What kind of stimulus travels from the axon terminal to the sarcolemma

The trigger for calcium release from the sarcoplasmic reticulum into the sarcoplasm is a neural signal. Each skeletal muscle fiber is controlled by a motor neuron, which conducts signals from the brain or spinal cord to the muscle. The area of the sarcolemma on the muscle fiber that interacts with the neuron is called the motor end plate. A small space called the synaptic cleft separates the synaptic terminal from the motor end plate.

The ability of cells to communicate electrically requires that the cells expend energy to create an electrical gradient across their cell membranes.

This charge gradient is carried by ions, which are differentially distributed across the membrane. Each ion exerts an electrical influence and a concentration influence. Just as milk will eventually mix with coffee without the need to stir, ions also distribute themselves evenly, if they are permitted to do so.

In this case, they are not permitted to return to an evenly mixed state. This alone accumulates a small electrical charge, but a big concentration gradient. This is the resting membrane potential.

Potential in this context means a separation of electrical charge that is capable of doing work. It is measured in volts, just like a battery. The nuclei are displaced peripherally within a cross section of the sarcoplasm while a large number of longitudinal myofibrils, groups of arranged contractile proteins, occupy most of the center space. The myofibril contains several important histological landmarks:. Each myofibril can be understood as a series of contractile units called sarcomeres that contains two types of filaments: thick filaments, composed of myosin, and thin filaments, composed of actin.

The individual filaments do not change in length during muscle contraction; rather the thin filaments slide over the thick filaments to shorten the sarcomere.

The nature of these filaments can be understood in the context of the histological landmarks of the myofibril. Skeletal muscles are divided into two muscle fiber types:. Most muscles contain a mixture of these extreme fiber types. In humans, the fiber types cannot be distinguished based on gross examination, but require specific stains or treatments to differentiate the fibers. Skeletal muscle cells are innervated by motor neurons.

A motor unit is defined as the neuron and the fibers it supplies. Some motor neurons innervate one or a few muscle cells whereas other motor neurons can innervate hundreds of muscle cells.

Muscles that require fine control have motor neurons that innervate fewer muscle cells; muscles that participate in less controlled movements may have many fibers innervated by each neuron. Motor axons terminate in a neuromuscular junction on the surface of skeletal muscle fibers.

The neuromuscular junction is composed of a pre-synaptic nerve terminal and a post-synaptic muscle fiber. Upon depolarization, the pre-synaptic vesicles containing the neurotransmitter acetylcholine fuse with the membrane, releasing acetylcholine into the cleft. Acetylcholine binds to receptors on the post-synaptic membrane and causes depolarization of the muscle fiber, which leads to its contraction. Typically, one action potential in the neuron releases enough neurotransmitter to cause one contraction in the muscle fiber.

In muscle cells, the sarcolemma or plasma membrane extends transversely into the sarcoplasm to surround each myofibril, establishing the T-tubule system. These T-tubules allow for the synchronous contraction of all sarcomeres in the myofibril. The T-tubules are found at the junction of the A- and I- bands and their lumina are continuous with the extracellular space. At such junctions, the T-tubules are in close contact with the sarcoplasmic reticulum, which forms a network surrounding each myofibril.

The part of the sarcoplasmic reticulum associated with the T-tubules is termed the terminal cisternae because of its flattened cisternal arrangement. When an excitation signal arrives at the neuromuscular junction, the depolarization of the sarcolemma quickly travels through the T-tubule system and comes in contact with the sarcoplasmic reticulum, causing the release of calcium and resulting in muscle contraction.

Smooth muscle forms the contractile portion of the wall of the digestive tract from the middle portion of the esophagus to the internal sphincter of the anus. It is found in the walls of the ducts in the glands associated with the alimentary tract, in the walls of the respiratory passages from the trachea to the alveolar ducts, and in the urinary and genital ducts.

The breakdown of one glucose molecule produces two ATP and two molecules of pyruvic acid , which can be used in aerobic respiration or when oxygen levels are low, converted to lactic acid Figure If oxygen is available, pyruvic acid is used in aerobic respiration. However, if oxygen is not available, pyruvic acid is converted to lactic acid , which may contribute to muscle fatigue. This occurs during strenuous exercise when high amounts of energy are needed but oxygen cannot be sufficiently delivered to muscle.

Glycolysis itself cannot be sustained for very long approximately 1 minute of muscle activity , but it is useful in facilitating short bursts of high-intensity output. This is because glycolysis does not utilize glucose very efficiently, producing a net gain of two ATPs per molecule of glucose, and the end product of lactic acid, which may contribute to muscle fatigue as it accumulates.

