Muscles Flashcards
Types of striated muscle
Skeletal, cardiac
Types of non striated muscle
Smooth
What is myoglobin? (4)
Structure similar to subunit of haemoglobin
Higher affinity for oxygen than Haemoglobin
especially in acidic conditions
Doesn’t bond to CO2
Muscle cell components (5)
Sarcolemma - outer membrane
Sarcoplasm - cytoplasm
Sarcoplasmic reticulum - endoplasmic reticulum
Sarcosome - mitochondria
Sarcomere - contraction unit ONLY IN STRIATED
What is Rhabdomyolysis?
What will be released into the blood stream?
Striated muscle death, myoglobin released into bloodstream
K ions will be released too - show lysis
Myoglobin present in urine is… (3)
Myoglobinuria
Tea coloured
Can damage kidneys
What is it called when myoglobin is released into bloodstream?
Myoglobinaemia
What does type of movement in muscle depend on?
The direction of muscle fibre contraction
Movement is always…
Along direction of fascicle
3 connective tissue layers in muscle
Epimysium - around whole muscle
Perimysium - around fascicles
Endomysium - between muscle fibres
Continuous to tendon
Where is tension created
Origin tendon point (rigid)
Where is movement created?
Insertion tendon point
What are extrinsic muscles?
Give examples of them in action
- Insertions into Bone and cartilage
- Extrinsic muscles protrude the tongue, retract it and move it from side to side
What are intrinsic muscles?
Give an example of them in action
- Not attached to bone
- Intrinsic muscles within tongue are not attached to bone. They allow the tongue to change shape but not position – these aid swallowing
What muscle allows us to stick out the tongue
Geniohyoid muscle (genio means chin)
What do perimysiums do?
Connective tissue surrounding fascicle, lubricate
Carry nerves and blood vessels
Why can skeletal muscle appear different in microscopic image
Some will be transverse and some longitudinal cross sections
Fibres and their requirement for blood
Thin fibres need less blood
Thick fibres need more
What is a striated muscle cell called
Fibre
What does a muscle fibres contain
Many myofibrils
Thin vs thick filaments and their bands/stain
Actin - thin Myosin - thick I band - just actin so stains lighter H zone - just myosin (stains darker) A band is overlap of myosin and actin so stains DARK
What length is a sarcomere
Z line to z line
Feature of skeletal muscle
Abundant mitochondria between myofibrils
Nuclei are peripheral
The 3 Muscle contraction speeds and staining
Fast - light/white (limited mitochondria)
Intermediate - light red/pink
Slow - red (abundant mitochondria)
What kinds of contraction speed is in a fascicles
There is at least one of each in east fascicle
Slow twitch vs fast twitch fibres
Slow- lots of mitochondria so many cytochromes, good blood supply, high myoglobin contracts slower and for longer periods of time, endurance activities, lots of ATP, CO2
Fast- low mitochondria so low cytochromes, poor blood supply, low myoglobin, contracts fast and for short periods of time, sprinting, lots of lactate, little ATP
Motor units and fibres
Each type of fibre has its own motor units
ie fast do not share with slow
Cardiac muscle features
Central nuclei Striated Intercalated discs - gap junctions (electrical and mechanical coupling with neighbour cells) Form branches Glycogen around cell T tubules along Z line
ANP and BNP
Released from heart during failure
ANP - atrial, congestive heart failure
BNP - ventricular hypertrophy (cells get bigger) mitral valve disease
Explain ANP and BNP
BNP - causes vasodilation, lowers BP
ANP - acts on kidney, increases GFR, increases fluid into bladder, more fluid released into urine, lowers blood volume
Both - lower renin
Hypertrophy
Cells get bigger
Hyperplasia
Cells get multiplied
Atrophy
Smaller than normal heart
Describe conducting system of heart
Action potential
Atria; Sinoatrial node
To atrial ventricular node - slowly give atria time to contract
Bundle of His
Pass across bundle branches rapidly
Distributed very QUICKLY by purkinkje fibres to ventricular walls
Ventricles contract in unison - strong
Cardiac vs Skeletal
Both - striated
Cardiac - nucleus are centre, sarcomere not as developed, one contract cell type - cardiomyocyte, intercalated discs, own isotopes of Troponin I and T
Skeletal - peripheral nucleus, sarcomere,
Smooth muscle characteristics
Single large nucleus
Not striated, no sarcomere, no T tubules
Stretch
Actin and myosin
Slower contraction, less ATP
Numerous stimuli can stimulate - nerves, hormones, drugs, blood gases
Sheets, bundles and layers
Smooth muscle cell cave-like invaginations
Pinocytic caveolae
Ultra structure of smooth muscle cell
Actin connects to dense plaque Actin connects to myosin Myosin connects to another actin Actin connects to dense plaque Gap junctions 2 actin vs 1 myosin
Where is smooth muscle found
Contractile walls - vascular structures, respiratory tract, gut
Clinical disorders smooth muscle
Involuntary muscle High BP painful menstruation Lung disease Abnormal movements of gut (IBS) Incontinence
Gut smooth muscle example
Longitudinal and circular
Peristalsis
Mucosal
How are smooth muscles stimulated
Neurotransmitters from varicosities to wide synaptic cleft
What often happens to smooth muscles
Tear - mild, moderate, severe
Muscle repair for skeletal
Skeletal - cells themselves cannot, regenerated via mitosis of satellite cells (hyperplasia). Satellite cells can also merge together multiple cells - hypertrophy.
