MUSCLE CONTRACTION

A top-down view of skeletal muscle

A muscle contraction (also known as a muscle twitch or simply twitch) occurs when a muscle cell (called a muscle fiber) shortens. Locomotion in most higher animals is possible only through the repeated contraction of many muscles at the correct times. Contraction is a duty of the central nervous system comprised of brain and spinal cord.

For most muscles, contraction occurs as a result of conscious effort originating in the brain. The brain sends signals, in the form of action potentials, through the nervous system to the motor neuron that innervates the muscle fiber. However, some muscles (such as the heart) do not contract as a result of conscious effort. These are said to be autonomic, or involuntary muscles. Also, it is not always necessary for the signals to originate from the brain. Some reflexes are fast, unconscious muscular reactions that occur due to unexpected physical stimuli. Other actions such as locomotion, breathing, chewing have a reflex aspect to them; the brain will start the contractions, but continuation of the movements can become reflexive. The action potentials for reflexes to unexpected stimuli originate in the grey matter within the spinal cord instead of the brain.

There are three general types of muscle contractions: skeletal muscle (voluntary) contractions, heart muscle (involuntary) contractions, and smooth muscle (involuntary) contractions.

For skeletal muscles, the force exerted by the muscle is controlled by varying the frequency at which action potentials are sent to muscle fibers. Action potentials do not arrive at muscles synchronously, and during a contraction some fraction of the fibers in the muscle will be firing at any given time. Typically when a human is exerting a muscle as hard as they are consciously able, roughly one-third of the fibers in that muscle will be firing at once, but various physiological and psychological factors (including Golgi tendon organs and Renshaw cells) can affect that.

Skeletal muscle contractions

Skeletal muscles contract according to the sliding-filament model:

1. An action potential originating in the CNS, reaches the axon of the motor neuron.
2. The action potential activates voltage gated calcium ion channels on the axon, and calcium rushes in.
3. The calcium causes the neurotransmitter, acetylcholine vesicles in the axon to fuse with the membrane, releasing the acetylcholine into the synapse between the axon and the motor end plate of the muscle fibre through the T tube system.
4. The acetylcholine diffuses across the synapse and binds to nicotinic receptors on the motor end plate, opening channels in the membrane for sodium and potassium. Sodium rushes in, while potassium trickels out through the sodium-potassium (Na/K) pump located in the sarcolemma. However, because sodium is more permeable, the muscle fibre membrane becomes more positively charged, triggering an action potential.
5. The action potential spreads through the muscle fibre's network of T tubules, depolarizing the inner portion of the muscle fibre.
6. The depolarization activates voltage-gated calcium channels in the T tubule membrane, which are in close proximity to calcium-release channels in the adjacent sarcoplasmic reticulum.
7. Activated voltage-gated calcium channels physically interact with calcium-release channels to activate them, causing the sarcoplasmic reticulum to release calcium.
8. The calcium binds to the troponin C present on the thin filaments of the myofibrils. The troponin then allosterically modulates the tropomyosin. Normally the tropomyosin sterically obstructs binding sites for myosin on the thin filament; once calcium binds to the troponin C and causes an allosteric change in the troponin protein troponin T allows tropomyosin to move, unblocking the binding sites.
9. Myosin (which is bound to ATP and is in a ready state) binds to the newly uncovered binding sites on the thin filament. It then hydrolyzes ATP to release ADP and inorganic phosphate, releasing energy to deliver a power stroke. The release of ADP and inorganic phosphate causes the myosin head to turn, causing a ratchet movement. Myosin is now bound to actin in the strong binding state. This will pull the Z-bands towards each other. It also shortens the sarcomere and the I-band.
10. ATP binds myosin, allowing it to release actin and be in the weak binding state. (A lack of ATP makes this step impossible, resulting in rigor mortis.) The myosin then hydrolyzes the ATP and uses the energy to move into the "cocked back" state while releasing ADP and inorganic phosphate.
11. Steps 7 and 8 repeat as long as ATP is available and calcium is present on thin filament.
12. All the while, the calcium is actively pumped back into the sarcoplasmic reticulum. When calcium is no longer present on the thin filament, the tropomyosin changes conformation back to its previous state so as to block the binding sites again. The myosin ceases binding to the thin filament, and the contractions cease.

The calcium ions leave the troponin molecule in order to maintain the calcium ion concentration in the sarcoplasm. The active pumping of calcium ions into the sarcoplasmic reticulum creates a deficiency in the fluid around the myofibrils. This causes the removal of calcium ions from the troponin. Thus the tropomyosin-troponin complex again covers the binding sites on the actin fiaments and contraction ceases.

Smooth muscle contraction

1. Contractions are initiated by an influx of calcium which binds to calmodulin.
2. The calcium-calmodulin complex binds to and activates myosin light-chain kinase.
3. Myosin light-chain kinase phosphorylates myosin light-chains, causing them to interact with actin filaments. This causes contraction.