How do the muscles work? The technical articles below explain in detail the structure and function of the muscles. This information is useful for anyone who is studying or is seriously interested in physiology for soccer.
About 35% of a person's bodyweight is attributed to muscle. As with all mammals, the human body's muscle tissue is categorized into three branches.
A. Cardiac muscles are only found in the heart. They make short rhythmic contractions and are controlled involuntarily. While nerves from the autonomic nervous system are present alongside cardiac muscles it has been noted that the autonomic impulses only alter the rate of contractions. Science has not yet proven what exactly causes the continuos rhythmic contractions. Cardiac muscles require constant supply of oxygen, and would quickly die (in a case of heart attack for example) if blood rich on oxygen fails to be delivered to them.
B. Smooth muscles are also considered visceral (involuntarily controlled) and are used in your skin, digestive system, excretory system, bladder, major blood vessels, airways and reproductive system. These muscles are capable of tetanus (prolonged) as well as twitch contractions.
C. Skeletal (striated) muscles are the only type that can be voluntarily controlled. They are attached to the skeleton (by a tissue called tendon) in pairs, so that they can move the bone in two opposite directions. Deep fascia is an irregular connective tissue, which wraps the muscles into functional and specific groups filling the space between them. Blood supply and nerves servicing the muscles all pass through the deep fascia. An outer layer of connective tissue (epimysium) surrounds skeletal muscles defining their shape and protecting them.
Sliding Filament Theory
According to the sliding filament theory, during a contraction, myosin filaments grab on to actin filaments by forming chemical bonds called crossbridges. By the use of these crossbridges, the thick filaments pull in the actins toward the center. Because the actins are attached to the Z-line, this sliding movement shortens the length of the entire sarcomere. Notice that during a contraction, the filaments maintain their original length and only the I band actually gets compressed. In a muscle fiber, the signal for contraction is synchronized over the entire fiber so that all of the myofibrils that make up the sarcomere shorten simultaneously.
At the molecular level, actin filaments (or thin filaments) are shaped like two strands of pearls twisted around each other. Imagine that each pearl is an actin molecule. Both strands of actins are also wrapped around with a strand of tropomyosin and interspersed toropnin. There are two structures in the grooves of each thin filament that enable them to slide along the thick ones: a long rod-like protein called tropomyosin and a shorter bead-like protein complex called troponin. Troponin and tropomyosin are the molecular switches that control the interaction of actin and myosin during contraction. The thick filaments are shafts of myosin molecules arranged in a cylinder. Myosin molecules are golf-club shaped. Their broader endings are called heads.
Running vertically down the Z-line is a small tube called the transverse or T-tubule, which is actually part of the cell membrane that extends deep inside the fiber. Stretching along the fiber's long axis, between T-tubules (Transverse tubule), is a membrane system called the sarcoplasmic reticulum. Calcium ions are stored in the sarcoplasmic reticulum. Energy (ATP) is required to maintain the calcium stored in the sarcoplasmic reticulum.
In the normal relaxed muscle fiber the intracellular calcium level of the sarcoplasma is maintained at a low concentration. When the calcium concentration is low, the regulatory proteins, troponin and tropomyosin, block the myosin binding sites on the actin proteins. When a muscle fiber is stimulated, calcium ions are released from storage (sarcoplasmic reticulum). The binding of calcium ions to the troponin complexes causes the regulatory proteins to shift over, opening up the binding sites along the actin protein. The myosin heads now move in contact with the actin binding sites and form chemical bonds called crossbridges. Initially, the crossbridges are extended with adenosine diphosphate (ADP) and inorganic phosphate (Pi) attached to the myosin. As soon as the crossbridge is formed, the myosin heads bend, thereby creating force and sliding the actin filament past the myosin. This process is called the power stroke. During the power stroke (which causes muscle shortening of only 1%), myosins release the ADP and Pi. Once ADP and Pi are released, a molecule of adenosine triphosphate (ATP) binds to the myosin. When the ATP binds, the myosin molecule releases the actin. When the actin is released, the ATP molecule gets split into ADP and Pi by the myosin. The energy from the ATP resets the myosin head to its original position. The process is repeated (up to when the muscle is shortened 35-50% of its relaxed length). The actions of the myosin molecules are not synchronized - at any given moment, some myosins are attaching to the actin filament, others are creating force and others are releasing the actin filament.
