C3 - HMS - Skeletal Muscle Flashcards
Where is muscle derived from?
Embryonic mesoderm
What is a fascicle?
A bundle of muscle fibres within the perimysium (connective tissue)
What is a muscle?
Bundle of fascicles surrounded by the epimysium (connective tissue)
What is a cell with many nuclei described as?
Coenocytic (if nuclei results from mitosis)
Syncytium (if nuclei results from fusion of many cells)
((MUSCLE FIBRES ARE BOTH)
What are thick + thin myofilaments usually?
Thick - Myosin
Thin - Actin
How long roughly is a sarcomere?
3 micrometers
Do the lengths of actin and myosin change?
NO
SLIDING FILAMENT THEORY OF MUSCLE CONTRACTION
What is the A band?
Entire length of Myosin so also a bit of Actin.
SLIDING FILAMENT THEORY OF MUSCLE CONTRACTION
What is the I band?
Actin up to the start of myosin
SLIDING FILAMENT THEORY OF MUSCLE CONTRACTION
What is the H zone?
JUST myosin
SLIDING FILAMENT THEORY OF MUSCLE CONTRACTION
What happens to the A band?
Same length
SLIDING FILAMENT THEORY OF MUSCLE CONTRACTION
What happens to the I band
Shortens
SLIDING FILAMENT THEORY OF MUSCLE CONTRACTION
What happens to the H zone
Shortens
How do nervous impulses cause muscles to contract?
In a process called ‘excitation-contraction coupling’.
What is the molecular mechanism of muscle contraction described by?
Sliding filament theory
What is meant by a Neuromuscular Junction?
Where motor neurones synapse w/ muscle fibres.
Describe the motor end plate at a NM junction
Folded to give large SA
Has receptor proteins for Acetylcholine
Describe what happens when an AP arrives at a NM junction
Vesicles of NT acetylcholine are released into synaptic cleft to then diff. across to bind to receptor proteins on motor end plate = Na+ channels to open = DEPOLARISES sarcolemma.
Sarcolemma carries depolarisation AWAY to the rest of the myofibril.
The ‘T tubule’ carries depolarisation deep into microfibril.
Sarcoplasmic reticulum releases Ca2+ = muscular contraction.
When does the sequence of the sliding filament theory repeat until?
Until the Ca2+ ions (ions that expose the myosin binding sites on the actin) are all actively pumped back into the sarcoplasmic reticulum.
Give an example of slow twitch (Type 1) muscles in humans
Back muscles + soleus muscle have about 80% slow twitch fibres.
Give an example of fast twitch (Type 2) muscles in humans
Eye muscles have about 85% fast twitch fibres.
Physiological features of slow twitch muscle fibres
Contract slowly
Contract for longer time before relaxing
Longer time before fatigue
Give 2 myofibril features of fast twitch muscle fibres
Few mitochondria
High density of myofibrils
Describe the respiration of slow twitch muscle fibres
Aerobic
High density of capillaries to deliver O2
Little glycogen as blood brings glucose
High conc. of myoglobin so O2 available even at low O2 pp.
Little lactate made
Describe the respiration of fast twitch muscle fibres
Anaerobic
Low density of capillaries as little O2 needed
High glycogen store to generate glucose for glycolysis.
Low conc. of myoglobin as no need for O2 store.
Lactate removed quickly by oxidation to pyruvate or reversion to glucose.
Colour difference of muscle fibre types
Slow twitch = Dark due to rich blood supply + high myoglobin con.
Fast twitch = Light due to little blood + low myoglobin conc.
What are the 2 types of fatigue?
Neural (when nerves initiating contraction can’t generate a sustained signal)
Metabolic (i.e shortage of substrates to provide energy, i.e glucose OR accumulation of metabolites i.e lactate)
Define a cramp
A severe, involuntary muscle contraction that can occur in striated or non-striated muscle.
How can skeletal muscle cramps be caused?
By fatigue as the lactate build up can inhibit the Cl- effect but not the K+ effect, so muscles would tend to contract, leading to cramp.
What does the amount of muscle glycogen store depend on?
