1.2-1.3 Introduction to muscle physiology

muscle relaxation

AP ends, electrical stimulation of SR stops Ca2+ pumped back into SR Stored until next AP arrives Requires ATP Without Ca2+, troponin and tropomyosin return to resting conformation Covers myosin-binding site Prevents actin-myosin cross-bridging

Molecular basis of contraction

(1) AP from alpha motor neuron (2)release ACh at neuromuscular junction (3) nicotinic ACh receptors in sarcolemma open (4) causes EPSP (5) AP travel down sarcolemma (6) into sarcoplasmic reticulum through opening into T-tubles (7) AP causes conformational change in tetrad and open Ca2+ release channels in SR (8) increase Ca2+ in cytosol (9) Ca2+ binds to troponin (10) Shifts tropomyosin (11) exposes myosin binding site on actin (12) myosin head binds actin (13) myosin pivots (14) ATP binds to myosin to disengage it from actin (15) cycle continues as long as Ca2+ is present

what is the RMP of muscle membrane?

-90 mv

What are the general mechanisms of a muscle contraction?

1. An action potential travels along a motor nerve to its endings on muscle fibers. 2. At each ending, the nerve secretes a small amount of the neurotransmitter acetylcholine. 3. Acetylcholine acts on a local area of the muscle fiber membrane to open acetylcholine-gated cation channels through protein molecules floating in the membrane. 4. The opening of acetylcholine-gated channels allows large quantities of sodium ions to diffuse to the interior of the muscle fiber membrane. This action causes a local depolarization that in turn leads to the opening of voltage-gated sodium channels, which initiates an action potential at the membrane. 5. The action potential travels along the muscle fiber membrane in the same way that action potentials travel along nerve fiber membranes. 6. The action potential depolarizes the muscle membrane, and much of the action potential electricity flows through the center of the muscle fiber. Here it causes the sarcoplasmic reticulum to release large quantities of calcium ions that have been stored within this reticulum. 7. The calcium ions initiate attractive forces between the actin and myosin filaments, causing them to slide alongside each other, which is the contractile process. 8. After a fraction of a second, the calcium ions are pumped back into the sarcoplasmic reticulum by a Ca 2+ membrane pump and remain stored in the reticulum until a new muscle action potential comes along; this removal of calcium ions from the myofibrils causes the muscle contraction to cease.

what are the 2 primary factors that can be adjusted to accomplish gradation of whole muscle tension?

1. number of muscle fibers contracting within a muscle 2. tension developed by each contraction fiber

One nerve impulse can release _______ Act vesicles

125

synaptic cleft

20-30 nm - space between the axon terminal and the muscle cell membrane - it contains the enzyme cholinesterase which can destroy Ach

what is the relationship of load to velocity of contraction in a skeletal muscle?

A skeletal muscle contracts rapidly when it contracts against no load to a state of full contraction in about 0.1 second for the average muscle. When loads are applied, the velocity of contraction decreases progressively as the load increases. When the load has been increased to equal the maximum force that the muscle can exert, the velocity of contraction becomes zero, and no contraction results, despite activation of the muscle fiber. This decreasing velocity of contraction with load occurs because a load on a contracting muscle is a reverse force that opposes the contractile force caused by muscle contraction. Therefore, the net force that is available to cause the velocity of shortening is correspondingly reduced.

The sarcolemma

A think membrane enclosing a skeletal muscle fiber that consists of a true cell membrane, called the plasma membrane, and an outer coat made up of a thin layer of polysaccharide material that contains numerous thin collagen fibrils

Ratchet theory of contraction

ATP is hydrolyzed, its chemical energy is stored in myosin head (re cocking) ADP remained bound - ATP is responsible for cocking (pulling back) the myosin head, ready for another cycle. When it binds to the myosin head, it causes the cross bridge between actin and myosin to detach - ATP then provides the energy to pull the myosin back, by hydrolyzing to ADP + Pi

synthesis and storage of Acetylcholine

Ach is synthesized locally in the cytoplasm of the nerve termite and is rapidly absorbed into the synaptic vesicles then they are carried by axoplasmic transport to the nerve terminal.

Troponin and Its Role in Muscle Contraction.

