Muscle action

Striated or skeletal muscle is made up of a syncitium of cells, ie the cells are not separated by cell membranes and therefore many nuclei are sharing the cytoplasm. Within the cytoplasm there are linear arrangements of contractile structures called sarcomeres. The cytoplasm is referred to as sarcoplasm and the plasma membrane is termed the sarcolemma. There are many mitochondria in the sarcoplasm. The sarcomeres contain small strands made up of the proteins actin and myosin. The actin is attached to the end walls or Z lines of the sarcomeres while the myosin is positioned in the central region. The actin and myosin strands overlap slightly.

The striated appearance of skeletal muscles is caused by the overlap of the proteins within many thousands of sarcomeres. When ATP is supplied to a sarcomere and there is a high level of Ca⁺⁺ in the sarcomere fluid, a cross-bridging reaction takes place between the actin and the myosin. The actin molecules have bridging sites along their lengths while the myosin has small arm like extensions from its sides. On the end of each arm there is a protein head which can attach to the bridging site and which will break down ATP when it does so. As the ATP is broken down the bridging head twists and then releases to become straight again. This puts it in line with the next bridging site and it will stick to it and go through the same series of changes once again. Each time a bridge is formed ATP is broken down. When hundreds of the bridges are being formed and broken the effect is that the actin strands are dragged along the myosin strands and each sarcomere gets shorter in length. The activation of bridging results from the movement of a spiral protein called tropomyosin which is wrapped around the actin strands.

The myosin strand with its bridging arms is lying next to the actin strand and the bridging arms react with the bridging sites:

The heads of the bridging arms then rotate and this pulls the actin across the myosin:

The arrow shows the relative movement of the myosin across the actin, however since both ends of the myosin are being ‘pulled’ by their reaction with the actin, the myosin cannot actually move in any direction so the actin strands slide across the myosin strands causing the sarcomere to shorten. When the bridges are broken the arms straighten and lie adjacent to the next bridging site along, which they join to if the Ca⁺⁺ are still present.

The control of muscle contraction

When an action potential reaches the motor end plate it releases neurotransmitter substances which open sodium channels in the sarcolemma (the muscle cellular membrane). The excitatory potential which develops travels along the sarcolemma causing Ca⁺⁺ channels to open along the T channels which run down by the Z lines of the sarcomeres. The influx of Ca⁺⁺ into the sarcomeres initiates the cross bridging of myosin with the actin molecules and this results in contraction of the sarcomeres. When the excitatory potential ends the Ca⁺⁺ are pumped out of the sarcomeres back into the T channel spaces and contraction ceases. Each motor end plate controls the contraction of one group of contractile fibrils in the muscle. The greater the number in the group the less precise the control of muscle contraction is.

In the eye muscle, each motor end plate controls about ten fibrils while in the biceps muscle there are about one hundred in each control group. Since muscles act in antagonistic pairs they are innervated so that as one muscle of the pair contracts, an inhibitory impulse is sent to the motor synapse of the other member of the pair preventing it’s contraction.

The banding pattern seen in skeletal muscle under the light microscope can be explained by the overlapping actin and myosin molecules in the sarcomeres of the muscle tissue. Because the sarcomeres are lined up in precise rows forming regular lines along the muscle fibrils the overlapping areas of actin and myosin form a dark stripe, the area with only actin present forms a slightly lighter stripe. when the muscle contracts the overlapping region becomes longer and the paler ends and centres of the sarcomeres become shorter.

How muscles cause movement:

Around each joint in the body there are pairs of muscles. Each pair works antagonistically to each other. One muscle of a pair can contract to pull the bone in one direction but when it relaxes it cannot push the bone back since the muscle simply becomes floppy. To move the bone back to its original position we need an antagonistic muscle which can contract to pull the muscle in the opposite direction. In the example opposite, which is a simplified elbow, the extensor straightens the arm while the flexor bends it. The more complex the movement of a joint is then the more sets of muscle that are needed to create that movement. Ball and socket joints which give movement in all three planes require many pairs of muscles to bring about the movement and therefore need large areas of flat bone in the region so that all of these muscles can be attached.