Skeletal Muscle Contraction

[여인호]

*muscle cell 의 종류 

-skeletal muscle , cardiac muscle , smooth muscle.

-skeletal muscle 만 voluntary.

-single skeletal muscle cell results from the fusion of hundreds of embryonic precursor cells called myoblasts. (syncytium)

*skeletal muscle 의 구조

- myofilament → myofibril → muscle fiber(cell) → fascicle → skeletal muscle

- striations of skeletal muscle cell are due to the organized arrangement of contractile proteins called thick and thin filaments.

-each fascicle contains hundreds or thousands of muscle cells(fibers).

-each muscle fiber runs the full length of the muscle.

-T tubules and sarcoplasmic reticulum play an important role in the activation of muscle contractions because they help transmit signals from the sarcolemma to the myofibrils, enabling a muscle cell to respond to neural input.

* sarcomere

- sarcomere (z band~ z band) 는 2.5mm

최대수축기에는 약 1.5㎛, 최대이완기에는 약 4.0㎛정도

- 근수축시 H band, I band 가 짧아짐.

- titin can be stretched to more than three times its unstressed length. it anchors the thick filaments in their proper positions relative to the thin filaments.when the force is removed, the muscle fibers and sarcomeres spring back to their origianl resting lengths automatically due to the actions of titin.

*thin filament

1.actin

-이중나선 구조

-each actin subunit has a specific binding site to which the myosin cross bridge binds.

2.tropomysin

-in the unstimulated muscle, the position of the tropomyosin covers the binding sites on the actin subunits and prevents myosin cross bridge binding.

3.troponin I,C,T

- to expose the binding sites for bending with myosin, the tropomyosin molecule must be moved aside. this is faciliated by presence of a third molecular complex called troponin.

-I : myosin 과 actin 이 못 만나게 막아줌.

C : 칼슘과 결합하는 부분

 (after an action potential, calcium ions are released from the terminal cisternae and bind to troponin. this cause conformational change in the tropomyosin-troponin complex. "dragging" the tropomyosin strands off the bind sites.)

T : (1)myosin 에 민감한 site

     (2)myosin 에 민감하지 않은 site

* thick filament

1. myosin

-head (cross bridge) has the ability to move back and forth (power stroke).

-head has ATP binding sites and actin binding site.

-the binding of ATP transfers energy to the myosin cross bridge as ATP is hydrolyzed into ADP and Pi. 

* muscle contraction cycle

- influx of calcium, triggering the exposure of binding sites on action. → the binding of myosin to actin →

power stroke of the cross bridge. it causes the sliding of the thin filaments. → the binding of ATP to the cross bridge, which result in the cross bridge disconnecting from actin. → the hydrolysis of ATP, which lead to the re-energizing and re-positioning of the cross bridge → the transport of calcium ions back into the sarcomere reticulum.

* motor end plate → 칼슘 releasing

1)Motor neuron의 action potential이 presynaptic membrane의 voltage gated Ca channel을 엽니다.

세포내 Ca의 증가는 Synaptic cleft로 Aceylcholine의 분비를 일으킵니다.

2) 분비된 Ach은 postsynaptic membrane의 ligand gated channel의 cholinergic receptor에 결합하면, channel이 열립니다.

3) 열린 channel을 통해 Na, K(주로 Na)이 세포내로 들어옵니다.

4) 이들 양이온의 influx는 postsynaptic membrane에 depolarization을 유발합니다. 이 때 발생하는 depolarization을 EPP(end plate potential)이라고 합니다. Synaptic region의 muscle membrane에는 voltage gated Na channel이 없기 때문에, EPP는 새로운 action potential을 유발하지 못하고 세포막을 따라 퍼져나가다가 voltage gated Na channel이 있는 부위에서 action potential을 발생시킵니다.

5)  새로만들어진 action potential은  postsynaptic membrane을 따라 퍼져나가 결국 T tubule로 이동을 합니다.

6) Action potential이 T-tubule의 L-type Ca²⁺ channel(dihydropyridine receptor)를 열어 sarcoplasmic reticulum 안으로 Ca을 이동시킵니다.