Aerobic respiration is the breakdown of glucose or other nutrients in the presence of oxygen O 2 to produce carbon dioxide, water, and ATP. Approximately 95 percent of the ATP required for resting or moderately active muscles is provided by aerobic respiration, which takes place in mitochondria.

The inputs for aerobic respiration include glucose circulating in the bloodstream, pyruvic acid, and fatty acids. Aerobic respiration is much more efficient than anaerobic glycolysis, producing approximately 36 ATPs per molecule of glucose versus four from glycolysis.

However, aerobic respiration cannot be sustained without a steady supply of O 2 to the skeletal muscle and is much slower Figure To compensate, muscles store small amount of excess oxygen in proteins call myoglobin, allowing for more efficient muscle contractions and less fatigue.

Aerobic training also increases the efficiency of the circulatory system so that O 2 can be supplied to the muscles for longer periods of time. Muscle fatigue occurs when a muscle can no longer contract in response to signals from the nervous system. The exact causes of muscle fatigue are not fully known, although certain factors have been correlated with the decreased muscle contraction that occurs during fatigue.

ATP is needed for normal muscle contraction, and as ATP reserves are reduced, muscle function may decline. This may be more of a factor in brief, intense muscle output rather than sustained, lower intensity efforts. Lactic acid buildup may lower intracellular pH, affecting enzyme and protein activity. Intense muscle activity results in an oxygen debt , which is the amount of oxygen needed to compensate for ATP produced without oxygen during muscle contraction. Oxygen is required to restore ATP and creatine phosphate levels, convert lactic acid to pyruvic acid, and, in the liver, to convert lactic acid into glucose or glycogen.

Other systems used during exercise also require oxygen, and all of these combined processes result in the increased breathing rate that occurs after exercise. Until the oxygen debt has been met, oxygen intake is elevated, even after exercise has stopped. Relaxing skeletal muscle fibers, and ultimately, the skeletal muscle, begins with the motor neuron, which stops releasing its chemical signal, ACh, into the synapse at the NMJ.

Without the ability to form cross-bridges between the thin and thick filaments, the muscle fiber loses its tension and relaxes. The number of skeletal muscle fibers in a given muscle is genetically determined and does not change. Muscle strength is directly related to the amount of myofibrils and sarcomeres within each fiber.

Factors, such as hormones and stress and artificial anabolic steroids , acting on the muscle can increase the production of sarcomeres and myofibrils within the muscle fibers, a change called hypertrophy, which results in the increased mass and bulk in a skeletal muscle.

Likewise, decreased use of a skeletal muscle results in atrophy, where the number of sarcomeres and myofibrils disappear but not the number of muscle fibers. It is common for a limb in a cast to show atrophied muscles when the cast is removed, and certain diseases, such as polio, show atrophied muscles.

Duchenne muscular dystrophy DMD is a progressive weakening of the skeletal muscles. Over time, as muscle damage accumulates, muscle mass is lost, and greater functional impairments develop. DMD is an inherited disorder caused by an abnormal X chromosome.

It primarily affects males, and it is usually diagnosed in early childhood. Generally, there are many folds and invaginations that increase surface area including junctional folds at the motor endplate and the T-tubules throughout the cells. The neurotransmitter acetylcholine is released when an action potential travels down the axon of the motor neuron, resulting in altered permeability of the synaptic terminal and an influx of calcium into the neuron.

The calcium influx triggers synaptic vesicles, which package neurotransmitters, to bind to the presynaptic membrane and to release acetylcholine into the synaptic cleft by exocytosis.

The balance of ions inside and outside a resting membrane creates an electric potential difference across the membrane. This means that the inside of the sarcolemma has an overall negative charge relative to the outside of the membrane, which has an overall positive charge, causing the membrane to be polarized.

Once released from the synaptic terminal, acetylcholine diffuses across the synaptic cleft to the motor end-plate, where it binds to acetylcholine receptors, primarily the nicotinic acetylcholine receptors.

This binding causes activation of ion channels in the motor end-plate, which increases permeability of ions via activation of ion channels: sodium ions flow into the muscle and potassium ions flow out.

Both sodium and potassium ions contribute to the voltage difference while ion channels control their movement into and out of the cell. This reduces the voltage difference between the inside and outside of the cell, which is called depolarization. As acetylcholine binds at the motor-end plate, this depolarization is called an end-plate potential. It then spreads along the sarcolemma, creating an action potential as voltage-dependent voltage-gated sodium channels adjacent to the initial depolarization site open.

