3.6.3 Skeletal muscles are stimulated to contract by nerves and act as effectors

Muscles are effector organs that respond to nervous stimulation by contracting and so bring about movement. They act in antagonistic pairs against an incompressible skeleton. There are three types:

• cardiac muscle (heart)
• smooth muscle (walls on blood vessels and the gut)
• skeletal muscle (attached to bone, under voluntary control)

Individual muscles are made up of tine fibres called myofibrils. They produce very little force but all together are extremely powerful. They are lined parallel to maximise force. Individual muscle cells do not have nuclei etc. The cells have become fused together into muscle fibres which share nuclei and cytoplasm (known as sarcoplasm). Within the sarcoplasm is a large concentration of mitochondria and endoplasmic reticulum.

Myofibrils are made up of two types of protein filament:

• actin
• this is thinner and consists of two strands twisted around eachother
• tropomyosin forms a fibrous strand around the actin filament
• myosin
• this is thicker and consists of long rod-shaped tails with bulbous heads that project to the side

Myofibrils appear striped due to alternating dark and light bands. Light bands are isotropic bands (I-bands) - here the thick (myosin) and thin (actin) filaments do not overlap hence they are lighter in colour. Dark bands are called anisotropic bands (A-bands) - here the myosin and actin filaments overlap hence it appears darker here. At the centre of each A-band is a lighter region known as the H-zone and at the centre of each I-band is a line called the Z-line. The sarcomere is the distance between adjacent Z-lines. When the muscle contracts the sarcomeres shorten.

There are two types of muscle fibre:

• slow-twitch fibres
• contract more slowly and provide less powerful contractions but over a long period
• adapted to endurance work (e.g running a marathon)
• they are suited to this role by being adapted to aerobic respiration to avoid a build up of lactic acid (this would cause them to function less effectively and prevent long-duration contraction)
• they have a large store of myoglobin, a rich supply of blood vessels (to deliver o2 and glucose for aerobic respiration), and numerous mitochondria to produce ATP
• fast-twitch fibres
• contract more rapidly producing more powerful contractions but only for a short period of time
• adapted to intense exercise so are more common in muscles that need to do short bursts of intense activity
• they have thicker and more numerous myosin filaments, a high concentration of glycogen, a high concentration of enzymes involved in anaerobic respiration which provide ATP rapidly, a store of phosphocreatine (a molecule that can rapidly generate ATP from ADP in anaerobic conditions)

A neuromuscular junction is the point where a motor neurone meets a skeletal muscle fibre. It is covered in 3.6.2.2.


The contraction of a skeletal muscle will move a part of the skeleton (e.g a limb) in one direction but the same muscle cannot move it in the other direction as muscles can only pull (not push). A second muscle working antagonistically is required to move the limb in the opposite direction.

The process of contraction involves the actin and myosin filaments sliding past one another so it is known as the sliding filament mechanism. This is supported by the changes seen in band pattern on myofibrils. When a muscle contracts...

• the I-band becomes narrower
• the Z-lines move closer together (the sarcomere shortens)
• the H-zone becomes narrower
• The A-band remains the same width as the width of this band is determined by the length of the myosin filaments and they do not get shorter.

Here's how the mechanism works:

• an action potential reaches many neuromuscular junctions simultaneously causing calcium ion protein channels to open and calcium ions to diffuse into the synaptic know
• the calcium 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 muscle cell surface membrane causing it to depolarise
• the action potential travels into the fibre through a system fo T-tubules that are extensions of the cell surface membrane and branch throughout the cytoplasm of the muscle (the sarcoplasm)
• the tubules are in contact with the endoplasmic reticulum of the muscle which has actively transported calcium ions from the cytoplasm of the muscle leading to a low concentration of calcium ions in the cytoplasm
• the action potential opens the calcium ion protein channels on the endoplasmic reticulum and calcium ions diffuse into the muscle cytoplasm down a concentration gradient
• the calcium ions cause the tropomyosin molecules the were blocking the actin binding sites to pull away
• ADP molecules attach to the myosin heads so now they are in a state to bind to actin filaments forming cross-bridges
• once attached to the actin filament the myosin heads change their angle pulling the actin filament along as they do so and releasing a molecule of ADP
• an ATP molecule attaches to each myosin head causing it to become detached from the actin filament
• the calcium ions activate the enzyme ATPase which hydrolyses ATP to ADP. This provides the energy for the myosin head to return to its original position
• the myosin head with an attached ADP molecule then reattaches itself further along the actin filament and the cycle is repeated as long as the concentration of calcium ions in the myofibril remains high
• when nervous stimulation ceases the calcium ions are actively transported back into the endoplasmic reticulum using energy from the hydrolysis of ATP
• the reabsorption of the calcium ions allows tropomyosin to block the actin filament binding sits
• myosin heads are now unable to bind to actin filaments and contraction ceases

So this all requires A LOT of energy. This is supplied by the hydrolysis of ATP to ADP + Pi. This energy is needed for the movement of myosin heads and the reabsorption of calcium ions into the endoplasmic reticulum by active transport. In an active muscle there is a great demand for ATP. Most energy is regenerated from ADP during the respiration of glucose in the mitochondria but this requires oxygen. In very active muscles we can rapidly generate ATP anaerobically using phosphocreatine