7) SR로 이동한 Ca²⁺은 Sarcoplasmic reticulum의 ryanodine receptor를 활성화시켜 Ca²⁺이 SR에서 ICF로 빠져나오게합니다. 

-when an action potential travels through the T tubules, these voltage sensors react and in so doing transmit a signal directly to the foot structures with which they are in contact. this signal triggers the opening of calcium channel pores within the foot structures, which allows 칼슘이온 to flow out of the SR. as the ions enter the cytosol, some of them bind to specific sites on other SR calcium channels and cause them to open. in this manner the initial release of calcium triggers the release of even more calcium from the SR.

when an action potentials triggers the release of calcium from the SR, this release does not continue indefinitely because as the cytosolic calcium concentration rises, calcium ions begin to bind to certain sites on the SR calcium channels, causing them to close. these sites are distinct from those that trigger channel opening and have a lower affinity for calcium, so they do not come into play until cytosolic calcium has risen to a sufficiently high level. the closure of these channels turns off the release of calcium and enables the active transport of calcium from the cytosol, which causes the calcium concentration to fall. 

this concentration change causes calcium to dissociate from troponin, which allows both troponin and tropomyosin to revert to their original positions. the number of exposed sites on the actin filament therefore decreases, leading to a decline in the number of active crossbridge. eventually, as calcium concentration returns to normal, the number of active crossbridges reaches zero, and the muscle contraction ends.

(it may be the result of a higher-than-normal calcium concentration in the cytosol between twitches, perhaps due to incomplete removal by the pump of the sarcoplasmic reticulum.)

-myosin head 가 actin과 떨어지는데 ATP는 에너지원으로 사용된 것이 아니라, myosin head의 allosteric modulation을 일으켜 myosin head와 actin과의 biding을 약화시키는 modulator의 역할을 한 것.

-high energy form : myosin-ADP-Pi (Because the myosin molecule stores energy that is released in the hydrolytic splitting of ATP.)

 low energy form : stored energy is released to drive the movement of the thin filament.

-Rigor; in releasing its stored energy, the myosin head returns to its low-energy form. at this point, myosin and actin are tightly bound together and unable to seperate, a condition called rigor.  (the stiffening of the body that occurs after death because the crossbridge cycle gets stuck at this step due to a lack of ATP. rigor mortis continues until enzymes leaked by disintegrating cellular components begin to break down the myofibrils.)

-although a given crossbridge generates force only part of the time while it is active (during power stroke), a muscle cell generates force continually during a contraction, because many crossbridges go through the cycle simultaneously but out of phase with each other. thus at any given time, some crossbridges are starting the cycle, others are finishing it, and still others are at various stages in between.

-multiple cross bridge cycling is coordinated sequentially to prevent all cross bridge from either being connected or dis connected at the same time.

-during a contraction, each myosin head completes only about five crossbridge cycles per second, but because each thick filament has several hundred head, thousands of power strokes can occur each second. for this reason, sarcomeres can shorten very rapidly, in many cases taking less than a tenth of a second to contract fully.

-when the cross bridge cycle stops and the contraction ends, the thin filaments passively slide back to their original position.(muscle returns back to its original length via the elasticity of the connective tissue elements, plus the contraction of antagonistic muscles, and gravity.).

*ATP supply

-the ATP that powers muscle contraction is produced in muscle cells, as in other cells, by substrate-level phosphorylation and oxidative phosphorylation. when a cell's rate of ATP utilization increases, the concentration of ATP inside the cell falls and the concentration of ADP rises. these and other changes then stimulate the enzymes that control ATP-producing reactions, such that ATP is generated at a higher rate. but even though this occurs once a muscle cell begins to contract, these reactions need a few seconds to come up to speed. to ensure a steady supply of ATP in the meantime, muscles rely on an immediately available store of high-energy phosphate that is present in the form of a compound calld creatine phosphate, which donates its phosphate to ADP to form ATP.

