Muscle 1 - 3

Question 1

skeletal muscle is responsible for:

Answer 1

voluntary movement of bones that underpin motion
control of inspiration by contraction of diaphragm
skeletal muscle pump - contraction of muscle helps with venous return to the heart

Question 2

sarcomere is made of

Answer 2

actin and myosin filaments

Question 3

sarcomere lines and bands (5)

during contraction:

Answer 3

Z line
I band
A band
M band
H band
during contraction - I band shortens, A bands are fixed and stay the same

Question 4

Z line

Answer 4

anchoring point for adjacent sarcomeres

Question 5

I band

Answer 5

actin fibres

light

Question 6

A band

Answer 6

mysoin and actin
overlapped - crucial for contraction
darkest
1 myosin for 6 actin filaments

Question 7

M band

Answer 7

where myosin projects out

Question 8

H band

Answer 8

just myosin

dark

Question 9

why does skeletal muscle look striated

Answer 9

due to how muscle reacts to polarised light

Question 10

intiating contraction

Answer 10

release of ACh at NMJ initiates action potential in plasma membrane
wave of depolarisation passes along sarcolemma and through t tubule network to reach interior of cell
in skeletl muscle, ER is specialised = sarcoplasmic reticulum
t tubule runs near 2 areas of SR forimg triad
depolarisation triggers an increase in intracellular calcium
number of muscle fibres stimulated depends on control needed
depolarisation travels through sarcolemma, along t-tubules and deep into cells
triad junction is between A and I bands

Question 11

Cross bridge formation in muscles

Answer 11

• ATP dependant process
  1 - rigid actin and nyosin are tightly bound, no ATP
  2 - ATP binds to myosin head, changes tightness of binding, myosin head dissociates from actin
  3 - ATP –> ADP + Pi, gives conformational change in shape of myosin head, ‘resting state’, extends limb
  4 - head can interact with actins further down chain, it binds and forms weak cross bridge
  5 - phosphate is released = strong cross bridge
  6 - conformational change in myosin head, causes power stroke, myosin back upright and pulls on actin so filaments slide past each other
  7 - ADP released, ready to start again
• each thick filament contains approx 300 myosin heads
• each head cycles 5 times a second

Question 12

summation of skeletal muscle

type = frequency

Answer 12

single muscle twitch = low frequency stimulation
temporal summation = inc freq before muscle has had change to relax (summation)
fused tetanus = contracted state is linked to recycling of Ca
contraction and relaxation is often slower than actual action potential

Question 13

classes of muscle fibres (3)

Answer 13

slow oxidative = type I
fast oxidative = type IIa
fast glycolytic = type IIx/IIb

Question 14

Slow oxidative muscle fibres - type I
fatigue
colour
metabolism
glycogen content
ATP synthesis
mitochondria
muscles

Answer 14

resistant
red
oxidative
low
aerobic
high
soleus (slow twitch)

Question 15

Fast oxidative muscle fibres - type IIa
fatigue
colour
metabolism
glycogen content
ATP synthesis
mitochondria
muscles

Answer 15

resistant
red
oxidative
abundant
aerobic
higher 
gastrocnemius (fast twitch)

Question 16

Fast glycolytic muscle fibres - type IIx/IIb
fatigue
colour
metabolism
glycogen content
ATP synthesis
mitochondria
muscles

Answer 16

fatiguable
white
glycolytic 
high 
anaerobic
fewer
biceps brachii

Question 17

Comparison of muscle fibres

- type I

Answer 17

very resistant to fatigue
control posture e.g. calf muscle
relies on oxidative phosphorylation
advantage = can generate force for a long time, generates some force, slowly

Question 18

Comparison of muscle fibres

- type IIa

Answer 18

for power
running / walking 
frequency needed to get to tetanus is higher
fatugues quicker
rapid generation of force

Question 19

Comparison of muscle fibres

- type IIx

Answer 19

biceps etc
tires fastest
rapid generation and rapid drop of force
high freq for tetanus
can't keep gneration of force for a long time

