MUSCLE PHYSIOLOGY




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www.occc.edu/biology/Documents/AandPII/Muscle%20Physiology.pptOVERVIEW
Your body has muscles that muscles and nerves that control your every move. Your muscles both contract and relax. There are several different kinds of muscle contraction. When a muscle contracts it gets shorter. For this to happen the muscle must gather up enough force to go against whatever is making it contract. During an isotonic contraction the muscles are shortening a lot because there is not very much resistance to them. During an isometric contraction the muscles would not shorten because there is too much force working against them. In an isometric contraction the muscle tension would match the load being lifted. A concentric contraction is also when the force on the muscle is greater than the load. An eccentric contraction is when the load is greater than the muscle contraction, even though the muscle may not want to stretch out it will anyway. I am sure that most everyone can relate these types of contraction to activities they have taken part in such as lifting weights or hiking in the mountains.JM



As we learned in this unit muscles have a very complicated physiological structure.


Skeletal Muscles
Lets start with skeletal muscles. Skeletal muscles are attached usually to bones by tendons. When muscles contract they pull on the tendons which pull on the bones therefore moving the bones. Tendons are connected to the muscles by connective tissue known as epimysium. The epimysium also extends within the muscle dividing it into fascicles. The connective tissue surrounding the fascicles is the perimysium. The fascicles of the muscles are composed of many muscle fibers surrounded by sarcolemma surrounded by connective tissue called endomysium. Skeletal muscles fibers are multinucleate. Muscle fibers are also striated which is due to dark A bands and light I bands which contain thin dark Z lines. When muscles form together to work as a unit each somatic motor neuron with all the muscle fibers that it innervates is known as the motor unit.


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Mechanisms of Contraction
Skeletal muscle cells contain many subunits or myofibrils. These are the A bands, I bands, and Z lines. Each myofibril contains myofilaments. A bands contain thick filaments composed of myosin which give them their dark appearance. I bands contain thin filaments composed of actin. In a muscle fiber the edges of A bands overlap with thin filaments of I bands The central region of the A band that does not overlap with the thin filaments of I bands is known as H bands.
The Sliding Filament Theory of Contraction has many steps. First the myofiber with all myofibrils shortens due to the movements of the insertion toward the origin of the muscle. The myofibril is shortened by shortening the sarcomeres which is the distance between Z lines. Sarcomeres are shortened by sliding the myofilaments (the filaments do not actually shorten they remain the same length during muscle contraction). Asynchronous power strokes of myosin cross bridges slide the filaments by pulling the thin filaments over the thick filaments. The thick filaments or A bands remain the same length during the contraction but are pulled toward the origin of the muscle. As the A bands are pulled closer together the I bands shorten. The H bands then shorten during contraction and the thin filaments on the sides of the sarcomeres are pulled toward the middle.


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Contraction of Skeletal Muscles
Contraction of skeletal muscles creates tension allowing the muscles to shorten and perform work. There are several types of muscle contractions. Twitch is the rapid contraction and relaxation of muscle fibers. When muscles contraction occurs back to back and overlap a bit it is known as summation. When summation is close enough together that the muscle contractions are smooth and sustained it is known as tetanus.
There are a few different types of muscle contractions. An isometric contraction is when a muscle exerts tension without actually shortening. An isotonic contraction occurs when the muscle exerts tension and does shorten. When a muscle contracts but the force exerted on the muscle is greater than the contraction strength the muscle will lengthen it is known as eccentric or lengthening contraction.
When muscles contract they must first pull tight the noncontractile parts of the muscle and connective tissue of the tendons because they are elastic and resist distention. This brings in the series-elastic component. This component which says these elastic components of the muscle must be stretched tight before the tension of a muscle contraction can cause movement.
There are many components that affect the strength of a muscle contraction. These include things like the number of fibers stimulated, the frequency of stimulation, the thickness of each muscle fiber and the length of the muscle fibers at rest.


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Energy Requirements of Skeletal Muscles
When muscles are at rest most of their energy comes from aerobic respiration of fatty acids. When exercising this is not enough energy and muscle glycogen and blood glucose are also used as energy. Energy that is obtained from cell respiration is used to make ATP.
Muscle fibers are divided based on their contraction speed. Slow-twitch fibers are able to maintain contraction for a long period of time without fatigue, have a rich capillary supply, numerous mitochondria and aerobic respiratory enzymes, and a high myoglobin concentration which also makes them known as red fibers. Fast-twitch fibers are adapted for anaerobic respiration, have fewer capillaries and mitochondria, have less myoglobin, and are also known as white fibers. Intermediate fibers are fast twitch but also are adapted for aerobic respiration.
Muscle fatigue is an exercise-induced reduction in the ability of a muscle to generate force. There are many types or causes of muscle fatigue. During a sustained maximal contraction when all motor units are used at a maximum firing rate there is an increase in extracellular K+. During moderate exercise there is a depletion of muscle glycogen and a reduced ability of sarcoplasmic reticulum to produce Ca2++. Fatigue can also be caused by changes in the CNS before the muscles are truly fatigued. This is known as central fatigue and reduces the force of voluntary contractions.