for the first few seconds of exercise, muscle rely on their own stored glycogen to supply glucose as fuel for ATP production. as exercise continues, they come to rely on glucose and fatty acids delivered to them by the bloodstream. after about 30 minutes, glucose utilization decreases, and fatty acids become the dominant energy source.

in heavy exercise, oxidative phosphorylation becomes less important as source of ATP, and substrate-level phosphorylation (particularly glycolysis) becomes more important. even though glycolysis is capable of producing ATP all by itself, one result is the production of lactic acid, which accumulates in muscle tissue and can spill over into the bloodstream. recall that in glycolysis, glucose is converted to pyruvate, which normally undergoes further oxidation in the Krebs cycle and oxidative phosphorylation. when pyruvate is produced at a rate exceeding the rate at which it is oxidized, it build up and is converted to lactic acid. this buildup of lactic acid is believed to be the reason for the burning sensation one feels in the muscles after heavy exercise.

-glycolysis : glucose + 2 ATP + 2 NAD → 2 pyruvate + 4 ATP + 2 NADH (산소 필요하지 않음.)

-pyruvate → 1 ATP + 4NADH + 1 FADH

* primary mode of ATP production. (glycolytic fibers, oxdative fibers)

-even though all muscle fibers have the ability to produce ATP by both oxidative phosphorylation and substrate-level phosphorylation, they differ in their capacities for doing so and are grouped into two general categories on this basis.

Glycolytic fibers have high cytosolic concentrations of glycolytic enzymes and therefore can generate ATP rapidly via glycolysis.(substrate-level phosphorylation). these fibers have a relatively low capacity for generating ATP via oxidative phosphorylation because they contain relatively few mitochondria, where oxidative phosphorylation occurs.

By contrast, oxidative fibers are rich in mitochondria and have a high capacity for producing ATP via oxidative phosphorylation. however, these fibers contain relatively low concentrations of glycolytic enzymes and therefore have a low glycolytic capacity. both fiber types are found in all muscles of the body, but their proportions vary among muscles.

Oxidative fibers are generally of smaller diameter and well-supplied with capillaries, the fiber's small diameter minimizes the distance oxygen must diffuse to reach the mitochondria. another difference between the fiber types is that oxidative fibers contain an oxygen-binding protein knwon as myoglobin, whereas glycolytic fibers lack it. myoglobin is a reddish molecule that binds oxygen reversibly. its function is to serve as an oxygen buffer to store a supply of oxygen that can be released whenever the oxygen concentration inside cells declines(as can happen when a muscle contracts strongly and compresses nearby blood vessels, thereby interrupting the blood supply.). Because this oxygen store is limited, however, it can supply adequate amounts of oxygen for only a short time before it must be replenished, which occurs when blood flow is restored and the oxygen concentration rises. because myoglobin imparts a reddish-brown color to oxidative fibers, these fibers are often referred to as red muscle.

Glycolytic fibers are of larger diameter and are surrounded by fewer capillaries. Glycolytic fibers, which lack myoglobin and this reddish color, are referred to as white muscle. glycolytic fibers produce ATP less efficiently than oxidative fibers because fewer ATP molecules are synthesized per unit of fuel consumed. however, glycolytic fibers are better able to produce ATP when oxygen avail-ability is low because glycolysis does not require oxygen. when glycolytic fibers are active and producing ATP at a high rate, lactic acid is produced as a by-product, because these cells have a low oxidative capacity in addition to their high glycolytic capacity. one consequence of these differing capacities is that pyruvate, the end-product of glycolysis, is generated faster than it can be consumed and therefore accumulates in these cells. as it accumulates, it is converted to lactic acid, which has been implicated as a cause of muscle fatigue. for this reason, glycolytic fibers fatigue more rapidly than oxidative fibers. in contrast, oxidative fibers produce little lactic acid so long as they are supplied with adequate amounts of oxygen, and as a consequence they are more resistant to fatigue.lactic acid does not normally accumulate in these cells(oxidative fibers) because their high oxidative capacity enables them to oxidize pyruvate as fast as it is produced.