Attached intermittently along the sides of the tropomyosin molecules are additional protein molecules called troponin. These protein molecules are actually complexes of three loosely bound protein subunits, each of which plays a specific role in controlling muscle contraction. One of the subunits (troponin I) has a strong affinity for actin, another (troponin T) for tropomyosin, and a third (troponin C) for calcium ions. This complex is believed to attach the tropomyosin to the actin. The strong affinity of the troponin for calcium ions is believed to initiate the contraction process

Researchers are studying muscle contraction in health subjects. volunteers are asked to contract the biceps agains resistance. which of the following will occur during this activity? a. tropomyosin moves into binding groove b. A band increases in size c. H band increases in size d. Myosin releases adenosine diphosphate e. troponin releases calcium

Answer D (CORRECT ANSWER): Muscle contraction begins when a motor neuron depolarizes a skeletal myocyte, triggering calcium release from the sarcoplasmic reticulum. calcium binds troponin, which removes tropomyosin from the myosin binding groove. myosin then binds actin and moves along the actin filament to cause contraction A. tropomyosin moves out of (not into) the myosin binding groove during contraction B. the A band is the region of the sarcomere where actin and myosin overlap. This band does not change in size during contraction C. The H band is located at the center of the sarcomere, this region shrinks during contraction E. Calcium binds to troponin to initiate muscle contraction

walk along theory of contraction

As soon as the actin filament is activated by the calcium ions, the heads of the cross-bridges from the myosin filaments become attracted to the active sites of the actin filament and initiate contraction. When a head attaches to an active site, this attachment simultaneously causes profound changes in the intramolecular forces between the head and arm of its cross-bridge. The new alignment of forces causes the head to tilt toward the arm and to drag the actin filament along with it. This tilt of the head is called the power stroke. Immediately after tilting, the head then automatically breaks away from the active site. Next, the head returns to its extended direction. In this position, it combines with a new active site farther down along the actin filament; the head then tilts again to cause a new power stroke, and the actin filament moves another step. Thus, the heads of the cross-bridges bend back and forth and, step by step, walk along the actin filament, pulling the ends of two successive actin filaments toward the center of the myosin filament.

Weight lifting can result in a dramatic increase in skeletal muscle mass. This increase in muscle mass is primarily attributable to which of the following? A. Fusion of sarcomere between adjacent myofibrils B. hypertrophy of individual muscle fibers C. increase in skeletal muscle blood supply D. increase in the number of motor neurons E. increase in the number of neuromuscular junctions

B. prolongated or repeated maximal contraction results in a concomitant increase in the synthesis of contractile proteins and an increase in muscle mass. This increase in mass or hypertrophy is observed at the level of individual muscle fibers

which of the following decreases in length during the contraction of a skeletal muscle fiber? a. A band of the sarcomere b. I band of the sarcomere c. thick filaments d. thin filaments e. z disks of the sarcomere

B. the physical lengths of the actin and myosin filaments do not change during contraction, therefore the A band, which is composed of myosin filaments, does not change either. The distance between z disks decreases, but z disks themselves do not change. Only the I band decreases in length as the muscle contracts

What happens during an end plate potential?

Binding of ACh with the ACh receptors in the post synaptic membrane of the motor end plates causes opening of ligand gated Na+ and K+ channels which causes greater influx of Na+ than efflux of K+ leading to localized depolarization of motor end plate to about +50-75 mv called as the end plate potential. EPP is not an action potential but it is simply depolarization of specialized motor end plate

Mechanism of action of tents toxin and botulinum toxin

Botulinum toxin imparts neuromuscular transmission by binding to the presynaptic terminal and entering the presynaptic terminal through endocytosis, cleaves the membrane docking proteins and prevents acetylcholine exocytosis Botulinum toxin A cleaves SNAP25 while botulinum toxin B cleaves synaptobrevin to limit exocytosis mechanism of tetanus toxin is similar to botulinum toxin the differences is, the tetanus toxin causes spastic paralysis instead of flaccid paralysis. it delivers toxin to inhibitory neurons by which GABA and glycine not produced that leads to overwhelming excitatory signals and extreme muscle spasm

Which of the following is the mechanism of action of rigor mortis? A. Withdrawal of Ca2+, which stops cycling at position 1 B. Cytosolic calcium rises and binds to troponin-C, exposing myosin-binding site on actin C. Depletion of ATP, which stops cycling at position 3 D. Depletion of calcium, which stops cycling at position 3 E. Depletion of actin-myosin cross bridging, which stops cycling at position 3

C. Depletion of ATP, which stops cycling at position 3

Which of the following is a characteristic of white muscle? A. It is responsible for slower muscle movements. B. It has a high mitochondria content. C. It primarily utilizes aerobic metabolism. D. It has a greater mass per motor unit. E. It contains high amounts of myoglobin