Question 20

Slow vs Fast twitch fibres

Answer 20

slow fibres = half diamete of fast, take longer to contract after nerve stimulation
fast fibres = 10 miliseconds or less to contract

Question 21

Neuromuscular junctions and inhibitors - muscle

Answer 21

calcium increase causes formation of vesicles so ACh can be released in synaptic cleft
depolarisation of axon = driven by Na channels, Na channels close, K channels open to bring mem potential back to resting
e.g. tetradotoxin inhibits Na channels = no depol = no action pot generated
e.g. dendrotoxin keeps membrane depolarised = continued release of ACh

Question 22

mechanism of botulinum toxins

Answer 22

most common casue of food poisoning
muscle weakness - paralysis - death
symptoms = dry mouth, diarrhea, paralysis
cleaves SNARE complex required for exocytosis of ACh in ANS
cant fuse vesicles to membrane
ACh cant be released = paralysis

Question 23

clinical use for botulinum toxin

Answer 23

treatment of cross eyes and uncontrolled eye movements

botox ( toxin A )

Question 24

aerobic endurance training

Answer 24

sustained, low level exercise
stimulation of slow fibres
conversion of IIx into IIa
increased fatigue resistance, blood capillaries
no change in muscle strength

Question 25

anaerobic endurance training

Answer 25

brief, intense exercise e.g. weight lifting stimulation of fast fibres no change in number of muscle fibres enlargement of myofibril size by addition of new myofilaments causes increased diameter of muscle fibre = hypertrophy

Question 26

types of energy delivery (3)

Answer 26

``` immediate non oxidative oxidative during initial 2 mins, body relies on 'stored energy' and anaerobic glycolysis stores have to be re - filled at the end ```

Question 27

immediate energy delivery

Answer 27

muscle cells have reserves of ATP and phosphocreatine ADP + PCr (using creatine kinase) = ATP + creatine as ADP accumulates: ADPs join together to form ATP and AMP using adenyl kinase build up of ADP, AMP and Pi will stimulate metabolic pathways involved in energy productions creatine = recycled into Phosphocreatine into mitochondria at rest

Question 28

non oxidative energy delivery (anaerobic)

Answer 28

using glycolysis muscle fibres store glycogen - 300-400g substrates enter glycolysis ar 2 points glycogenolysis of glycogen produces glucose-1-phosphate - converted into glucose-6-phsophate = enters glycolysis at reaction 2 - uptake of glucose from blood by GLUT4, glucose enter glycolysis pathway pyruvate produced, pyruvate - converted to lactic acid/lactate - process is very inefficient - 2 x ATP molecules per glucose - H+ from lactic acid lowers cell pH = muscle fatigue used at start of exercise/peak activity advantage = produces ATP in absence of O2 disadvantage = ATP yield low and toxic products made

Question 29

oxidative energy delivery (aerobic)

Answer 29

as tissue O2 delivery increases, energy production via oxid phos is stimulated process is slower but more efficient = 30 molecules of ATP per glucose molecule glucose sourced from blood, following breakdown of glycogen stored in liver lactate converted back into pyruvate - feeds oxid phos type IIx fibres release lactate into circulation - can enter other skeletal muscle cells or utilised by liver

Question 30

extended periods of exercise

Answer 30

lactate and alanine used by liver to generate new glucose during exercise - lactate cna be released from non exercising muscles, body acts to redistribute glycogen stores mobilisation of non muscle lipids = increase in circulating fatty acids - taken by muscle breakdown of triacylgylcerols stored in muscle cells generate ATP through aerobic metabolism in mitochondria or via glycolysis (anaerobic) in cytoplasm = 38 x ATP at ideal conditions

Question 31

muscle fatigue

Answer 31

inability to maintain desired output, decline in force and velocity of muscle shortening

Question 32

central fatigue

Answer 32

minor factor in trained exercise | brain is telling us to stop

Question 33

types of peripheral fatigue (5)

Answer 33

``` high frequency low frequency ATP depletion lactic acid build up glycogen depletion ```

Question 34

high frequency fatigue

Answer 34

altered Na/K cell balance, relevant more so to type II muscle fibres

Question 35

low frequency fatigue

Answer 35

decreased release of calcium from sarcoplasmic reticulum = more apparent at low level stimulation - type I fibres