* types of skeletal muscle fibers (slow oxidative, fast oxidative, and fast glycolytic fibers)

-myosin ATPase activity :  low   /     high      /      high

-myoglobin content :   high     /      high      /      high

-when different muscles are stimulated to contract isometrically, some take longer to reach peak tension than others. the reason is these muscles contain different populations of fibers. some muscles contain mostly slow twitch fibers, which contract relatively slowly. in other muscles, the predominant fibers are fast twitch fibers, which contract relatively quickly.

the difference between fast twitch and slow twitch fibers is based on not on their size or shape, but instead on the type of myosin present in their thick filaments. so-called fast myosin has the inherent ability to hydrolyze ATP at a faster rate than slow myosin, and this ATPase rate has been found to correlate strongly with a fiber's speed of contraciton. the higher ATPase rate of fast myosin implies that this form of myosin can complete more crossbridge cycles per second, which means that sarcomeres shorten faster, all else being equal.

-muscles generally contain all three fiber types, but in different proportions.

As their name implies, slow oxidative fibers contain slow myosin and have a high oxidative capacity, producing most of their ATP by oxidative phosphorylation.

Fast oxidative fibers also have a high oxidative capacity, but they contain fast myosin.(actually, the myosin ATPase activity in these fibers is intermediate between the slowest and fastest myosin.) 

Fast glycolytic fibers contain fast myosin and have a high glycolytic capacity, producing most of their ATP through glycolysis.

although there is no direct connection between a muscle fiber's type and its ability to generate force, there is an indirect connection because the three fiber types also differ in diameter.

Slow oxidative fibers are the smallest in diameter and are therefore capable of generating only small forces.

Fast glycolytic fibers have the largest diameter and generate the highest forces, whereas fast oxidative fibers are intermediate in terms of diameter and force-generating capacity.

*sequence of motor unit recruitment

1. small, type 1 motor unit (slow twitch)

2. type 2a motor unit (fast twitch oxidative glycolytic)

3. large , type 2b motor unit (fast twitch glycolytic)

*force generating capacity

1. frequency of stimulation (summation of contractions)

2. fiber diameter (number of sarcomeres in parallel)

3. changes in fiber length (length of individual sarcomeres)

4. recruitment of motor units

*frequency of stimulation (summation of contractions)

-latent period is the delay of a few milliseconds that occurs between the action potential in a muscle cell and the start of contraction, when the cell first begins to generate force. this time lag exists because the events of excitation-contraction coupling must occur before crossbridge cycling can begin.

-compared to an action potential, which takes at most a few milliseconds to complete, a muscle twitch is fairly slow, taking anywhere from tens to hundreds of milliseconds to complete. 

Because of this, a muscle fiber can have several action potential in the time it takes to complete on twitch. when a muscle is stimulated repetitively such that additional action potentials arrive before twitches can be completed, the twitches superimpose on one another, yielding a force greater than that of a single twitch. this process is called summation.

however, when stimuli are delivered over a prolonged time period, the force does not continue to mount but instead reaches a plateau, during which it oscillates about a constant average level. under these conditions, the muscle is said to be in a state of incomplete (unfused) tetanus.

(the term "tetanus" also refers to a disease in which toxins produced in a bacterial infection cause motor neurons to stimulate muscle contraction inappropriately.)

if the muscle is stimulated with still greater frequency, the individual twitches become indistinguishable because they follow each other so closely. in this case the tension rises swiftly and smoothly at the beginning of stimulation and eventually reaches a higher plateau. this condition is called complete (fused) tetanus. if the stimulus frequency is increased still further, tetanic tension increase, but only up to a point; further increases in frequency beyond this point yield no further increases in force. under these conditions the muscle is generating all the force it can, which is referred to as maximum tetanic tension.

-an action potential in a motor neuron triggers contraction of all the muscle cells that are connected the that neuron, and it is not possible to stimulate on cell without stimulating the others. a twitch is the mechanical response of an individual motor unit to a single action potential.