D. It has a greater mass per motor unit.

end plate potential (EPP)

Depolarization of the membrane potential of skeletal muscle fiber, caused by the action of the transmitter acetylcholine at the neuromuscular synapse to which sodium channels open and sodium diffuses into the muscle causes a local, non propagated potential

Fast fibers

Fast Fibers (Type II, White Muscle) The following are characteristics of fast fibers: 1. Fast fibers are large for great strength of contraction. 2. Fast fibers have an extensive sarcoplasmic reticulum for rapid release of calcium ions to initiate contraction. 3. Large amounts of glycolytic enzymes are present in fast fibers for rapid release of energy by the glycolytic process. 4. Fast fibers have a less extensive blood supply than slow fibers because oxidative metabolism is of secondary importance. 5. Fast fibers have fewer mitochondria than slow fibers, also because oxidative metabolism is secondary. A deficit of red myoglobin in fast muscle gives it the name white muscle.

Lever systems of the body

In short, an analysis of the lever systems of the body depends on knowledge of the following: (1) the point of muscle insertion; (2) its distance from the fulcrum of the lever; (3) the length of the lever arm; and (4) the position of the lever. Many types of movement are required in the body, some of which need great strength and others that need large distances of movement. For this reason, there are many different types of muscle; some are long and contract a long distance, and some are short but have large cross-sectional areas and can provide extreme strength of contraction over short distances. The study of different types of muscles, lever systems, and their movements is called kinesiology and is an important scientific component of human physiology.

Describe the activation of actin filament by calcium ions

In the presence of large amounts of calcium ions, the inhibitory effect of the troponin-tropomyosin on the actin filaments is itself inhibited. When calcium ions combine with troponin C, each molecule of which can bind strongly with up to four calcium ions, the troponin complex then undergoes a conformational change that in some way tugs on the tropomyosin molecule and moves it deeper into the groove between the two actin strands. This action uncovers the active sites of the actin, thus allowing these active sites to attract the myosin cross-bridge heads and allow contraction to proceed. Although this mechanism is hypothetical, it emphasizes that the normal relationship between the troponin-tropomyosin complex and actin is altered by calcium ions, producing a new condition that leads to contraction.

muscle fatigue

Inability of muscle to maintain its strength of contraction or tension; may be related to insufficient oxygen, depletion of glycogen, and/or lactic acid buildup Prolonged strong contraction of a muscle leads to the well-known state of muscle fatigue. Studies in athletes have shown that muscle fatigue increases in almost direct proportion to the rate of depletion of muscle glycogen. Therefore, fatigue results mainly from the inability of the contractile and metabolic processes of the muscle fibers to continue supplying the same work output. However, experiments have also shown that transmission of the nerve signal through the neuromuscular junction can diminish at least a small amount after intense prolonged muscle activity, thus further diminishing muscle contraction. Interruption of blood flow through a contracting muscle leads to almost complete muscle fatigue within 1 or 2 minutes because of the loss of nutrient supply, especially the loss of oxygen.

frequency summation and tetanization

Individual twitch contractions occurring one after another at low frequency of stimulation are displayed on the left. Then, as the frequency increases, there comes a point when each new contraction occurs before the preceding one is over. As a result, the second contraction is added partially to the first, and thus the total strength of contraction rises progressively with increasing frequency. When the frequency reaches a critical level, the successive contractions eventually become so rapid that they fuse together, and the whole muscle contraction appears to be completely smooth and continuous, as shown in the figure. This process is called tetanization. At a slightly higher frequency, the strength of contraction reaches its maximum, so any additional increase in frequency beyond that point has no further effect in increasing contractile force. Tetany occurs because enough calcium ions are maintained in the muscle sarcoplasm, even between action potentials, so that a full contractile state is sustained without allowing any relaxation between the action potentials.

Neuromuscular blocking agents

Inhibit transmission of nerve impulses by binding with cholinergic receptor sites, antagonizing action of acetylcholine.

What is sarcoplasm?

It is the intracellular fluid between myofibrils

What are transverse tubules?