The action potential moves across the entire cell membrane, creating a wave of depolarization. After depolarization, the membrane needs to be returned to its resting state. This is called repolarization, during which sodium channels close and potassium channels open. During repolarization, and for some time after, the cell enters a refractory period, during which the membrane cannot become depolarized again.

This is because in order to have another action potential, sodium channels need to return to their resting state, which requires an intermediate step with a delay. Propagation of an action potential and depolarization of the sarcolemma comprise the excitation portion of excitation-contraction coupling, the connection of electrical activity and mechanical contraction.

The structures responsible for coupling this excitation to contraction are the T tubules and sarcoplasmic reticulum SR. The T tubules are extensions of the sarcolemma and thus carry the action potential along their surface, conducting the wave of depolarization into the interior of the cell.

T tubules form triads with the ends of two SR called terminal cisternae. When tropomyosin moves, the myosin binding site on the actin is uncovered. Low sarcoplasmic calcium levels prevent unwanted muscle contraction. Acetylcholine , often abbreviated as ACh, is a neurotransmitter released by motor neurons that binds to receptors in the motor end-plate.

It is an extremely important small molecule in human physiology. On the neuron side of the synaptic cleft, there are typically , vesicles waiting to be exocytosed at any time and each vesicle contains up to 10, molecules of acetylcholine. ACh is produced by the reaction of Acetyl coenzyme A CoA with a choline molecule in the neuron cell body. After it is packaged, transported, and released, it binds to the acetylcholine receptor on the motor end-plate; it is degraded in the synaptic cleft by the enzyme acetylcholinesterase AChE into acetate and acetic acid and choline.

The choline is recycled back into the neuron. AChE resides in the synaptic cleft, breaking down ACh so that it does not remain bound to ACh receptors, which would interrupt normal control of muscle contraction. In some cases, insufficient amounts of ACh prevent normal muscle contraction and cause muscle weakness. Botulinum toxin prevents ACh from being released into the synaptic cleft.

With no ACh binding to its receptors at the motor end-plate, no action potential is produced, and muscle contraction cannot occur.

Botulinum toxin is produced by Clostridium botulinum , a bacterium sometimes found in improperly canned foods. Ingestion of very small amounts can cause botulism, which can cause death due to the paralysis of skeletal muscles, including those required for breathing. ATP supplies the energy for muscle contraction to take place. Muscle contraction does not occur without sufficient amounts of ATP. The amount of ATP stored in muscle is very low, only sufficient to power a few seconds worth of contractions.

As it is broken down, ATP must therefore be regenerated and replaced quickly to allow for sustained contraction. One ATP moves one myosin head one step. This can generate three picoNewtons pN of isometric force, or move 11 nanometers. Three pN is a very small force—a human bite, generated by muscle, can generate trillion pN of force. And 11 nm is a very small distance— one inch has 25 million nanometers. There are three mechanisms by which ATP can be regenerated: creatine phosphate metabolism, anaerobic glycolysis, and aerobic respiration.

Creatine phosphate is a phosphagen, which is a compound that can store energy in its phosphate bonds. In a resting muscle, excess ATP adenosine triphosphate transfers its energy to creatine, producing ADP adenosine diphosphate and creatine phosphate. When the muscle starts to contract and needs energy, creatine phosphate and ADP are converted into ATP and creatine by the enzyme creatine kinase. This reaction occurs very quickly; thus, phosphagen-derived ATP powers the first few seconds of muscle contraction.

However, creatine phosphate can only provide approximately 15 seconds worth of energy, at which point another energy source has to be available. Glycolysis is an anaerobic process that breaks down glucose sugar to produce ATP; however, glycolysis cannot generate ATP as quickly as creatine phosphate. The sugar used in glycolysis can be provided by blood glucose or by metabolizing glycogen that is stored in the muscle. Each glucose molecule produces two ATP and two molecules of pyruvate, which can be used in aerobic respiration or converted to lactic acid.

If oxygen is available, pyruvic acid is used in aerobic respiration. However, if oxygen is not available, pyruvic acid is converted into lactic acid, which may contribute to muscle fatigue and pain. This occurs during strenuous exercise when high amounts of energy are needed but oxygen cannot be delivered to muscle at a rate fast enough to meet the whole need. Anaerobic glycolysis cannot be sustained for very long approximately one minute of muscle activity , but it is useful in facilitating short bursts of high-intensity output.

Glycolysis does not utilize glucose very efficiently, producing only two ATP molecules per molecule of glucose, and the by-product lactic acid contributes to muscle fatigue as it accumulates. Lactic acid is transported out of the muscle into the bloodstream, but if this does not happen quickly enough, lactic acid can cause cellular pH levels to drop, affecting enzyme activity and interfering with muscle contraction.