the tension
- walls of uterus, bladder, blood vessels, GI tract, etc.
ATP
- produced aerobically and anaerobically by glycolysis
- smooth muscle consumes much less than skeletal muscle
three muscle types: microscopic appearance and features
skeletal = striated
cardiac = striated
smooth = not striated (smooth)
three muscle types: location
skeletal = most commonly attached by tendons to bones
cardiac = heart
smooth = walls of hollow viscera, airways, iris and ciliary body of the eye, arrector pili, muscles of skin
three muscle types: fiber diameter
skeletal = very large (10-100um)
cardiac = large (10-20 um)
smooth = small (3-8 um)
three muscle types: fiber length
skeletal = 100um-30cm
cardiac = 50-100um
smooth = 20-200um
three muscle types: contractile proteins organized into sarcomeres
skeletal = yes
cardiac = yes
smooth = no
three muscle types: sarcoplasmic reticulum
skeletal = abundant
cardiac = some
smooth = small amount
three muscle types: transverse tubules present
skeletal = yes
cardiac = yes
smooth = no
three muscle types: auto rhythmicity
skeletal = no
cardiac = yes
smooth = yes, in a single unit smooth muscle
three muscle types: source of Ca2+ for contraction
skeletal = sarcoplasmic reticulum
cardiac = sarcoplasmic reticulum and extracellular fluid
smooth = sarcoplasmic reticulum and extracellular fluid
three muscle types: regulator proteins for contraction
skeletal = troponin and tropomyosin
cardiac = troponin and tropomyosin
smooth =calmodulin, and myosin light chain kinase
three muscle types:
skeletal =
cardiac =
smooth =
three muscle types: speed of contraction
skeletal = fast
cardiac = moderate
smooth = slow
three muscle types: nervous control
skeletal = voluntary (somatic nervous system)
cardiac = involuntary (autonomic nervous system)
smooth = involuntary (autonomic nervous system)
three muscle types: contraction regulated by…
skeletal = acetylcholine released by somatic motor neurons
cardiac = acetylcholine and norepinephrine released by autonomic motor neurons
smooth = acetylcholine and norepinephrine released by autonomic motor neurons; several hormones; local chemical changes; stretching
three muscle types: capacity for regeneration
skeletal: limited, via satellite cells
cardiac: limited, under certain conditions
smooth: considerable, via pericytes (compared with other muscle tissues, but limited compared with epithelium)
hypertropy
- enlargement of existing cells (increase in size of cells and increase in number of myofibrils)
- occurs in skeletal, cardiac, and smooth muscles
can help repair damaged tissue
hyperplasia
increase in the number of cells = myofibers
- occurs via cell division
- can occur in limited types of smooth muscle
- some literature records of hyperplasia after muscle damage in skeletal mucle
muscle pathologies
atrophy, dystrophy, and hypertrophy
