Session 7 Flashcards
What are the derivations of muscle related words?
myalgia, muscle pain myasthenia, weakness of the muscle myocardium, muscular component of the heart myopathy, a disease of the muscles myoclonus, a muscle spasm
Describe the muscle cell hierarchy
striated
skeletal-
myoglobin present, voluntary control, direct nerve to muscle communication
heart-
myoglobin present, involuntary control, indirect nerve to muscle communication
non striated
smooth-
myoglobin absent, involuntary control, no nerve to muscle communication
What is myoglobin?
red protein that is structurally similar to a single subunit of haemoglobin
oxygen storing molecule, has a higher affinity for oxygen than haemoglobin and provides oxygen to working striated muscle
haemoglobin gives up oxygen to myoglobin, especially at low pHs
when striated muscle dies, the myoglobin is released into the bloodstream and the urine
this can cause renal damage
if many striated muscles break down then the collecting tubes and ducts in the kidneys can become blocked and the kidneys can become ischemic
What are the muscle cell components terminology?
sarcolemma- outer membrane
sarcomere- the contractional unit in striated muscle
sarcoplasmic reticulum- smooth endoplasmic reticulum
sarcoplasm- cytoplasm
sarcosome- mitochondrion
What is the structure and function of skeletal muscle?
3 parts to the structure
epimysium- surrounds the whole tissue/ muscle
perimysium- surrounds each fascicle
endomysium- surrounds individual muscle fibres
function, to contract
Describe the direction of movement
always in the direction of the muscle fibre
tension is created at the centre of the tendon
movement is created at the insertion of the tendon
Describe the muscles in the mouth
extrinsic muscles to the tongue allows for protruding of the tongue, retraction of the tongue and to move it side to side
the geniohyoid muscle permits us to stick out our tongue
(genio means chin so the muscle in the chin)
the intrinsic muscles within the tongue allow us to change shape of the tongue but not position as they are not attached to a bone
Explain the skeletal muscle histology including the fascicles and mitochondria
perimysium is a connective tissue carrying nerves and blood vessels
the dark longitudinal streaks are mitochondria
the nuclei are peripheral in transverse section and in rows in longitudinal sections
Describe the capillary network surrounding skeletal muscle fibres
stain using dark red gelatine
long muscle fibres stain orange
thin muscle fibres have less blood
thick muscle fibres have more blood
Summarise the structure of skeletal muscles
striated muscle cells are called muscle fibres
each fibre contains multiple myofibrils
Describe the myofibril structure (including the components)
a band I band z line m line h zone actin myosin
What are the muscle contraction speeds?
slow
fast
intermediate
each fascicle has at least one of each
Describe the muscle fibre types, including the amounts of ATP
slow twitch: rich capillary supply aerobic many mitochondria and cytochromes high myoglobin levels red fatigue resistant endurance type activities standing and walking fatty acids as fuel lots of ATP and carbon dioxide produced
fast twitch type 2A: rich capillary blood supply aerobic many to intermediate mitochondria many cytochromes high myoglobin levels red to pink moderate fatigue resistant assist type 1 and 2B activities fatty acids and glycogen as fuel initially lots ion carbon dioxide then lots of lactate produced
fast twitch type 2B: poor capillary blood supply anaerobic low myoglobin levels few mitochondria and cytochromes white rapidly fatigue strength and anaerobic type activities jumping, running, sprinting glycogen as fuel (breaks down to glucose) lots of lactate and little ATP produced
Describe the structure cardiac muscle fibres
striated
centrally positioned nuclei
intercalated disks, allow for electrical and mechanical coupling with adjacent cells
branching
What is ANP and BNP?
ANP atrial natriuretic peptide
released by the atria
released in heart failure, eg congestive heart failure
BNP brain type natriuretic peptide
released by ventricles
released in heart failure, eg mitral valve disease
both act to reduce arterial pressure by decreasing the blood volume and the systemic valvular resistance
What is hypertrophy and hyperplasia?
hypertrophy
where the cells enlarge in the heart
hyperplasia
where the cells in the heart multiply
the heart can do both of these all the time, however hyperplasia can not occur in adulthood from puberty on as cardiac myocytes can’t multiply
Explain how the heart works
action potential (AP)
sinoatrial node (SA)
atrioventricular node (AV)
bundle of his (B)
AP in the SA
travels across the atrial wall from the SA to the AV
AP passes slowly thought the AV to give the atria time to contract
then passes rapidly down the B and divides into left and right bundle branches
AP is carried by the Purkinjie fibres in the branches to the ventricular walls
the rapid conduction from the B to the ends of the Purkinjie fibres allows the ventricular muscle cells to contract in unison, providing a strong contraction
Explain electrical transmission with the Purkinjie fibres
have:
abundant glycogen
sparse myofibrils
extensive gap junctions
because they are able to transmit the action potential so rapidly, you get synchronous contraction of the ventricles
How does cardiac muscle differ to skeletal muscle?
