Skeletal Muscle Contractions

Steps of a skeletal muscle contraction:

• An action potential reaches the axon of the motor neuron.
• The action potential activates voltage gated calcium ion channels on the axon, and calcium rushes in.
• The calcium causes acetylcholine vesicles in the axon to fuse with the membrane, releasing the acetylcholine into the cleft between the axon and the motor end plate of the muscle fiber.
• The skeletal muscle fiber is excited by large mylenated nerve fibers which attach to the neuromuscular junction. There is one neuromuscular junction for each fiber.
• The acetylcholine diffuses across the cleft and binds to nicotinic receptors on the motor end plate, opening channels in the membrane for sodium and potassium. Sodium rushes in, and potassium rushes out. However, because sodium is more permeable, the muscle fiber membrane becomes more positively charged, triggering an action potential.
• The action potential on the muscle fiber causes the sarcoplasmic reticulum to release calcium ions(Ca++).
• The calcium binds to the troponin present on the thin filaments of the myofibrils. The troponin then allosterically modulates the tropomyosin. Normally the tropomyosin physically obstructs binding sites for cross-bridge; once calcium binds to the troponin, the troponin forces the tropomyosin to move out of the way, unblocking the binding sites.
• The cross-bridge (which is already in a ready-state) binds to the newly uncovered binding sites. It then delivers a power stroke.
• ATP binds the cross-bridge, forcing it to conform in such a way as to break the actin-myosin bond. Another ATP is split to energize the cross bridge again.
• Steps 7 and 8 repeat as long as calcium is present on thin filament.
• Throughout this process, the calcium is actively pumped back into the sarcoplasmic reticulum. When no longer present on the thin filament, the tropomyosin changes back to its previous state, so as to block the binding sites again. The cross-bridge then ceases binding to the thin filament, and the contractions cease as well.
• Muscle contraction remains as long as Ca++ is abundant in sarcoplasm.

Types of Contractions:

• Isometric contraction--muscle does not shorten during contraction and does not require the sliding of myofibrils but muscles are stiff.
• Isotonic contraction--inertia is used to move or work. More energy is used by the muscle and contraction lasts longer than isometric contraction.
• Twitch--exciting the nerve to a muscle or by passing electrical stimulus through muscle itself. Some fibers contract quickly while others contract slowly.

The Efficiency of Muscle Contraction:

• Only about 20% of input energy converts into muscular work. The rest of the energy is heat.
• 50% of energy from food is used in ATP formation.
• If a muscle contraction is slow or without movement, energy is lost as maintenance heat.
• If muscle contraction is rapid, energy is used to reduce friction.

Summation of Muscle Contraction: It is the adding together of individual muscle twitches to make strong muscle movements.

• Multiple motor unit summation--increasing number of motor units contracting simultaneously.
• Wave summation--increasing rapidity of contraction of individual motor units.
• Tetanization--higher frequency successive contractions fuse together and cannot be distinguished from one another.

Sliding Filament theory

When a muscle contracts, the actin is pulled along myosin toward the center of the sarcomere until the actin and myosin filaments are completely overlapped. The H zone becomes smaller and smaller due to the increasing overlap of actin and myosin filaments, and the muscle shortens. Thus when the muscle is fully contracted, the H zone is no longer visible (as in the bottom diagram, left). Note that the actin and myosin filaments themselves do not change length, but instead slide past each other.

Cellular Action of Skeletal Muscles

During cellular respiration the mitochondria, within skeletal muscle cells, convert glucose from the blood to carbon dioxide and water in the process of producing ATP (see cell physiology). ATP is needed for all muscular movement. When the need of ATP in the muscle is higher than the cells can produce with aerobic respiration, the cells will produce extra ATP in a process called anaerobic respiration. The first step of aerobic respiration(glycolysis) produces two ATP per glucose molecule. When the rest of the aerobic respiration pathway is occupied the pyruvate molecule can be converted to lactic acid. This method produces much less ATP than the aerobic method, but it does it faster and allows the muscles to do a bit more than if they relied solely on ATP production from aerobic respiration. The drawback to this method is that lactic acid accumulates and causes the muscles to fatigue. They will eventually stop contracting until the breakdown of lactic acid is sufficient to allow for movement once again. People experience this most noticeably when they repeatedly lift heavy things such as weights or sprint for a long distance. Muscle soreness sometimes occurs after vigorous activity, and is often misunderstood by the general public to be the result of lactic acid buildup. This is a misconception because the muscle does fatigue from lactic acid buildup, but it does not stay in the muscle tissue long enough to cause tissue breakdown or soreness. During heavy breathing, following exercise, the cells are converting the lactic acid either back into glucose or converting it to pyruvate and sending it through the additional steps of aerobic respiration. By the time a person is breathing normally again the lactic acid has been removed. The soreness is actually from small tears in the fibers themselves. After the fibers heal they will increase in size. The number of mitochondria will also increase if there is continued demand for additional ATP. Hence, through exercise the muscles can increase in both strength and endurance.

Another misconception is that as the muscle increases in size it also gains more fibers. This is not true. The fibers themselves increase in size rather than in quantity. The same holds true for adipose tissue--fat cells do not increase in number, but rather the amount of lipids (oil) in the cells increase.

Muscle fibers are also genetically programmed to reach a certain size and stop growing from there, so after awhile even the hardest working weightlifter will only reach a certain level of strength and endurance. Some people will get around this by taking steroids. The artificial steroids cause all sorts of trouble for the person. They can cause the adrenal glands to stop producing corticosteroids and glucosteroids. This leads to the atrophy of the gland's medulla and causes permanent loss of the production of these hormones. The testicles may also atrophy in response to steroids. Eventually the testes will stop making testosterone and sperm, rendering the male infertile.

One of the more serious problems associated with abnormal gain of muscle mass is heart failure. While for most people gaining muscle and losing fat is desirable, a body builder is at risk of producing more muscle mass than the heart can handle. One pound of fat contains about 3.5 miles of blood vessels, but one pound of muscle has about 6.5 miles. Hence, additional muscle causes the heart to pump more blood. Some people that have too much muscle will be very strong but will not have a healthy aerobic endurance, in part because of the difficulty of providing oxygenated blood to so much tissue.