Muscle repair for cardiac
Incapable of regeneration
After damage, fibroblasts invade and lay scar tissue
Muscle repair for smooth and example
Repair themselves
Pregnant uterus
Purkinje fibres
Modified myocytes SPECIALISED Receive impulse from AV node transmit it to ventricle walls Lots of glycogen Lots of gap junctions
Cardiac vs smooth
Both - central nucleus, one contractile type (fast and slow in skeletal), syncytium (wave) gap junctions
Cardiac - specialised cells/routes (purkinje fibres for conduction), striated, intercalated discs
Smooth - no sarcomeres, not striated
Cardiac nerve supply and contraction
Nerve sits far away to allow neurotransmitter to spread (wave like)
Parasympathetic - slows down, straight to heart only to SA node
Sympathetic - speeds up, via spinal cord, cardiac nerve, to whole heart
Cardiac contraction
Receptor is activated by acetylcholine binding
Cause action potential
DHP voltage sensitive calcium channels open
Calcium flows through
Calcium binds to TN-C
Allows myosin-actin complex
Pulls actin towards M line
Smooth muscle nerve supply
Varicosities supply - sits far away neurotransmitter spreads (same as cardiac, wave like)
Neurotransmitter causes depolarisation, opens Ca voltage gated channels, calcium in, contraction
Contraction doesn’t stop until Ca decreases
Skeletal muscle nerve supply
Neuromuscular junction - nerve meets muscle at motor end plate Swellings on axon contain acetylcholine Nerve impulse releases it Binds to receptors on sarcolemma Action potential along muscle
Innervation ratio
More fibres per motor unit allow for more power, less allow for finer control
Kranocyte
Found at neuromuscular junction
Covers Schwann cell
Maybe anchors nerve to muscle cell
T tubules
Allow rapid transmission of action potential
Associated with sarcoplasmic reticulum and mitochondria
Skeletal muscle contraction (DETAIL IONS)
Nerve impulse arrives at neuromuscular junction
Acetylcholine is released to synaptic cleft
Sarcolemma LOCALLY depolarised
Voltage gated Na channels open, Na ions enter
Depolarisation of whole sarcolemma to T tubules
Voltage sensitive T tubule proteins conformational change
Voltage gated Ca channels open
Ca into sarcoplasm
binds to TnC subunit of troponin
Contraction
Ca ions return to sarcoplasmic reticulum
Myasthenia gravis
Skeletal muscle Autoimmune disease Antibodies block Ach receptor Smaller invaginations in synaptic cleft Reduced synaptic transmission Muscle weakness
Sliding filament theory outline
Cardiac, Skeletal
Myosin anchored to M line
Actin anchored to Z line (moves from each end)
Myosin and actin form cross bridges, myosin pulls actin
Muscle parts
Fibres, myofibrils, sarcomere
Sliding filament theory
ATP hydrolysed and binds - causes myosin head to extend (attached as ADP and Pi)
Attaches to binding site on actin - cross bridge
ADP pi detach
Power stroke pulls actin filament towards M line
Shortens sarcomere
Myosin remains attached until more ATP
Tropomyosin and troponin sliding filament theory
Controlled by calcium - stored in sarcoplasmic reticulum
Blocks cross bridge binding sites on actin
Calcium binds to troponin, displaces tropomyosin
Exposes binding sites
Cross bridge can be formed
How is calcium release controlled
Stored in sarcoplasmic reticulum Neurotransmitter released from neuron Bind to receptor Depolarisation - electrical impulse travels down T tubules Opens Ca channels Ions float to troponin
Myosin structure
Rod like
2 Heads protrude
Actin structure
2 protein
F-actin fibres
G actin fibres
Tropomyosin-troponin complex sits over actin binding sites
M line
Centre
Void of myosin heads
Actin pulled towards it during contraction
Roles of troponin and creatine kinase
TnC - calcium binding site
TnI - inhibits, binds tropomyosin and TnT to actin over binding site, dissociates when Ca attaches
TnT - moves tropomyosin