Neural Control of Skeletal Muscles
Lower Motor Neurons or motoneurons have cell bodies in the spinal cord and axons within nerves that stimulate muscle contraction. These neurons are influenced by sensory feedback of muscles and tendons and facilitory and inhibitory effects for upper motor neurons.
To control skeletal movements the nervous system must receive sensory information from the Golgi tendon organs which provides the tension the muscle exerts on the tendons, and the muscle spindle apparatus which provides the muscle length. Alpha motoneurons innervate the extrafusal muscle fibers. Gamma motoneurons innervate the intrafusal fibers. Alpha motoneurons are faster conducting and can cause muscle contractions that result in skeletal movement. Gamma motoneurons are thinner and cannot cause skeletal movement.
Skeletal muscles are generally voluntary muscles, however they can contract unconsciously as in a reflex as a result from certain stimuli. Golgi tendon organs monitor tension in the tendons produced by muscle contraction. As tension in the tendons increase the Golgi tendon organs sensory neurons inhibit the activity of alpha motoneurons. This is known as a disynaptic reflex because sensory neurons synapse with interneuron's which make inhibitory synapse with motoneurons.


Cardiac and Smooth Muscles
Cardiac muscle is regulated by somatic motor neurons and are involuntary. Myocardial cells are striated and contain actin and myosin filaments arranged in sarcomeres and contract by sliding filament mechanism. Myocardial cells are tubular and joined to other myocardial cells by gap junctions. This makes it so action potentials can cross from one myocardial cell to another.
Smooth Muscle is arranged in circular layers in the walls of blood vessels and bronchiles. There are circular and longitudinal smooth muscle layers in the tubular digestive tract, ureters, ductus deferentia, and uterine tubes. They do not contain sarcomeres but do contain actin and some myosin. The thin filaments in smooth muscle are long compared to skeletal muscle. Myosin proteins are stacked vertically to form cross bridges with actin.


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JD.





ESSENTIAL QUESTIONSDescribe the sliding filament theory of muscle contraction and why it is called the sliding filament theory. Describe the action of the cross bridges that cause a power stroke. What is the role of Ca2+ and ATP in muscle contraction and relaxation?
As a muscle contracts it shortens. The shortening of the muscle is caused by the myofibrils shortening. The A bands move closer instead of shortening like the sarcomers. The distance between the sarcomers and the A bands is called an I band. The I bands will also get shorter. The I band is composed of thin filaments that do not get shorter. The sarcomers shorten because the thin filaments slide over the thick filaments. Cross bridges are formed when the myosin head attaches to the actin. The myosin heads contain ATP-binding sites. These heads can act as myosin ATPase enzymes which will eventually turn into ADP and Pi. ADP must be present on the myosin heads in order for them to bind to actin. A power stroke, which is what pulls the thin filaments into the A band center, happens after the Pi is released from the cross bridge. After the power stroke has happened the myosin head will break its bond with the actin and ATP will be released from the ADP that was bound to the myosin head. After all of this is complete this whole process should start all over again with a newly formed cross bridge. Cross bridges are prevented by tropomyosin when a muscle is relaxed. When the cross bridge is prevented from forming there becomes a decreased level of Ca2+ in the sarcoplasm. With stimulation, the Ca2+ level in the sarcoplasm become high very quickly. When this happens some of the Ca2+ will bind with troponin. This will cause a conformation change and the troponin and the tropomyosin will move allowing a cross bridge to form. So as you can see Ca2+ is very important in muscle contractions because if it is not there the cross bridges can not form and therefore there can be now muscle contraction.


SUMMARY

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Skeletal Muscles

One doesn’t normally think about their muscles, much less what they are made of or how they work. This is a pretty interesting chapter. I imagine if we didn’t have muscles, we would all be flopping around like jellyfish. That would be a mess, good thing we do!!!
The skeletal muscles are formed almost like boxes inside of each other. You start with a muscle, but that is actually made of lots of bundles called fascicles. Inside of the fascicles there are more bundles called myofibrils. Now each of the myofibrils are made up of many fibers called myofilaments. These myofibrils are the muscle cells and the cells span the length of the muscle it forms. Each one has the same organelles as other cells, but they are also multinucleated. Each of the parts of the muscle are covered with epithelial cells. The epimysium covers the whole muscle, where the perimysium covers each fascicle. The endomysium covers the myofibrils, confused yet? Each myofibril has a plasma membrane called a sarcolemma.