Membranous channels that extend inward from the plasma membrane of the muscle cell and pass all the way through the cell the overlie the z lines between the adjacent sarcomeres between A and I bands they are a path for rapid transmission of action potential from cell membrane to all the fibrils at once of a muscle fiber

Isometric contractions

Muscle contracts but there is no movement, muscle stays the same length

When does maximum efficiency of muscle contraction occur?

ordinarily, maximum efficiency occurs when the velocity of contraction is about 30% of maximum

miniature end plate potential (MEPP)

Small, spontaneous depolarization of the membrane potential of skeletal muscle cells, caused by the release of a single quantum of acetylcholine. usually amount 0.5 mv significance is not known, probably responsible for the tone of muscle

Sources of energy for muscle contraction

Phosphocreatine, glycolysis, oxidative metabolism Most of the energy required for muscle contraction is used to trigger the walk-along mechanism whereby the cross-bridges pull the actin filaments, but small amounts are required for the following: (1) pumping calcium ions from the sarcoplasm into the sarcoplasmic reticulum after the contraction is over; and (2) pumping sodium and potassium ions through the muscle fiber membrane to maintain an appropriate ionic environment for the propagation of muscle fiber action potentials. The third and final source of energy is oxidative metabolism , which means combining oxygen with the end products of glycolysis and with various other cellular foodstuffs to liberate ATP. More than 95% of all energy used by the muscles for sustained long-term contraction is derived from oxidative metabolism.

Rigor Mortis

Several hours after death, all the muscles of the body go into a state of contracture that is, the muscles contract and become rigid, even without action potentials. This rigidity results from loss of all the ATP, which is required to cause separation of the cross-bridges from the actin filaments during the relaxation process. The muscles remain in rigor until the muscle proteins deteriorate about 15 to 25 hours later, which presumably results from autolysis caused by enzymes released from lysosomes. All these events occur more rapidly at higher temperatures.

Slow fibers

Slow Fibers (Type 1, Red Muscle) The following are characteristics of slow fibers: 1. Slow fibers are smaller than fast fibers. 2. Slow fibers are also innervated by smaller nerve fibers. 3. Slow fibers have a more extensive blood vessel system and more capillaries to supply extra amounts of oxygen compared with fast fibers, 4. Slow fibers have greatly increased numbers of mitochondria to support high levels of oxidative metabolism. 5. Slow fibers contain large amounts of myoglobin, an iron-containing protein similar to hemoglobin in red blood cells. Myoglobin combines with oxygen and stores it until needed, which also greatly speeds oxygen transport to the mitochondria. The myoglobin gives the slow muscle a reddish appearance—hence, the name red muscle.

what is summation?

Summation means the adding together of individual twitch contractions to increase the intensity of overall muscle contraction. Summation occurs in two ways: (1) by increasing the number of motor units contracting simultaneously, which is called multiple fiber summation ; and (2) by increasing the frequency of contraction, which is called frequency summation and can lead to tetanization

The pathway that appears to account for much of the protein degradation in a muscle undergoing atrophy is the

TP-dependent ubiquitin-proteasome pathway . Proteasomes are large protein complexes that degrade damaged or unneeded proteins by proteolysis , a chemical reaction that breaks peptide bonds. Ubiquitin is a regulatory protein that basically labels which cells will be targeted for proteosomal degradation.

central fatigue

caused by the CNS and psychological mechanisms and manifests as feeling "tired" or not wanting to go on

what is the first source of energy for muscle contraction?

The first source of energy that is used to reconstitute the ATP is the substance phosphocreatine , which carries a high-energy phosphate bond similar to the bonds of ATP. The high-energy phosphate bond of phosphocreatine has a slightly higher amount of free energy than that of each ATP bond Therefore, phosphocreatine is instantly cleaved, and its released energy causes bonding of a new phosphate ion to ADP to reconstitute the ATP. However, the total amount of phosphocreatine in the muscle fiber is also small, only about 5 times as great as the ATP. Therefore, the combined energy of both the stored ATP and the phosphocreatine in the muscle is capable of causing maximal muscle contraction for only 5 to 8 seconds

What is the Fenn effect?

