How does excitation contraction coupling work

Therefore, beta-adrenergic stimulation increases the force and shortening velocity of contraction i. There are investigational drugs that enhance TN-C calcium affinity and thereby exert a positive inotropic influence on the heart. One potential downside with these drugs, however, is that enhanced TN-C binding to calcium can reduce the rate of relaxation, thereby causing diastolic dysfunction.

In systolic heart failure , ECC can be impaired at several different sites. First, there can be decreased influx of calcium into the cell through L-type calcium channels resulting from impaired signal transduction , which decreases subsequent calcium release by the SR. There can also be a decrease in TN-C affinity for calcium, so that a given increase in calcium in the vicinity of the troponin complex has less of an activating effect on cardiac contraction.

In some forms of diastolic heart failure , there is evidence that the function of the SR ATP-dependent calcium pump is impaired. This reduces the voltage difference between the inside and outside of the cell, which is called depolarization. As ACh binds at the motor end plate, this depolarization is called an end-plate potential.

The depolarization then spreads along the sarcolemma and down the T tubules, creating an action potential. ACh is broken down by the enzyme acetylcholinesterase AChE into acetyl and choline. AChE resides in the synaptic cleft, breaking down ACh so that it does not remain bound to ACh receptors, which would cause unwanted extended muscle contraction. Learning Objectives Explain the process of excitation-contraction coupling and the role of neurotransmitters.

Key Points A motor neuron connects to a muscle at the neuromuscular junction, where a synaptic terminal forms a synaptic cleft with a motor-end plate.

The neurotransmitter acetylcholine diffuses across the synaptic cleft, causing the depolarization of the sarcolemma. In the absence of ATP, the myosin head will not detach from actin. ATP binding causes the myosin head to detach from the actin Figure The energy released during ATP hydrolysis changes the angle of the myosin head into a cocked position Figure The myosin head is now in position for further movement. When the myosin head is cocked, myosin is in a high-energy configuration. This energy is expended as the myosin head moves through the power stroke, and at the end of the power stroke, the myosin head is in a low-energy position.

After the power stroke, ADP is released; however, the formed cross-bridge is still in place, and actin and myosin are bound together. As long as ATP is available, it readily attaches to myosin, the cross-bridge cycle can recur, and muscle contraction can continue. Note that each thick filament of roughly myosin molecules has multiple myosin heads, and many cross-bridges form and break continuously during muscle contraction.

Multiply this by all of the sarcomeres in one myofibril, all the myofibrils in one muscle fiber, and all of the muscle fibers in one skeletal muscle, and you can understand why so much energy ATP is needed to keep skeletal muscles working.

In fact, it is the loss of ATP that results in the rigor mortis observed soon after someone dies. With no further ATP production possible, there is no ATP available for myosin heads to detach from the actin-binding sites, so the cross-bridges stay in place, causing the rigidity in the skeletal muscles. 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. There are three mechanisms by which ATP can be regenerated: creatine phosphate metabolism, anaerobic glycolysis, fermentation and aerobic respiration. Creatine phosphate is a molecule that can store energy in its phosphate bonds.

This acts as an energy reserve that can be used to quickly create more ATP. When the muscle starts to contract and needs energy, creatine phosphate transfers its phosphate back to ADP to form ATP and creatine. This reaction is catalyzed by the enzyme creatine kinase and occurs very quickly; thus, creatine phosphate-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 used Figure Glycolysis is an anaerobic non-oxygen-dependent process that breaks down glucose sugar to produce ATP; however, glycolysis cannot generate ATP as quickly as creatine phosphate.

Thus, the switch to glycolysis results in a slower rate of ATP availability to the muscle. The sugar used in glycolysis can be provided by blood glucose or by metabolizing glycogen that is stored in the muscle. 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.