4 minute read
Sequence of Muscle Contraction Events
spinal cord to the individual muscle cells. These axons can be up to three feet long, forming bundles called nerves similar to individual wires bundled in a cable.
When the nerve cell is activated, it releases acetylcholine, its neurotransmitter, that crosses the synaptic cleft, which is the space between the nerve cell and the motor end plate of the muscle cell. It binds to the muscle cell receptors at the motor end plate, causing positively charged ions to pass through the cell membrane, raising the membrane potential so that it is less negative. This is called depolarization. This depolarization triggers the action potential that spreads to all parts of the muscle cell. In the meantime, there is an enzyme called acetylcholinesterase that degrades the acetylcholine so it can no longer act on the motor end plate.
Advertisement
When the muscle cell is activated with an action potential, there are invaginations of the sarcolemma (cell membrane) called T-tubules or transverse tubules. They ensure that the activated membrane can get closer to the sarcoplasmic reticulum. This is where it can affect the calcium transport inside or outside the sarcoplasmic reticulum. The Ttubule with membranes of the sarcoplasmic reticulum on either side is called a triad. The triad surrounds the myofibril, which is what contains actin and myosin.
SEQUENCE OF MUSCLE CONTRACTION EVENTS
In understanding the structure of the muscle fiber, you need to see that the shortening of these long, thin muscle cells involves two kinds of fiber in them, which are actin and myosin. The shortening relies on the presence of calcium ions in the cytoplasm of the muscle cell, which causes un-shielding of actin binding sites, which had been shielded by troponin and tropomyosin. Calcium also activates enzymes that will activate the myosin heads. Figure 3 shows actin and myosin in the muscle cell.
The signal must first be received in order to have muscle contraction. This happens when the neurotransmitter acetylcholine acts on receptors on the motor end plate of the muscle fiber. Each muscle fiber has a motor end plate. The attachment of acetylcholine results in depolarization or change in energy potential across the cell membrane of the muscle fiber because sodium ions enter the cell. It ultimately causes an action potential that spreads down the muscle fiber.
This action potential—an electrical potential across the membrane—triggers the release of calcium ions from their storage in the sarcoplasmic reticulum, which is the specific endoplasmic reticulum within muscle cells. The calcium initiates the contraction, which is sustained by adenosine triphosphate or ATP, which is the energy currency of the muscle cell and indeed, all cells. The muscle will continue to contract as long as ATP is available.
The cessation of muscle contraction starts with signaling from the motor neuron ends, which causes repolarization of the muscle cell, closing the calcium channels in the sarcoplasmic reticulum. The calcium ions are pumped back into the sarcoplasmic reticulum, causing tropomyosin to reshield or recover the actin strands binding strands.
Another thing that can stop muscle contraction is when the muscle cell runs out of ATP, becoming fatigued.
The molecular events of muscle fiber shortening occurs within the sarcomeres themselves. The muscle fiber has thousands of linearly-arranged myofibrils that shorten as the myosin heads pull upon the actin filaments. The region where thick and thin filaments overlap is dense in appearance, with little space between the filaments. As mentioned, the thin filaments are attached by the Z-discs but do not connect in the middle of the myofibril. In the same way, the thick filaments are not connected to the Zdiscs but line up between the thin filaments.
The sliding (or contraction) can only happen when the myosin-binding sites on the actin filaments are exposed by steps that start when calcium is released by the sarcoplasmic reticulum. Tropomyosin is the main protein that winds around the chains of actin filaments, covering the binding sites and preventing the contraction from occurring. Tropomyosin forms a complex with troponin that together prevent myosin from binding to actin.
The troponin protein binds to calcium, allowing the tropomyosin to slide away from the myosin binding sites on the actin molecule. Cross-bridges form between the actin and myosin, pulling the actin toward the center of the sarcomere. This is temporary and requires ATP to allow for the pulling of the actin and myosin further along each other. The cross-bridges re-cock and allow the myosin heads to attach to other binding sites further down the actin molecule so that actin and myosin can together contract the myofibril—and the muscle itself.
As actin is pulled, the filaments move approximately 10 nanometers toward the M-line, which is the center line that indicates the center attachment of the myosin molecule. This movement of one part of the myosin molecule down the actin molecule, is called a “power stroke.” Without ATP, only one stroke can happen. The myosin head attachment to actin will not reverse itself and detach without the action of ATP.
Myosin has ATPase activity that converts ATP to ADP and phosphate, releasing the cross-bridge so that the myosin head can be in position for further movement. Many cross-bridges break and re-form on a continuous basis along the molecule, with each