The greater the amount of work performed = the greater the amount of ATP that is cleaved When a muscle contracts, work is performed, and energy is required. Large amounts of ATP are cleaved to form ADP during the contraction process, and the more work performed by the muscle, the more ATP that is cleaved; this phenomenon is called the Fenn effect. The following sequence of events is believed to be the means whereby this effect occurs: 1.Before contraction begins, the heads of the cross-bridges bind with ATP. The ATPase activity of the myosin head immediately cleaves the ATP but leaves the cleavage products, ADP plus phosphate ion, bound to the head. In this state, the conformation of the head is such that it extends perpendicularly toward the actin filament but is not yet attached to the actin. 2. When the troponin-tropomyosin complex binds with calcium ions, active sites on the actin filament are uncovered, and the myosin heads then bind with these sites 3. The bond between the head of the cross-bridge and the active site of the actin filament causes a conformational change in the head, prompting the head to tilt toward the arm of the cross-bridge and providing the power stroke for pulling the actin filament. The energy that activates the power stroke is the energy already stored, like a cocked spring, by the conformational change that occurred in the head when the ATP molecule was cleaved earlier. 4. Once the head of the cross-bridge tilts, release of the ADP and phosphate ion that were previously attached to the head is allowed. At the site of release of the ADP, a new molecule of ATP binds. This binding of new ATP causes detachment of the head from the actin. 5. After the head has detached from the actin, the new molecule of ATP is cleaved to begin the next cycle, leading to a new power stroke. That is, the energy again cocks the head back to its perpendicular condition, ready to begin the new power stroke cycle. 6 .When the cocked head (with its stored energy derived from the cleaved ATP) binds with a new active site on the actin filament, it becomes uncocked and once again provides a new power stroke. Thus, the process proceeds again and again until the actin filaments pull the Z membrane up against the ends of the myosin filaments or until the load on the muscle becomes too great for further pulling to occur.

Muscle Hypertrophy and Muscle Atrophy

The increase of the total mass of a muscle is called muscle hypertrophy. When the total mass decreases, the process is called muscle atrophy

maximum strength of contraction

The maximum strength of tetanic contraction of a muscle operating at a normal muscle length averages between 3 and 4 kg/cm 2 of muscle, or 50 pounds/inch 2 . Because a quadriceps muscle can have up to 16 square inches of muscle belly, as much as 800 pounds of tension may be applied to the patellar tendon. Thus, one can readily understand how it is possible for muscles to pull their tendons out of their insertions in bone.

Remodeling of muscle to match function

The muscles of the body continually remodel to match the functions required of them. Their diameters, lengths, strengths, and vascular supplies are altered, and even the types of muscle fibers are altered, at least slightly. This remodeling process is often quite rapid, occurring within a few weeks. Experiments in animals have shown that muscle contractile proteins in some smaller, more active muscles can be replaced in as little as 2 weeks.

The ___________ is a thin membrane enclosing and skeletal muscle fiber

The sarcolemma is a thin membrane enclosing a skeletal muscle fiber

What is the second source of energy for muscle contraction?

The second important source of energy, which is used to reconstitute both ATP and phosphocreatine, is a process called glycolysis —the breakdown of glycogen previously stored in the muscle cells. Rapid enzymatic breakdown of the glycogen to pyruvic acid and lactic acid liberates energy that is used to convert ADP to ATP; the ATP can then be used directly to energize additional muscle contraction and also to re-form the stores of phosphocreatine. The importance of this glycolysis mechanism is twofold. First, glycolytic reactions can occur even in the absence of oxygen, so muscle contraction can be sustained for many seconds and sometimes up to more than 1 minute, even when oxygen delivery from the blood is not available. Second, the rate of ATP formation by glycolysis is about 2.5 times as rapid as ATP formation in response to cellular foodstuffs reacting with oxygen. However, so many end products of glycolysis accumulate in the muscle cells that glycolysis also loses its capability to sustain maximum muscle contraction after about 1 minute

What is the final source of energy in muscle?

The third and final source of energy is oxidative metabolism , which means combining oxygen with the end products of glycolysis and with various other cellular foodstuffs to liberate ATP. More than 95% of all energy used by the muscles for sustained long-term contraction is derived from oxidative metabolism. The foodstuffs that are consumed are carbohydrates, fats, and protein. For extremely long-term maximal muscle activity—over a period of many hours—the greatest proportion of energy comes from fats but, for periods of 2 to 4 hours, as much as one half of the energy can come from stored carbohydrates.

What are I bands?

They are the light bands, containing thin filaments (actin) but no thick filaments. They also contain the protein titin, which helps return myofilaments to their original position after contraction. They are isotropic to polarized light

what causes the actin filaments to slide inward among the myosin filaments?

This action is caused by forces generated by interaction of the cross-bridges from the myosin filaments with the actin filaments. Under resting conditions, these forces are inactive, but when an action potential travels along the muscle fiber, this causes the sarcoplasmic reticulum to release large quantities of calcium ions that rapidly surround the myofibrils. The calcium ions, in turn, activate the forces between the myosin and actin filaments, and contraction begins. However, energy is needed for the contractile process to proceed. This energy comes from high-energy bonds in the ATP molecule, which is degraded to adenosine diphosphate (ADP) to liberate the energy.