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Inside of a myofibril there are many myofilaments. There are two types, thick-myosin and thin-actin-filaments. These myofilaments are actually very short, but they are structured to overlap the length of the fiber. The sections where the myofilaments overlap give the skeletal muscle its striated look. One section of a muscle fiber is called a sarcomere. It consists of myosin in the middle and actin on the edges. The actin fibers are attached to the actin fibers of the next sarcomere. This is known as the Z line. A sarcomere spans the length from one Z line to the next. Where the myosin and actin overlap at rest is called the A band and where there is only myosin in the middle it is known as the H zone. These thick and thin myofilaments slide over each other, shortening the sarcomere and contracting the muscle. This is called the Sliding Filament Theory of contraction. This theory is explained in more detail in the essential questions section.
The skeletal muscles are stimulated by somatic motor neurons. The neuromuscular junction is where the neurons join with the muscle. The muscle and neuron form a motor end plate. This is where the neurotransmitter from the neuron releases to stimulate the muscle fiber. A somatic neuron can innervate more than one muscle fiber. A motor unit is considered a somatic neuron and all the muscle fibers it innervates. Innervation ratios vary from 1:100 to 1:2000. Fine neural control is best when there are many small motor units being stimulated. Neurons that innervate less muscle cells have a lower stimulation level so they are used more often. If then more strength is needed for contraction larger motor units are stimulated in a process called recruitment of motor units.



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Metabolism of Skeletal Muscles

The cardiopulmonary system need time to sufficiently increase the oxygen supply to our exercising muscles, so the skeletal muscle metabolize anaerobically for about the first minute and a half for moderate to heavy exercise. During moderate exercise, after the first two minutes, aerobic respiration contributes the major portion of skeletal muscle energy. Maximal oxygen uptake is the maximum rate of oxygen consumed in the body, also termed aerobic capacity. The aerobic capacity is determined by an individual’s age, size and sex. The range for aerobic capacity is about 12 mL of oxygen per minute per kg of body weight for an older or inactive individual but can be as high as 84 mL per minute for young male athletes. Lactate threshold (anaerobic threshold) is the intensity of exercise. The lactate threshold is the percentage of the maximal oxygen uptake where there is a significant rise in blood lactate levels. In healthy individuals significant amount of blood lactate appears when exercise is performed at about 50-70% of the aerobic capacity.

Most of the exercising muscles energy is obtained from aerobic respiration of fatty acids during light exercise. The fatty acids come mainly from the stored fat in adipose tissue. When exercising just below the lactate threshold, skeletal muscle energy is equally pulled from the fatty acids and from blood glucose. During heavy exercise two-thirds of skeletal muscle energy comes from glucose. GLUT-4, a carrier protein, is used for the diffusion of glucose. GLUT-4 moves into the muscle’s plasma membrane so the cell can take in an increased amount of glucose. This process is about 15-30% of the muscle’s energy needs during moderate exercise and goes up to 40% for heavy exercising.



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The rate of oxygen uptake does not immediately return to normal when you stop exercising. Breathing heavily after exercise helps the body to “pay off” its oxygen debt. When exercising, oxygen is pulled from the hemoglobin in the blood and myoglobin in the muscles. The extra oxygen obtained from breathing heavily after exercise allows the replacement of the oxygen used from the oxygen stores in the body to return to normal.

Muscle activity requires the use of ATP, which may be used faster than it can be produced in the body. Another high-energy phosphate compound called phosphocreatine can be used to form ATP the muscles need during activity. Phosphocreatine concentration is three times the concentration of ATP, so it is a ready reserve of energy phosphate that is donated to ADP. ATP production from ADP and phosphocreatine is very efficient, allowing ATP concentrations to only decrease slightly even though the rate of ATP breakdown is increased from rest to exercise.