Creatine Kinase - produce ATP
Lengths of sections during contraction
Actin and myosin DO NOT CHANGE - overlap more
sarcomeres shorten
Innervation and contraction explained skeletal
Nerve impulse causes nerve to release acetylcholine to synaptic cleft
Acetylcholine binds to receptors on motor end plate
Action potential generated, travels down T tubules
Ca are released by Sarcoplasmic reticulum
Ca ions bind to TnC on tropomyosin-troponin complex
Exposes binding sites
ATP hydrolysis causes myosin to cock head and bind to actin
Releases ADP and Pi
Pulls actin towards M line - power stroke
Ca is taken up by sarcoplasmic reticulum
Tropomyosin slips back, covers binding site
Origin vs insertion
Origin - Bone, proximal (close to midline), more stable, greater mass
Insertion - muscle attaches, moved by contraction, distal, bone/tendon/connective tissue, more motion
Agonist
2 muscles working together, prime movers (main muscles responsible for movement)
Antagonist
Oppose prime movers (agonists)
Synergists
Assist prime movers (can’t act alone)
Neutralisers
Prevent unwanted movement that agonists can do
Fixators
Hold body part in place while another is moving
First class lever
See-saw Load on one end Effort downwards on other Fulcrum central Extension of head
Second class lever
Wheelbarrow Load ‘in wheelbarrow’ so central Effort one end Fulcrum at other end Standing on ball of foot
Third class lever
Fishing rod Effort in middle Load one end, fulcrum other Hard to perform Most common
How are skeletal muscles grouped together
In compartments
Similar actions, thick dense fascia
Location eg, anterior, posterior, lateral or medial
Compartment syndrome
Trauma to one compartment
Internal bleeding - exerts pressure on blood vessels and nerves
Compartment syndrome symptoms
Deep pain - not localised Aggravated by stretch Pins and needles (parathesia) Tense and firm compartment Swollen shiny skin Long time for capillary to refill (white skin for long time when pressed)
What are clinical markers of striated muscle death in blood
K ions, troponin (I, T and C), creatine kinase
Clinical markers for smooth muscle death
K ions
Name 5 muscular dysfunction
Duchene muscular dystrophy Rhabdomyolysis Myocardial infarction Botulism and organophosphate poisoning Malignant hypothermia
Duchene muscular dystrophy
X linked Recessive gene
Most Common
Mutation of dystrophin gene (joins sarcolemma to actin)
Absence of dystrophin
Dystrophin absence causes…
Excess calcium to enter cell
Calcium and water absorbed by mitochondria
Mitochondria burst
Muscle cell bursts (rhabdomyolysis)
Creatine kinase and myoglobin levels HIGH
Creatine kinase
Diagnose heart attacks (lots of enzyme = lots of damage)
Important in metabolically active tissues
Released into blood by damaged skeletal muscle
What can cause a rise in creatine kinase
Myocardial infarction Vigorous exercise Vaccination A fall Rhabdomyolysis Kidney injury (myoglobin not removed) Muscle wastage
Troponin assays…
Assess myocardial damage - cardiac isachaemia
Measure troponin (I and T) - specific isoforms in cardiac muscle - levels not proportional to damage
Measure within 20 hours
Botulism and Botox
Toxin produced by clostridium botulinum Blocks neurotransmitter release Causes paralysis of skeletal muscle Cosmetically for wrinkles Treat muscle spasm
Organophosphate poisoning
Pesticides
Inhibits Ach esterase
Ach activity stronger
Effects somatic and autonomic signalling
Symptoms of poisoning organophosphate (muscarinic)
SLUDGE Salivation Lacrimation (crying) Urination Defecation GI cramps Emesis (vomitting)
Symptoms of organophosphate poisoning (nicotinic)
MTWTF Muscle cramps Tachycardia Weakness Twitching Fasciculations
Malignant hyperthermia
Reaction to anaesthetics
Muscle rigidity lots of Ca
Hot and metabolic acidosis
Muscle breakdown (high k ions)