Duchenne muscular dystrophy(DMD)

This disease affects only males because it is transmitted as an X-linked recessive trait and is caused by mutation of the gene that encodes for a protein called dystrophin , which links actins to proteins in the muscle cell membrane. Dystrophin and associated proteins form an interface between the intracellular contractile apparatus and extracellular connective matrix. Although the precise functions of dystrophin are not completely understood, lack of dystrophin or mutated forms of the protein cause muscle cell membrane destabilization and activation of multiple pathophysiological processes, including altered intracellular calcium handling and impaired membrane repair after injury. One important effect of abnormal dystrophin is an increase in membrane permeability to calcium, thus allowing extracellular calcium ions to enter the muscle fiber and initiate changes in intracellular enzymes that ultimately lead to proteolysis and muscle fiber breakdown. Symptoms of DMD include muscle weakness that begins in early childhood and rapidly progresses, so that the patient is usually in wheelchairs by age 12 years and often dies of respiratory failure before age 30 years

What molecules keep the myosin and actin filaments in place?

Titin filamentous molecules

What is the binding site for Ca2+ that helps to alter positions of troponin I and tropomyosin thus expose the active sites of actin to initiate the contraction?

Troponin C

What along with tropomyosin, helps in the inhibition of the active sites of actin

Troponin I

what binds components to tropomyosin?

Troponin T

Hyperplasia of muscle fibers

Under rare conditions of extreme muscle force generation, the actual number of muscle fibers has been observed to increase (but only by a few percent), in addition to the fiber hypertrophy process. This increase in fiber number is called fiber hyperplasia. When it does occur, the mechanism is linear splitting of previously enlarged fibers.

coactivation of agonist and antagonist muscles

Virtually all body movements are caused by simultaneous contraction of agonist and antagonist muscles on opposite sides of joints. This process is called coactivation of the agonist and antagonist muscles , and it is controlled by the motor control centers of the brain and spinal cord.

Energetics of Muscle Contraction

When a muscle contracts against a load, it performs work. To perform work means that energy is transferred from the muscle to the external load to lift an object to a greater height or to overcome resistance to movement. W = L X D which W is the work output, L is the load, and D is the distance of movement against the load. The energy required to perform the work is derived from the chemical reactions in the muscle cells during contraction, as described in the following sections.

Muscle Denervation Causes Rapid Atrophy

When a muscle loses its nerve supply, it no longer receives the contractile signals that are required to maintain normal muscle size. Therefore, atrophy begins almost immediately. After about 2 months, degenerative changes also begin to appear in the muscle fibers. If the nerve supply to the muscle grows back rapidly, full return of function can occur in as little as 3 months but, from then onward, the capability of functional return becomes less and less, with no further return of function after 1 to 2 years. In the final stage of denervation atrophy, most of the muscle fibers are destroyed and replaced by fibrous and fatty tissue. The fibers that do remain are composed of a long cell membrane with a lineup of muscle cell nuclei but with few or no contractile properties and little or no capability of regenerating myofibrils if a nerve does regrow. The fibrous tissue that replaces the muscle fibers during denervation atrophy also has a tendency to continue shortening for many months, a process called contracture. Therefore, one of the most important problems in the practice of physical therapy is to keep atrophying muscles from developing debilitating and disfiguring contractures. This goal is achieved by daily stretching of the muscles or use of appliances that keep the muscles stretched during the atrophying process.

Recovery of Muscle Contraction in Poliomyelitis: Development of Macromotor Units

When some but not all nerve fibers to a muscle are destroyed, as occurs in poliomyelitis, the remaining nerve fibers branch off to form new axons that then innervate many of the paralyzed muscle fibers. This process results in large motor units called macromotor units , which can contain as many as five times the normal number of muscle fibers for each motoneuron coming from the spinal cord. The formation of large motor units decreases the fineness of control one has over the muscles but allows the muscles to regain varying degrees of strength

All the muscle fibers innervated by a single nerve fiber are called

a motor unit

Myofibrils are composed of

actin and myosin filaments

What are actin filaments composed of?

actin, tropomyosin, troponin The backbone of the actin filament is a double-stranded F-actin protein molecule , represented by the two lighter-colored strands. The two strands are wound in a helix in the same manner as the myosin molecule. Each strand of the double F-actin helix is composed of polymerized G-actin molecules. Attached to each one of the G-actin molecules is one molecule of ADP. These ADP molecules are believed to be the active sites on the actin filaments with which the cross-bridges of the myosin filaments interact to cause muscle contraction. The active sites on the two F-actin strands of the double helix are staggered, giving one active site on the overall actin filament about every 2.7 nanometers.The bases of the actin filaments are inserted strongly into the Z disks; the ends of the filaments protrude in both directions to lie in the spaces between the myosin molecules

what binds actin to z lines?

