Lecture 9- Muscle tissue introduction Flashcards
‘myos’
muscle
myalgia
muscle pain
myasthenia
weakens the muscle
myocardium
muscular component of the heart
myopathy
any disease of the muscles
myoclonus
sudden muscle spasm
myoclonus
sudden muscle spasm
two types of muscle
striated and non-striated
striated
skeletal muscle
cardiac muscle
non-striated
smooth muscle
skeletal muscle is under
voluntary control
nerve muscle interactions in skeletal muscle
direct nerve-muscle communication
cardiac muscle is under
involuntary control
nerve-muscle interaction in cardiac muscle
indirect nerve-muscle communication
is myoglobin present in striated muscle
YES
is myoglobin present in non-striated muscle
NO
is smooth muscle under involuntary control
NO
nerve-muscle communication in smooth muscle
No direct nerve-muscle communication
myoglobin is a what colour protein
red
myoglobin is structural similar to
Hb (single unit)
myoglobin function
oxygen string molecule which provides oxygen to working striated muscle
at low pH Hb ..
gives up oxygen to myoglobin
when striated muscles dies (necrosis)
myoglobin is released onto the bloodstream
what removes myoglobin from the blood
the kidneys
- excreted in the urine- myoglobinurea
excess myoglobin in the blood can
damage kidneys
sarcolemma
outer membrane of muscle cell
sarcoplasm
cytoplasm of a muscle cell
sarcosome
mitochondrion
sarcomere
contraction unit in striated muscle
sarcoplasm retioculum
smooth endoplasmic reticulum of a muscle cell 9high [Ca2+]
what is the contraction unit in striated muscle
the sarcomere
which types of muscle are under voluntary control
skeletal muscles
which types of muscle have dire nerve- muscle communication
skeletal
each muscle fibre contains
myofibrils
myofibrils are made up of
repeating subunits called sarcomeres
myofibrils are made up of which proteins
- actin
- myosin
- tropomyosin
thin filaments
composed of actin
thick filaments
composed of myosin
thin and thick filaments
partially overlap and form functional units called sarcomeres (why myofibrils ahem dark and light bands- striated)
how do myofibrils bring about muscle contraction
via the sliding-filament theory
the sarcomere A band
dark band composed of thick filaments and some thin filaments
the sarcomeres H band
centre of the A band- only thick filament present
I band
light bands composed of actin (thin) alone
Z band
found at the centre of I bands
Z bands are made of
alpha-actinin
- anchors actin filaments and acts as a boundary between sarcomere units
z to z=
width of sarcomere
contraction energy source
glycogen- glucose storage meolcile
what provides phosphate for ADP-ATP
creatine phosphate
glycogen is converted to ATP through
glycolysis and aerobic resp
contraction of sarcomere powered through
hydrolysis of ATP–> ADP and inorganic phosphate
when muscle are at rest
there is an incomplete overlap between the thick and thin filaments with some areas containing only one of the two types
when muscle are at rest the ATP molecule is attached to
globular myosin head on myosin filaments
when muscles are contracting
the sarcomeres shorten in length due to the thick and thin filaments sliding over each other resulting in greater overlap between the filaments and a narrowing of the H zones
- the I bands will come closer together
- Size of the A band will stay the same
MOA: muscles contraction
- Ca2+ binds to troponin C on the actin filament (thin)- causing a conformational change in troponin
- This causes Tropomyosin to move allowing interaction of actin and myosin (tropomyosin previously blocking myosin binding site on actin)
- ATP molecule attached to myosin head is hydrolysed, changing its conformation
- Myosin head binds actin and forms cross bridge and ‘power stroke occurs
- Calcium is transported back to SR by (SERCA ATPase) and the muscle relaxes due to active site on actin being blocked by tropomyosin once again
outline Excitation-contraction coupling (long)
- Action potential at NMJ causes Ach release at synaptic cleft- depolarises the sarcolemma
- Action potential propagated down t-tubule of muscle
- Depolarisation triggers conformation change in L-type channels which opens Ryanodine receptors
- Ryanodine receptors open causing calcium from the SR to flood into the sarcoplasm
- Ca2+ binds to troponin C on the actin filament (thin)- causing a conformational change in troponin
- This causes Tropomyosin to move allowing interaction of actin and myosin (tropomyosin previously blocking myosin binding site on actin)
- ATP molecule attached to myosin head is hydrolysed, changing its conformation
- Myosin head binds actin and forms cross bridge and ‘power stroke’ occurs
- Calcium is transported back to SR by (SERCA ATPase) and the muscle relaxes due to active site on actin being blocked by tropomyosin once again