Flashcards in Muscle Contraction Deck (14):
What are muscles?
Muscles are effector organs that respond to nervous stimulation by contracting and so bring about movement.
There are three types of muscle model?
- is found exclusively in the heart.
- is found in the wall of blood vessels and the gut.
- bulk of body muscle in vertebrates.
- attached to bone and acts under voluntary, conscious control.
Why are muscles so strong?
Individual's muscles are made up of million of tiny muscle fibres called myofibrils- they produce almost no force while collectively they can be extremely powerful.
Why is it if muscle were made up of individual cells joined end to end it would not be able to perform the function of contraction very efficiently?
This is because the junction between adjacent cells would be a point of weakness- reduce the overall strength.
Separate cells (which share nuclei and also a cytoplasm called sarcoplasm) have to be fused together.
What are slow twitch fibres?
Contract more slowly and provide less powerful contractions over a longer period.
This is suited for aerobic respiration in order to avoid a buildup of lactic acid.
What are fast twitch fibres?
Contract more rapidly and produce a powerful contraction but only for a short period.
thicker and more numerous myosin filaments.
a high concentration of enzymes involved in anaerobic respiration.
a store of phosphocreatine- a molecule that can rapidly generate ATP from ADP in anaerobic conditions and so provide energy for muscle contraction.
What are the changes to the sarcomere during the sliding filament theory?
I bands become narrower.
Z lines move closer together- the sarcomere shortens.
H zone becomes narrower.
A band remains the same width- the width of this band is determined by the length of the myosin filaments.
nervous stimulation ceases, Ca+ ions are actively transported back into the endoplasmic reticulum using energy from the hydrolysis of ATP.
this reabsorption of the Ca+ ions allows tropomyosin to block the actin filament again.
myosin heads are now unable to bind to actin filaments and contraction ceases.
an action potential reaches many neuromuscular junctions simultaneously- causing Ca+ ion channels to open and so move into the synaptic knob.
the Ca+ ions cause the synaptic vesicles to fuse with the presynaptic membrane and release their acetylcholine into the synaptic cleft.
acetylcholine diffuses across the synaptic cleft and binds with receptors on the postsynaptic membrane, causing depolarisation.
Sliding filament mechanism of muscle contraction.
The action potential opens the Ca+ ion channels on the endoplasmic reticulum and so they flood into the muscle cytoplasm down a diffusion gradient
Ca+ released from the endoplasmic reticulum remove tropomyosin that is blocking
Myosin can now bind to site on actin.
Head of myosin changes angle moving the actin filament along as it does so. The ADP molecule is released.
ATP fixes to myosin head, causing it to detach from actin.
Hydrolysis of ADP to ATP by ATPase provides the energy for the myosin head to return to its normal position.
Myosin head reattaches further down the actin filament and cycle continues.
How is the shape of the myosin molecule adapted to its role in muscle contraction?
Made of two proteins
- fibrous protein is long and thin in shape, which enables it to combine with others to form a long thick filament along which the actin can move.
- the globular protein forms two bulbous structures, the head and the tail. This allows it to exactly fit with the actin molecule. It also means it can be moved at an angle when attached to actin and so move it along causing the muscle to contract.
Trained sprinters have high levels of phosphocreatine in their muscles, explain the advantage of this.
Phosphocreatine stores phosphate which is used to generate ATP from ADP in anaerobic conditions.
Why does rigor mortus often occur after death?
Death = no ATP production and ATP attaches to myosin head, causing them to detach from actin so the muscle relaxes.