actinin

What happens after Ach acts on the receptors?

after Ach acts on the receptors, it is hydrolyzed by the enzyme cholinesterase into acetate and choline the choline is actively reabsorbed into the nerve terminal to be used again to form ACh this whole process of ACh release, action, and destruction takes about 5-10 ms

ATP, myosin head

allows myosin head to detach from actin, and ready for next contraction. the myosin head that is essential for muscle contraction is that it functions as an adenosine triphosphatase (ATPase) enzyme. this property allows the head to cleave ATP and use the energy derived from the ATP's high-energy phosphate bond to energize the contraction process.

Virtually all muscle hypertrophy results from

an increase in the number of actin and myosin filaments in each muscle fiber, causing enlargement of the individual muscle fibers; this condition is called simply fiber hypertrophy

Which of the following properties of depolarizing blocking agents allow them to be successful ACh agonists? a. they have a high affinity for DHP receptors than ACh b. they are more resistant to degradation than ACh c. they prevent Ca+ from entering the post-synaptic membrane to cause depolarization d. they prevent Na+ from entering the pre-synaptic membrane to cause depolarization

b. they are more resistant to degradation than ACh

Activation of the Actin filament by

calcium ions

non depolarizing blocking agents

classify as competitive acetylcholine antagonists, which directly bind to the alpha subunits of nicotinic receptors on the postsynaptic membrane and maintains the polarized motor endplate. this metabolic process leads to muscular paralysis, a favorable condition for patients undergoing preoperative procedures

Thin filaments

composed of actin

Thick filaments

composed of myosin

What is the neuromuscular junction?

connection between the motor neuron and the muscle fiber; the nerve fiber branches at its end to form a complex branching nerve terminals, which invaginates into muscle fiber but lie outside the muscle fiber plasma membrane (motor end plate)

axon terminal

contains around 300,00 vesicles which contain the neurotransmitter acetylcholine (Ach)

What are A bands?

dark bands, made of overlapping myosin filaments, has m-lines in the center and are anisotropic to polarized light

what binds the plasma membrane to z lines?

desmin

what binds actin to plasma membrane?

dystrophin

What are terminal cisternae?

enlarged areas of the sarcoplasmic reticulum surrounding the transverse tubules. they are arranged near cell membrane and store Ca2+ for muscle contraction. Extensive in rapidly contracting types of muscle fibers and helps in muscle metabolism

excitation-contraction coupling

events that link the action potentials on the sarcolemma to activation of the myofilaments, thereby preparing them to contract

Z disk

filamentous network of protein. Serves as attachment for actin myofilaments

active tension

force applied to an object to be lifted when a muscle contracts. it is initiated by cross bridge formation and movement of thin and thick filaments. the amount of tension generated depends on neuronal factors (frequency, number and size of the motor unit) and mechanical properties (isometric length tension relationship and force velocity relationship) of muscle

muscular dystrophy

group of inherited diseases characterized by progressive weakness and degeneration of muscle fibers without involvement of the nervous system

When a muscle remains unused for many weeks, the rate of degradation of the contractile proteins

is more rapid than the rate of replacement. Therefore, muscle atrophy occurs. The pathway that appears to account for much of the protein degradation in a muscle undergoing atrophy is the ATP-dependent ubiquitin-proteasome pathway . Proteasomes are large protein complexes that degrade damaged or unneeded proteins by proteolysis , a chemical reaction that breaks peptide bonds. Ubiquitin is a regulatory protein that basically labels which cells will be targeted for proteosomal degradation.