Question 36

ATP depeletion

Answer 36

intense stimulation can cause large drops in ATP near sites of cross bridg formation and ATPases

Question 37

lactic acid build up

Answer 37

high rates of lactate production leads to cellular acidification

Question 38

Cardiac muscle

Answer 38

specific to heart cardiomyocytes also striated like skeletal muscle myocytes are shorter and more balanced, join together at intercalated disks electrical coupling between adjacent myocytes at intercalated disk by gap junctions action potential initiated in pacemaker cells of Sino-atrial node and propagates between cells via gap junctions

Question 39

Smooth muscle

Answer 39

involved in mechanical control of organ systems e.g. digestive, urinary and reproductive system and control of blood vessels and airway diameter control of smooth muscle more complex, cna involve circulating hormones, ANS input or inflammatory mediators e.g. histamine

Question 40

2 classes of smooth muscle

Answer 40

multiunit - electrical isolation of cells allows finer motor control unitary - gap junctions permit co-ordinated contraction non striated, multiple actin fibres join at 'dense bodies' and thick filaments intersperse around thin filaments large variations in action potential depending on muscle type, some cells can't generate action potenitals but respond to graded changes in membrane potential - has impact on ion channels, allows Ca in or K out, can control muscle contraction

Question 41

mechanisms for increasing intracellular calcium | - in skeletal muscle

Answer 41

excitation - contraction coupling known as triad, at AI barrier depolarisation activates L type Ca channels in the t tubule membrane = 2 effects 1 - leads to opening of L type Ca channels and influx of calcium into cell 2 - causes a mechanical tethering between L type Ca chanels in t tubule and Ca release channels (aka ryanodine receptors) in SR membrane = muscle contraction Ca release channels in SR open and Ca moves into cytoplasm

Question 42

mechanisms for increasing intracellular calcium | - in cardiac muscle

Answer 42

excitation - contraction cardiac muscle does have t tubules but only close to on branch of SR = dyad lie at Z line region mo mechanical tethering between voltage gated Ca channels in t tubule to ryanodine receptors in SR influx of Ca through t tubule channels activates ryanodine receptors = calcium induced calcium release (CICR) needs source of extracell calcium for contraction to occur

Question 43

removal of calcium from cytoplasm:

Answer 43

terminates muscle contraction 1 - across cell mem by plasma mem calcium ATPase (PMCA) or electrogenic Na/Ca exchanger (NCX) 2 - back into SR via sarco-endoplasmic reticulum ATPase

Question 44

mechanisms for increasing intracellular calcium | - smooth muscle

Answer 44

excitation - contraction smooth muscle lacks t tubule and triad/dyad structures, instead shallow invaginations = caveolae peripheral SR - encircles caveolae central SR - runs through cell change in mem potential = action potenital can activate L type Ca channels leads to CICR via activvation of ryanodine receptors in SR membrane activation of GPCR leads to IP3 production and sitmulation of IP3 receptors in SR membrane

Question 45

sarcomere contraction

Answer 45

``` similar to skeletal and cardiac troponin couple: TnC = calcium binding complex TnT = interacts with tropomyosin TnI = inhibits actin binding sites ```

Question 46

role of calcium and troponin in skeletal and cardiac muscle in cross bridge formation

Answer 46

inc Ca in cell means it binds to troponin complex = conformational change moves tropomyosin and TnI = reveals actin binding sites contraction continues whilst Ca levels are high Ca drops = comes off complex and shifts tropomyosin back covers actin binding site = contraction stops

Question 47

contraction in smooth muscle

Answer 47

NO TROPONIN IN SMOOTH MUSCLE 2 other proteins - calponin and caldesman, tonically inhibit interaction of myosin and actin Ca binds to calmodulin = myosin light chain kinase (MLCK) activated, which phosphorylates myosin head and activates it activation of MLCK removes inhibtory effects of calponin and caldesmon facilitating cross bridge formation and contraction to stop contraction - need to de-phosphorylate MLC which involves MLCP - myosin light chain phosphotase