Skeletal muscles are stimulated to contract by nerves and act as effectors (A-level only) Flashcards
Bones
Tendons attach skeletal muscles to bones.
The muscles work in a pair to move the bones.
A pair of muscles is called an antagonistic pair.
In an antagonistic pair, one muscle contracts when the other muscle relaxes.
Antagonist
The muscle that is relaxing is called the antagonist.
Which muscle in a pair is the antagonist can vary depending on the movement.
E.g. When you bend your arm, your tricep muscle relaxes (it is the antagonist).
When you straighten your arm, the tricep muscle contracts (it is the agonist).
Agonist
The muscle that is contracting is called the agonist.
Which muscle in a pair is the agonist can vary depending on the movement.
E.g. When you bend your arm, your bicep muscle contracts (it is the agonist).
When you straighten your arm, the bicep muscle relaxes (it is the antagonist).
Muscle fibres
Skeletal muscle consists of many bundles of muscle fibres.
Muscle fibres are long, specialised cells.
Sarcolemma
The membrane of muscle fibres is called the sarcolemma.
The sarcolemma folds inwards to the sarcoplasm (muscle fibre cytoplasm) at certain points.
The inwards folds are called transverse (T) tubules.
The tubules are very important in initiating muscle contraction.
Sarcoplasmic reticulum
The sarcoplasmic reticulum (SR) is an organelle in the sarcoplasm.
The SR is a store for calcium (Ca2+) ions. This is important in muscle contraction.
Mitochondria and nuclei
Muscle fibres also have many mitochondria and nuclei.
The mitochondria provide lots of ATP to power muscle contraction.
Myofibrils
Myofibrils are cylindrical organelles that run along the length of muscle fibres.
Myofibrils are the site of muscle contraction.
Myofibril components
Sarcomere
Myofilaments
Myosin filaments
Actin filaments
Sarcomere
Myofibrils are made of multiple units that run end-to-end along the myofibril.
These units are called sarcomeres.
The end of a sarcomere is called the Z-line.
Myofilaments
Sarcomeres are made from two types of myofilaments.
The two myofilaments slide past each other.
This movement is what makes muscles contract.
The two types of myofilaments are:
Thick myofilaments - made of myosin protein.
Thin myofilaments - made of actin protein.
Myosin filaments
Myosin and actin filaments are arranged in an alternating pattern in sarcomeres.
Thick myosin filaments overlap with the thin actin filaments at each end.
The overlapping region is called the A-band.
The region with only myosin filament is called the H-zone.
Actin filaments
Thin actin filaments only overlap with myosin filaments in the middle of the sarcomere.
The middle is called the M-line.
The region with only actin filament is called the I-band.
Sliding filament theory
The sliding filament theory explains how muscle contraction is coordinated in myofibrils.
Stages of sliding filament theory:
Depolariation of the sarcolemma
Contraction of the sarcomeres
Muscle contraction
Muscle relaxation
Depolarisation of the sarcolemma
Muscle contraction is initiated when an action potential arrives at the muscle cells.
The action potential depolarises the sarcolemma.
Contraction of the sarcomeres
Depolarisation of the sarcolemma causes the myosin and actin filaments to slide over each other.
The sliding movement causes the sarcomeres to contract.
Muscle contraction
There are multiple sarcomeres along the length of myofibrils.
As many sarcomeres contract simultaneously, the muscle fibres contract.
Contraction of the muscle fibres causes the whole muscle to contract.
Muscle relaxation
After the muscle has contracted, the sarcomeres relax.
The filaments slide back over each other and the muscle relaxes.
3 myosin head components aiding sliding filament theory:
Globular head
Binding site
Tropomyosin
Globular head
Myosin filaments have globular heads.
Globular heads can move back and forth.
The movement of the globular heads is what allows actin and myosin filaments to slide past each other in muscle contraction.
Binding site
There are two binding sites on every myosin head:
One site can bind to actin.
One site can bind to ATP.
There is also a binding site for the myosin heads on actin filaments.
This is called the actin-myosin binding site.
Tropomyosin
Tropomyosin is a protein that is located on actin filaments.
Tropomyosin plays an important role in muscle contraction because it blocks the actin-myosin binding site when muscle fibres are at rest.
When muscle fibres are stimulated, the tropomyosin protein is moved so that myosin heads can bind to the actin-myosin binding site.
When actin and myosin bind, they can slide past each other to cause muscle contraction.
Ways to make ATP:
Aerobic respiration
Anaerobic respiration
Phosphocreatine
Aerobic respiration
Aerobic respiration makes ATP through oxidative phosphorylation.
Aerobic respiration requires oxygen.
It is mainly used for extended periods of low-intensity muscle use (e.g. jogging 5km).
Anaerobic respiration
Anaerobic respiration makes ATP by glycolysis and lactate fermentation.
Lactate is produced by lactate fermentation.
The build-up of lactate in the muscles can cause fatigue.
Anaerobic respiration is mainly used short periods of high-intensity muscle use (e.g. sprinting 100m).