#treppe

-all-or-nothing events only if a muscle is stimulated at a frequency low enough to ensure that twitches are well seperated in time. when a muscle is stimulated at a sufficiently high frequency, such that twitches follow one another closely, peak tension rises in a step-wise fashion with each twitch , until eventually it reaches a constant level. this step-wise increase in peak tension is a called treppe. the cause of treppe is not known, but it may be the result of a higher-than-normal calcium concentration in the cytosol between twitches, perhaps due to incomplete removal by the pump of the sarcoplasmic reticulum.

* fiber diameter (number of sarcomeres in parallel)

-force generating capacity of a muscle fiber depends on both the number of crossbridges in each sarcomere and geometrical arrangement of the sarcomeres. in addition, a muscle that has more sarcomeres, hence more thick and thin filaments, arranged in parallel can generate more force than a muscle with fewer sarcomeres arranged in parallel. because the number of thick and thin filaments per unit of cross-sectional area does not vary significantly from one muscle to another, a fiber's diameter is the crucial variable that determines its force-generating capacity. the greater the fiber diameter, the greater its cross-sectional area, and more force it can generate. note that although the number of parallel sarcomeres strongly affects a muscle's force generating capacity, the force generating capacity does not depend on the number of sarcomeres that are joined in series. this means that two muscle, on longer than the other but otherwise identical, have the same force generating capacity. assuming that the weight of the chain itself is negligible, each of its links exerts on its neighbors a force that is equal to the force exerted on the chain by the weight. this will be true regardless of the number of links in the chain.

*changes in fiber length (length of individual sarcomeres)

-changes in fiber's length do influence its ability to generate force. for each fiber, maximum force generating capacity occurs over a certain range of lengths (length-tension relationship). when a fiber either shortens beyond or is stretched beyond this optimum range, its force generating capacity decreases, because such changes in length alter the length of individual sarcomeres and reduce their ability to generate force.

-if the muscle is significantly shorter than its optimum length, tension declines in two stages as the length decrease.

As sarcomeres shorten beyond their optimum length, the thin filaments at opposite ends of the sarcomere begin to overlap each other, which interferes with their movement. then, as the sarcomeres shorten beyond a point, Z lines eventually come into contact with thick filaments, so most of the force generated by crossbridges is exerted on the sarcomere itself instead of being transmitted to the ends of the muscle fiber.

-The muscle can withstand (briefly) a heavier load when forcibly stretched than it can develop isometrically. 

The strength of the crossbridge attachment to the thin filament is greater than the force generated by its movement. Consequently, muscles can bear a load larger than the maximum active force, before the crossbridge attachment is mechanically broken and rapid lengthening occurs. This situation has physiological relevance when a muscle is contracted to decelerate the body when a person is walking or running downhill.

* force regulation (recruitment, size principle)

-when you use a particular set of muscles for different activities. for example, using your arm to pick up a chair, as opposed go picking up a paper clip. the muscle's contractile force varies because the nervous system alters the pattern of commands it sends to them. one way it does this is by varying the action potential frequency in individual motor units. another way is by varying the number of motor units stimulated at any given time.

the most force a single muscle fiber can develop contracting isometrically is the maximum tetanic tension, which for most muscle fibers is only about five times greater than peak tension in a single twitch. given that muscular tension can vary over several orders of magnitude, it is clear that variation in action potential frequency can account for only a small fraction of the range of forces a muscle can generate.

when a muscle contracts, only rarely do all of its fibers actively generate force. some motor units are active, but the fibers in other motor units simply go along for the ride passively shortening in response to forces generated by actively contracting fibers. when larger forces are needed, the nervous system can activate some of these extra fibers, thereby increasing the total number of active fibers. indeed, the nervous system exerts most of its control over muscular force by varying the number of active motor units; variation in the frequency of stimulation of individual fibers plays a secondary role.

an increase in the number of active motor unit is called recruitment.

-within a muscle, fibers belonging to a given motor unit are intermixed with fibers from other motor units. they often differ in size. 