Synaptic gutter (Synaptic trough)

it is the muscle cell membrane which is in contact with the nerve terminal. it has many folds called sub neural clefts, which greatly increase the surface area, Ach receptors (nicotinic receptors) are located here

What is preload?

load applied on the muscle before it contracts (e.g. holding a ball before throwing it) It increases muscle length

acetylcholine receptors

muscarinic and nicotinic Ach-gated ion channels has 5 subunits: 2a, 1b, 1y and 1e - 2 ach molecules binds to 2a subunits - opening of the channel to cations - influx of Na+ ions - End plate potential

isotonic contractions

muscle length changes and moves the load, the tension remains relatively constant through the rest of the contractile period; come in two flavors concentric and eccentric

staircase effect (treppe)

occurs when a muscle has been relaxed for some period of time and then is stimulated to contract. In this case, the first few contractions is stronger than the previous contractions. In treppe, calcium slowly accumulates in the sarcoplasm until a maximum contraction can occur. Although all the possible causes of the staircase effect are not known, it is believed to be caused primarily by increasing calcium ions in the cytosol because of the release of more and more ions from the sarcoplasmic reticulum with each successive muscle action potential and failure of the sarcoplasm to recapture the ions immediately

What does more work, preload or after load?

preload does more work than after load because the fore of contraction is directly proportional to the initial length of the muscle (within physiological limits)

generation and propagation of neuromuscular junction action potential

presynaptic membrane calcium influx to release acetylcholine. Ach travels to ligand-gated channel to open sodium channels on the nicotinic receptors.

Multiple fiber summation

results from an increase in the number of motor units contracting simultaneously (fiber recruitment) When the central nervous system sends a weak signal to contract a muscle, the smaller motor units of the muscle may be stimulated in preference to the larger motor units. Then, as the strength of the signal increases, larger and larger motor units begin to be excited, with the largest motor units often having as much as 50 times the contractile force of the smallest units. This phenomenon, called the size principle , is important because it allows the gradations of muscle force during weak contraction to occur in small steps, whereas the steps become progressively greater when large amounts of force are required. This size principle occurs because the smaller motor units are driven by small motor nerve fibers, and the small motoneurons in the spinal cord are more excitable than the larger ones, so naturally they are excited first. Another important feature of multiple fiber summation is that the different motor units are driven asynchronously by the spinal cord; as a result, contraction alternates among motor units one after the other, thus providing smooth contraction, even at low frequencies of nerve signals.

Molecular mechanisms of muscle contraction occurs by a

sliding filament mechanism

passive tension

tension applied to load when a muscle is stretched but not stimulated. Refers to tension developed in parallel elastic component also knowns as non contractile tension.

Skeletal muscle tone

the "normal" amount of contraction that occurs within skeletal muscles to maintain normal body posture Even when muscles are at rest, a certain amount of tautness usually remains, called muscle tone. Because normal skeletal muscle fibers do not contract without an action potential to stimulate the fibers, skeletal muscle tone results entirely from a low rate of nerve impulses coming from the spinal cord. These nerve impulses, in turn, are controlled partly by signals transmitted from the brain to the appropriate spinal cord anterior motoneurons and partly by signals that originate in muscle spindles located in the muscle

what is after load?

the load applied on the muscle with it is contracting (e.g. picking up a bucket of water)

Titin

the side-by-side relationship between the myosin and actin filament sis maintained by a large number of filamentous molecules of a protein called titin. Act as a framework that holds the myosin and actin filaments in place so that the contractile machinery of the sarcomere will work. One end of the titin molecule is elastic and is attached to the Z disk, acting as a spring and changing length as the sarcomere contracts and relaxed. The other part of the titin molecule tethers it to the myosin thick filament. The titin molecule may also act as a template for the initial formation of portions of contractile filaments of the sarcomere, especially the myosin filaments

What binds myosin to Z lines?

titin

What inhibits the active sites of actin?

tropomyosin

Becker muscular dystrophy (BMD)

very similar to, but less sever than, Duchenne muscular dystrophy is also caused by mutations of the gene that encodes for dystrophin but has a later onset and longer survival. It is estimated that DMD and BMD affect 1 of every 5,600 to 7,700 males between the ages of 5 through 24 years. Currently, no effective treatment exists for DMD or BMD, although characterization of the genetic basis for these diseases has provided the potential for gene therapy in the future.

Acetylcholine release

when a nerve impulse reaches the nerve terminal, it opens calcium channels calcium diffuses from the ECF into the axon terminal Ca++ releases Ach from vesicles by a process of exocytosis

depolarizing blocking agent

work by depolarizing the plasma membrane of the muscle fiber, similar to acetylcholine these agents are more resistant to degradation by acetylcholinesterase, the enzyme responsible for degrading acetylcholine, and can thus more persistently depolarize the muscle fibers. this differs from acetylcholine, which is rapidly degraded and only transiently depolarizes the muscle the constant depolarization and triggering of the receptors keeps the endplate resistant to activation by acetylcholine. a normal neuron transmission to muscle cannot cause contraction of the muscle because the endplate is depolarized and thereby the muscle paralyzed