Physical training
Basal metabolic rate
Eating habits
How can ‘Hitting the wall’ be avoided? (3)
High glycemic index foods
Endurance training so that slow twitch muscle fibres become more efficient + use fats rather than glycogen for energy.
CHO loading
Why is fat harder to transport in the blood than glycogen?
Non-polar and the oxidation of fat reserves requires more O2 than the oxidation of glycogen.
Physiologists conducting experiments used tissue from the same organism. Suggest factors that would need to be controlled.
Temp of solution.
pH of solution
Conc. of solution
Same muscle type.
Why might no tension be generated
Because the actin + myosin filaments don’t overlap so no cross-bridges can form to enable contraction.
State 3 roles of ATP in muscle contraction
Actively pumps Ca2+ back into sarcoplasmic reticulum = muscle relaxes
ATP binds to myosin heads = erect high energy state.
Release of energy from hydrolysis of ATP causes change in shape of myosin cross bridge, resulting in a bending action = POWER STROKE
Where do calcium ions come from?
Sarcoplasmic reticulum, from ‘T’ tubules
What is the role of calcium ions?
Bind to troponin + change shape = tropomyosin changes position.
= Exposing myosin binding sites on actin.
= Heads on myosin can now attach too actin.
What is the mechanism of muscle contraction called?
Ratchet mechanism
What is myosin’s functional role in muscle movement
Has moveable head that provides a power stroke when activated.
Rigor mortis is a state of partial contraction of the muscle that occurs after death. During rigor mortis, the muscles are locked and the body is stiff.
Suggest why muscle enters this state
Because there’s no longer ATP to provide energy to change the shape of the myosin cross bridge.
What is the process in the sliding filament hypothesis
Actin binding sites are blocked by tropomyosin + troponin.
B4 muscle contraction, ATP binds to myosin heads = erect high energy state.
Arrival of AP = release of Ca2+ from sarcoplasmic ret.
Ca2+ binds to troponin + causes blocking molecules to move so that myosin binding sites on actin are exposed.
Myosin heads attach to binding sites on actin filament.
Release of energy from hydrolysis of ATP causes change in shape of myosin cross bridge, resulting in a bending action = POWER STROKE
== actin fil. slide past myosin fil.
New ATP attached to myosin, releasing them from binding sites + reprising them for repeat movement. They become attached further along actin chain as long as ATP + Ca2+ are available.
What does muscle contraction require?
Ca2+ and ATP
Define synergists
Muscles that assist the agonist + may be involved in the fine-tuning of the direction of the movement.
What is the Muscle spindle?
Where can it be found?
A stretch receptor located in skeletal muscle, parallel to muscle fibres.
What does the muscle spindle do?
Stimulated in response to sustained or sudden stretch on the central region of its specialised intrafusal fibres.
Sensory info from muscle spindle is relayed to spinal cord.
Motor response adjusts degree of stretch of the muscle. = Help in coordination + efficiency of contr.
Why are muscle spindles important?
Maintenance of muscle tone, postural reflexes + movement control.
What is the role of PC in providing energy for muscle contraction?
Produces ATP
Are slow twitch muscle fibres found near the surface or deeply situated?
Deeply situated
Damaged muscle fibres have an increased mRNA conc. and a higher rate of O2 consumption, at rest, than undamaged muscle fibres.
Explain the increased mRNA conc.
Proteins need repairing so protein synthesis is required.
== More transcription + translation i.e pf troponin or myosin
Damaged muscle fibres have an increased mRNA conc. and a higher rate of O2 consumption, at rest, than undamaged muscle fibres.
Explain the higher rate of O2 consumption
Rest = aerobic resp which requires O2 so more ATP produced.
= For condensation formation of peptide bond formation of extra mRNA
How does the body provide the muscle with more O2 to meet increased O2 consumption?
⬆️ HR, breathing + ventilation rate
Vasoconstriction/dilation
What is the effect of the increase in lactate levels in the muscle?
⬆️ acidity = contractile proteins become less sensitive to Ca2+ = ⬇️ ability to contract
Suggest why during prolonged exercise, i.e marathon, the blood urea conc increases
aa are deaminated in liver == ammonia is converted to urea whilst remainder is used in respiration as another source of energy