their nucleus is central not peripheral
sarcomere not so developed
few to no t-tubules in the sarcoplasmic reticulum
only one cell contractile type, the cardiomyocytes
cardiomyocytes communicate through gap junctions in the intercalated disk
Describe smooth muscle
no sarcomeres, no t tubules
capable of being stretched substantially
contraction still relies on actin-myosin interactions
contraction is slower and more sustained, requires less ATP
may remain contracted for hours or days
respond to stimuli in form of nerve signals, hormones, drugs or local concentrations of blood gases
numerous caveolae- small cave like invaginations
in cytoplasm there is myofilaments and intermediate filaments which upon receiving a signal, will gather in dense bodies
How is smooth muscle distributed?
often forms contractile walls of passageways of cavities, eg in the gut
the role of this is to modify volume
clinically important (as SMC have a mind of their own) in disorders such as; incontinence painful menstruation bronchospasm high blood pressure abnormal gut motility
Explain how the smooth muscle cells in the gut work
most SMC are innervated by the autonomic nervous system fibres that release neurotransmitters from varicosities into a wide synaptic cleft
the synaptic cleft is wide to allow the biggest chance at sending as much neurotransmitter over as possible
SMC activated when receiving neurotransmitter
What are the types of muscle tearing?
smooth
skeletal
cardiac- tear here can be catastrophic and lead to death
Explain the muscle repair of each type of muscle
skeletal
the cells cannot divide but can regenerate by mitotic division of satellite cells, so that hyperplasia follows the injury
satellite cells can also merge with existing cells so you get hypertrophy and increased muscle mass
cardiac
cells are incapable of repair
the fibroblasts invade and divide and lay down scar tissue
smooth
cells retain their mitotic activity so can form new SMCs
this is particularly evident in the uterus where the muscle wall becomes thicker by hypertrophy
Compare cardiac and smooth muscle, their similarities and their differences
similarities central nuclei only one contractile unit act as syncytium communicate through gap junctions
differences
no troponin in smooth muscle
no sarcomeres in smooth muscle
specialised cells in cardiac muscle to allow for electrical conduction
Explain how the cardiac muscles contract
the action potential acts on the membrane and passes down into the T tubule in the sarcomere where it activates the DHP receptors
this pumps Ca into the sarcoplasmic reticulum and activates the ryanodine receptors to release Ca from the sarcoplasm reticulum so that Ca can interact with the contraction machinery in the sarcomere
Explain, if not already done so, the ultrastructure of the smooth muscle cell
s
How do the smooth muscle cells contract? Explain
hormone binds to its receptor on sarcolemma
this changes a second messengers activity which results in Ca being released by the SER and opens the voltage gated Ca channel so there is an influx of Ca into the cell
calcium binds to a protein called calcitonin forming a Ca- calcitonin complex
myosin light chain kinase (MLCK)) then binds to the complex to create an activated enzyme which goes on to phosphorylate myosin light chains so the two heads on the chain are now able to bind to actin and cause contraction
when Ca concentration decreases, myosin light chain is acted on by phosphatase which inactivates the myosin and causes it to warp up into a circle
What is the kranocyte?
might be a connective tissue cell
resides over the Schwann cell
might anchor nerve to the muscle
other functions unsure of
What are the events leading to skeletal muscle cell contraction?
- nerve impulse travels along the axon and arrives at the neuromuscular junction
- action potential prompts release of ACh into synaptic cleft causing local depolarisation
- voltage gated Na channels open and Na enters cell
- general depolarisation spreads over membrane and into T-tubules
- voltage sensor proteins of T-tubule membrane change their conformation
- voltage gated Ca channels open
- Ca ions are rapidly released into sarcoplasm
- Ca binds to TnC subunit of troponin and contraction cycle initiated
- Ca ions are returned to the terminal cisternae of SER
What is myasthenia gravis?
endplate invaginations reduced
Describe myosin and actin
individual myosin molecule has a rod like structure from which two heads protrude
each thick filament consists of many myosin molecules, whose heads protrude at opposite ends of the filament
actin has two protein components
F-actin fibres
G-actin globules
actin is bound to tropomyosin, troponin complexes are also bound to the tropomyosin
together they make the tropomyosin- troponin complex that is the thin filament
Describe the functional contraction unit of a myosin filament
tropomyosin molecules coil around the actin helix. reinforcing it
a troponin complex is attached to each tropomyosin molecule
in the centre of the sarcomere the thick filaments are devoid of myosin heads
the myosin heads extend up towards the actin filaments in regions of potential overlap
What is the role of Ca in the contraction mechanism?