Phosphocreatine
Phosphocreatine is a molecule that can supply ATP for muscle contraction.
During intense muscular effort, phosphocreatine donates phosphate to ADP to produce ATP.
The ATP produced is used to sustain muscle contraction.
During low periods of muscle activity, ATP can be used to phosphorylate creatine back to phosphocreatine.
This process is anaerobic and produces no lactate but phosphocreatine is in short supply.
Role of calcium ions
When muscle cells are stimulated, there is an influx of calcium ions.
The ions play an important role in initiating muscle contraction.
Stages involved to initiate muscle contraction via calcium ions:
Depolarisation
Influx in calcium ions
Tropomyosin
Actin-myosin cross bridge
ATP hydrolase
Depolarisation
Muscle contraction is initiated when an action potential arrives at a neuromuscular junction from a motor neurone.
The action potential causes depolarisation of the sarcolemma.
Depolarisation spreads along the T tubules and into the sarcoplasm.
Influx of calcium ions
Depolarisation of the T tubules stimulates the sarcoplasmic reticulum (SR).
The SR releases Ca2+ ions into the sarcoplasm.
Tropomyosin
Ca2+ ions bind to a protein attached to tropomyosin.
Tropomyosin is a protein that blocks the actin-myosin binding site.
Binding of Ca2+ ions causes the protein to change shape.
Altering the protein causes tropomyosin to be moved.
The actin-myosin binding site is no longer blocked by tropomyosin.
Actin-myosin cross bridge
The myosin head can now bind to the actin filament.
The bond between actin and myosin is called the actin-myosin cross bridge.
ATP hydrolase
Ca2+ ions also activate ATP hydrolase.
ATP hydrolase is an enzyme that hydrolyses ATP to ADP and inorganic phosphate.
This process releases energy that can power muscle contraction.
Roles of actin-myosin cross bridges are:
Bending of myosin heads
Breaking of cross bridge
Forming a new cross bridge
Contraction
Bending of myosin heads
When Ca2+ ions activate ATP hydrolase, ATP is hydrolysed and energy is released.
The energy released from this reaction causes the myosin head to bend.
The movement of the myosin head causes the actin filament to slide past the myosin filament.
The actin filament is pulled by the myosin head because of the actin-myosin cross bridge.
Breaking of the cross bridge
After the actin filament has slid past the myosin filament, the actin-myosin cross bridge is broken.
This is driven by energy from ATP.
The myosin head is no longer attached to the actin filament.
Forming a cross bridge
The myosin head bends back to its original position after it is released from the actin binding site.
The myosin forms a new cross bridge with a binding site further along the actin filament.
Contraction
The cycle of forming and breaking actin-myosin cross bridges occurs quickly and continuously.
As actin filaments are pulled past the myosin filaments, the overall result is the shortening of the sarcomere.
Shortening of the sarcomere causes muscle contraction.
Halting contraction
Muscle contraction is stopped when the muscle cells are no longer stimulated.
Stages involved in halting contraction:
Removal of calcium ions
Movement of tropomyosin
Sarcomere lengthens
Removal of calcium ions
If action potentials are no longer stimulating the muscle cells, the release of Ca2+ ions by the sarcoplasmic reticulum (SR) will stop.
The Ca2+ ions are transported back into the SR by active transport.
Movement of tropomyosin
Removal of Ca2+ ions means that the protein attached to tropomyosin undergoes a conformational change.
The protein changes shape.
This causes tropomyosin to shift so that it is blocking the actin-myosin binding sites.
Myosin heads can no longer bind to actin filaments.
Sarcomere lengthens
Myosin heads can no longer bind to actin filaments.
The actin filaments return to their resting position.
The sarcomere lengthens again.
The muscle is no longer contracting.
Key differences between slow and fast twitch muscle fibres:
Location
Adaptation to function
Energy source
Cell structure
Location
Slow twitch fibres -
Found in muscles used for posture such as the back and neck.
Fast twitch fibres -
Found mainly in muscles such as the arms and legs.
Adaptation to function
Slow twitch fibres -
Adapted for endurance and slow movement over long periods of time.
Muscle fibres are long and thin.
The muscles fatigue slowly and contract slowly.
Fast twitch fibres -
Adapted for fast or strong movement over short periods of time.
Muscle fibres are short and wide.
The muscles fatigue quickly and contract quickly.
Energy source
Slow twitch fibres -
Rely on energy released through aerobic respiration.
Fast twitch fibres -
Rely on energy released through anaerobic respiration.
Cell structure
Slow twitch fibres -
Lots of mitochondria to maintain aerobic respiration.
Lots of capillaries to supply muscle fibres with oxygen.
Low levels of glycogen.
Low levels of phosphocreatine.
Large stores of myoglobin (pigment that stores oxygen), so appear reddish.
Less sarcoplasmic reticulum (contains calcium ions).
Fast twitch fibres -
Fewer mitochondria.
Fewer capillaries.
High levels of glycogen.
High levels of phosphocreatine.
Small stores of myoglobin.
More sarcoplasmic reticulum.