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Cardiac and Smooth MuscleCardiac Muscle



Cardiac muscles are similar to skeletal muscles in that they have a striated look, but are like smooth muscle because they are not under voluntary control. The muscle fibers do not span the length of the muscle and the fibers are attached to each other by intercalated discs where there are gap junctions. The gap junctions are the electrical synapses that allow the electrical impulses to be conducted through the myocardial cell. The myocardial cells also contain sarcomeres with myosin and actin filaments and contract by means of the sliding filament theory like the skeletal muscles. The mass of myocardial cells are also known as the myocardium. Action potentials can originate at any point in the myocardium and spread through the myocardial cells by the gap junctions. This allows the myocardium to act as one functional unit. Unlike skeletal muscles where the contraction depends on the number of cells stimulated and because all of its cells contribute to contraction, the myocardium contracts to its full extent at each contraction.As discussed in chapter 14, cardiac muscle is able to produce action potentials automatically. Their action potentials originate in the pacemaker, but the rate of the spontaneous depolarization and rate of the heartbeat are regulated by the autonomic nervous system.


Myocardial cells also differ from skeletal muscle cells in the process of excitation-contraction coupling. In skeletal muscle there is a direct excitation-contraction coupling between the transverse tubules and sarcoplasmic reticulum. In myocardial cells the voltage-gated calcium channels in the plasma membrane and sarcoplasmic reticulum do not directly interact (connect). This difference means that the calcium that enters the cytoplasm via voltage-gated calcium channels in the transverse tubule stimulates the opening of the release channels for calcium in the sarcoplasmic reticulum. This is known as calcium-induced calcium release. In this way calcium serves as the second messenger that goes from the voltage-gated channels to the release channels. Because the transverse tubules and sarcopolasmic reticulum do not directly interact, it makes the excitation-contraction coupling slower in myocardial cells as compared to skeletal muscle.






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Smooth Muscle

In the walls of blood vessels and bronchioles smooth muscle is arranged in circular layers, but in the digestive tract, ureters, ductus deferntia, and fallopian tubes it is arranges in circular and longitudinal layers. Perstalsis occurs because of the way the circular and longitudinal layers contract with each other. This propels the contents of the tube in one direction. Smooth muscles do not contain sarcomeres, but do contain the myofilaments actin and myosin. The actin is found in a ratio of 16 to 1 to myosin. The myofilaments of smooth muscle are long and attach to regions of the plasma membrane or to cytoplasmic structures called dense bodies which are similar to the Z discs of skeletal muscle. Proper smooth muscle function is enabled by the arrangement of the contractile apparatus and because it is not organized into sarcomeres. This allows the muscle to contract even when greatly stretched. The smooth muscle of the bladder may stretch up to two and a half times its resting length where the smooth muscle of the uterus can stretch up to eight times its original length during pregnancy.


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Contraction of smooth muscle is stimulated by an increase in the calcium concentration in the cytoplasm of the muscle cell. In smooth muscle the sarcoplasmic reticulum is less developed than in skeletal muscle so calcium is only released by it to activate the initial phase of contraction. For sustained contraction the extracellular calcium diffuses through the plasma membrane. The extracellular calcium enters the plasma membrane through voltage-gated calcium channels. These channels are graded by the amount of depolarization so the greater the depolarization more calcium will enter the cell and the contraction will be stronger. After the calcium enters the cytoplasm it combines with calmodulin, which is a protein that is structurally similar to troponin. This complex then combines with and activates MLCK (myosin light-chain kinase). MLCK is an enzyme that catalyzes the phosphorylation of myosin light chains which is a component of myosin cross bridging. Smooth muscle can produce graded depolarization and contractions without producing action potentials. Greater depolarization allows greater diffusion of calcium and more MLCK enzymes are activated. As more MLCK enzymes become activated, more cross bridges will become phosphorylated to bind with actin, so a stronger depolarization leads to a stronger contraction.



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Fox, Stuart Ira. (2009). Human Physiology. New York, NY: McGraw-Hill.


LJ


APPLICATION
As a nurse I would need to know that if the troponin level in a blood sample is elevated it would be indicative of a myocardial infarction.JM


As a nurse I will be working with the elderly and I as a nurse will have to understand that with patients who are bed ridden or patients with a cast muscles can become smaller and decline in strength. And with patients who have a cast, this decline is much faster. This is why, usually when the cast is removed the affected leg is smaller then the non-affected leg or extremity. It is still important to continue with exercise to the non-affected extremity. Also as a nurse i will work with patients with certain diseases that affect the muscles such as ALS amyotrophic lateral sclerosis where as a nurse I am able to recognize the disease as a rapidly, progressive, fatal neurologic disorder resulting in destruction of motorneurons of the cortex, brain stem and spinal cord. The motorneurons that are affected are known as the lower and higher motorneurons. Lower motorneurons are neurons whose axons control the skeletal muscles and signs of damage to these motorneurons would be muscle weakness and muscle atrophy ( as we discussed above, is the size reduction of the muscle with the decline in muscle strength). Upper or Higher motorneurosn are neurons in the brain that control skeletal movements and act by facilitating or inhibiting the activity of the lower motorneurons. Signs of damage to these motorneurons include spasticity, brisk reflexes, and a positive Babinski sign, which is when the lateral side of the sole of the foot is rubbed with a blunt object and the great toes dorsiflexes and the other toes fan out. I as a nurse need to recognize the a positive Babinski sign and be able to notice the signs and symptoms to diseases so this information may be passed along to the MD. Also as a nursing consideration, as a nurse I an provide physical, spiritual and emotional support the the family and patient. Some of the treatments include a drug that can prolong survival is Riluzole and the additional treatments include only palliative treatments with support and symptom management. I also understand that ALS has no cure or therapy that will slow the progression of the disease process. AR