when calcium binds to TnC a conformational change moves the tropomyosin molecule away from actin’s binding sites
allows myosin to bind to actin
the tropomyosin sits in the cleft of G-actin spheres- supports the TnC protein
Describe the sliding filament theory
contraction begins when bound ATP to the myosin is hydrolysed to ADP and Pi
this causes the myosin head to extend and attach to the binding site on actin, forming a cross bridge
the working/ power stroke is triggered, allowing myosin to pull the actin filament towards the M line by shortening the sarcomere
ADP and Pi are released during the power stroke and myosin remains attach to actin until ATP binds, freeing myosin to either go through another cycle of binding and contraction or remain unattached to allow for relaxation of the muscle
How long are the actin and myosin filaments?
the lengths of the myosin and actin remain the same during the contraction
the z lines come closer together
Describe what is meant by origin and insertion of muscles
the part of the bone that has greater mass and is more stable during contraction than the muscle’s insertion- ORIGIN
the INSERTION is the structure the muscles attach to, tends to be moved by contraction
can be bone, tendon or connective tissue
greater motion than origin during contraction
Explain the muscle roles in movement
agonists, antagonists, synergists, neutralisers and fixators
agonists- prime movers antagonists- oppose prime movers synergists- assist prime movers neutralisers- prevent the unwanted actions of the agonist fixators- hold a body part immobile whist another body part is moving
Explain the different types of levers in the body
first class- effort and load are at opposite ends eg flexion of head second class- effort and fulcrum (pivot) at opposite ends eg plantar flexion of foot third class- load and fulcrum are at opposite ends most common in body - mechanical disadvantage as if the load is too heavy, you can't produce enough effort to lift it
Explain the skeletal muscles as levers
muscles with similar actions group together
they are separated by thick dense fascia
separated into compartments based on location:
anterior, posterior, medial and lateral
What is compartment syndrome?
trauma to one of the compartments causing internal bleeding with in turn exerts pressure on the nerves and blood vessels
treated with a fasciotomy and covered with a skin graft
typical symptoms include:
deep, poorly localised pain
aggravated pain with passively stretching the muscle
parasthesia
may feel tense and warm
prolonged capillary refill time
swollen shiny skin
What is muscle tone? How is it regulated?
muscle tone is defined as the tension in the muscle at rest
muscle strength is the ability of the muscle to contract and create tension in response to resistance
regulated by:
motor neurone activity
muscle elasticity
use
gravity
– healthy muscle is never fully relaxed
it retains the amount of tension and stiffness and it ready to react
improves with exercise
Describe the muscle remodelling
continual
replacement of contractile proteins is 2 weeks
if the rate of decay of contractile proteins and myofibrils is greater than the replacement- atrophy
if the rate of decay of contractile proteins and myofibrils is less than the replacement- hypertrophy
as the number of fibres decrease, the fascicle size decreases too
What is the mechanism behind muscle hypertrophy?
overstretching causes the a band and I band to stop engaging with each other
new muscle fibrils are produced
new sarcomeres are formed in the middle of existing sarcomeres
new muscle fibres are created from mesenchymal cells
it is thought that overstretching features in some cardiac pathologies
What is the mechanism behind muscle atrophy?
happens due to:
disuse, surgery and disease
diseases- loss of protein, reduced fibre diameter, loss of muscle power
nerve regeneration will occur but takes 3 months
50%of muscle loss by 80 years
What is Duchene Muscular Dystrophy?
X linked recessive disorder mutation in dystrophin gene absence of dystrophin causes: ca enters the cell taken up by mitochondria water follows mitochondria burst muscle cells die creatine kinase and myoglobin levels are extremely high in blood
muscle cells are replaced by adipose tissue
because the muscle cell bursts, the satellite cells die too and so cannot simply regenerate the muscle cells
symptoms related to skeletal muscles
What is creatine kinase?
an important enzyme used in metabolically active tissues
was used to signify a heart attack- now tend to use troponin-I assays
can also be released into the blood by damaged skeletal and brain tissues
raised levels in plasma can be due to:
- a fall
- rhabdomyolysis
- intramuscular injection
- acute kidney damage
- muscular dystrophy
- vigorous exercise
How can troponin assays be used as a diagnostic tool?
troponin I and T forms used as a marker for cardiac ischaemia (there are specific isoforms of cardiac T and I)
released from ischaemic cardiac tissue within the hour
measure within 20 hours for absolute accuracy
the smallest change in troponin levels in the plasma is indicative of a heart attack
quantity of troponin is not necessarily proportional to the degree of muscle damage
What is the effect of botox on the muscles?
the toxin blocks the neurotransmitter release at the motor end plate
causes non contractile state of muscle
used clinically to treat muscle spasms
when the toxin is released into the synaptic cleft, it can now be taken back through the nerves and into the CNS
What is malignant hyperthermia?
a severe reaction to anaesthetics (succinylcholine)
- autosomal dominant inheritance pattern, RyR1 gene
males > females
massive contractile fasciculation
- muscle rigidity caused by increase calcium release
- outcome of this is excessive heat and metabolic acidosis
increased muscle breakdown and hyperkalaemia
mortality risk 75% without treatment, 5% with treatment