CASE STUDY

http://www.sciencecases.org/teeth/teeth.asp


Part 1: The Hospital

1.) How is heat generated in the body?
Muscles in the body generate about 85% of the total body heat (due to contraction and relaxation). Heat is also the by-product of metabolic processes; large organs such as the liver produce substantial amount of heat for the body.

2.) In this case, where halothane-induced heat production quickly elevated Mr. Thompson's body temperature, where do you think most of the heat is generated?
I think the heat is coming from the increased amount of Ca2+ entering his skeletal muscles from the endoplasmic reticulum, causing an increase in muscular contraction through the use of energy (ATP), thus, producing large amount of heat.

3.) What chemical reaction is responsible for generating the huge amount of heat?
ATP (adenosine triphosphate), which will be broken down into ADP-P (adenosine diphoshpate and a phosphate).

4.) Which processes use ATP as an energy source in skeletal muscle?
Both contraction and relaxation of skeletal muscles requires the use of ATP. ATP is needed for the movement of the cross bridges in muscle contraction and the pumping of Ca2+ into the sarcoplasmic reticulum for muscle relaxation.

Part 2: The Motor Neuron
An action potential enters the presynaptic terminal. Voltage-gated channels open and Ca2+ and Na+ ions enter the presynaptic terminal. Ca2+ ions cause neurotransmitter containing vesicles to fuse with the presynaptic membrane. Acetylcholine is liberated into the synaptic cleft.

Part 3: The Chemical Synapse
Acetylcholine is secreted into the cleft by the motor axon. The neurotransmitter reacts with nicotinic acetylcholine receptors on the muscle membrane. Channels open and the muscle membrane depolarizes. This produces and end-plate potential in the muscle membrane.
Acetylcholine is secreted into the cleft by the motor axon. The neurotransmitter reacts with nicotinic acetylcholine receptors on the muscle membrane.The neurotransmitter is broken down by enzyme acetylcholinesterase in the synaptic cleft. Choline is taken up into the presynaptic cleft.


Part 4: The Muscle
Acetylcholine binding opens the channels and the muscle membrane becomes depolarized. This creates an action potential which travels along the sarcolemma. The action potential travels down the T-tublules, the impulse passes to the sarcoplasmic reticulum and stimulates voltage-sensitive calcium gates. Calcium ions are released into the sarcoplasm from the sarcoplasmic reticulum. Calcium binds to troponin. Tropomyosin moves to expose the myosin binding sites on actin. Cross bridge cycling causes the sarcomeres to shorten (contract). Calcium is taken up into the sarcoplasmic reticulum to terminate the contraction.


Part 5: Hypothesis

The anesthetic Halothane stimulates contraction Ca2+ release from the sarcoplasmic reticulum in normal skeletal muscles.
Hypothermia is a reaction that occurs in individuals with an inherited (genetically-linked trait) abnormality of skeletal-muscle sarcoplasmic reticulum that causes a rapid increase in the intracellular Ca2+ levels in response to halothane and other inhalation anesthetics
A drug called Dantrolene Sodium is an antidote when a person is having a reaction to halothane or other inhalation anesthetics. Dantrolene Sodium is a muscle relaxant that acts by stopping excitation-contraction coupling in muscle cells, by interfering with the release of Ca++ from the sarcoplasmic reticulum in skeletal muscles. This drug is the only specific and effective drug for malignant hyperthermia, triggered by anesthesia.

































Sources:
http://www.answers.com/topic/thermoregulation-1
http://www.ojrd.com/content/2/1/21
http://faculty.taftcollege.edu/dsheehy/includes/courses/Physiology7/Documents/8%20Muscular%20System%20Intro.pdf
Fox, Stuart Ira. (2009). Human Physiology. New York, NY: McGraw-Hill.
http://www.drugs.com/pro/halothane.html