Because a muscle may contain hundreds of motor units, muscular tension can be varied over a wide range merely by varying the number of active motor units.

muscle differ in regard to the numbers of motor units they contain, from a handful in the muscles that control movements of the eye to hundreds in larger muscles such as the biceps. 

when a muscle is called upon to generate small forces, generally only the smaller motor units come into play. when larger forces are needed, larger motor units are recruited. this correspondence between the size of motor units and the order of recruitment is known as the size principle. in addition, when contractions are sustained over a long time, motor units are activated asynchronously as one becomes active, another ceases its activity. in this manner the total force of the muscle is maintained at a constant level without overworking any of the individual motor units. 

the fact that motor units differ in size has practical implications for precise control of muscular force.

-the basis for the size principle is not only that motor units vary in size, but that the motor neurons that control them also vary in size. larger motor units are controlled by motor neurons with larger-than-average cell bodies and axon diameters, whereas smaller motor units are controlled by neurons with smaller-than-average cell bodies and axon diameters. larger cells are harder to depolarize to threshold; more excitatory synaptic input is required to induce a larger neuron to fire. thus, when gradually increasing synaptic input is delivered to a set of motor neurons, the small neurons will fire first and the large ones last.

motor units become active in order of increasing size. each motor unit is recruited, the force increases in stepwise increments that reflect both increased number of fibers in the larger units and the larger size of those fibers.  

# recruitment를 좋게하기 위해서는 어떻게 해야 할까? 장력이 변하는 세라밴드를 사용? 

- 우선 coordination → stabilization → strengthening 으로 나눠서 하자. 

나중에 functional 하게 적용할 수도 있을듯...

* isometric , isotonic , isokinetic

-isotonic means same tension.

-as the load increases, the velocity of shortening gradually decreases, eventually reaching zero when the load is equal to or greater than the maximum tension that can be generated by muscle, and that velocity of shortening is greatest when no load is placed on the muscle. 

-isometric contraction : when a muscle contracts isometrically, its sarcomeres shorten even though the whole muscle does not. this is possible because the sarcomeres do not extend the entire length of each muscle fiber and therefore do not transmit force directly to the ends of the cells. instead, the force is transmitted through certain cellular components that connect the myofibrils to the ends of the cells and then through connective tissue that anchors the ends of the cells in place and extends through the tendons. those parts of a muscle that do not actively generate force but only serve to passively transmit force to the ends of the muscle are collectively referred to as the muscle's series elastic component. when a muscle contracts isometrically , the contractile component shortens and stretches the SEC, causing it to pull on the ends of the muscle. in so doing, the SEC lengthens as the CC shortens, giving an overall length change of zero.

#stretch shortening cycle

#power (일률)이 가장 높은 구간은?? (다이어트에 적용가능?)

-The Y axis at the left of the figure is the velocity of shortening or lengthening, the X-axis is the magnitude of the load against which the muscle is contracting.

-the maximal shortening velocity (Vo) is limited by the rate at which a particular isoenzymatic form of myosin synthesized in a cell can interact with actin and release the energy stores in ATP. 

-Work (W) is defined in your physics book as the force (F) applied to a mass times the distance (d) the mass or load has been moved with that force, W = F • d. If a muscle contracts isometrically, no shortening (d) is produced. Therefore, since d=0 from the physics point of view, no work is done. On the other extreme, in a pure isotonic contraction, no mass or load is lifted, and since force is equal to mass times acceleration (F = m • a) and there is no mass (m=0) to be lifted, there is no force (F=0) and work has a value of zero (W=F•d). In other words, the apparent work done under these circumstances is zero. We can say that a muscle activated at the two extremes (isometric or isotonic), apparently produces no "external work", but that, indeed work is done which appears as heat. Furthermore, there is a linear relationship between the heat produced during activation and the amount of ATP split during it. We can express the above by saying that the total work done by the muscle when it is activated consists of two components: external work, i.e., work that can be appreciated as "productive" plus the heat that is produced as ATP splits. 

- If the load is very light, the muscle will lift it very fast and will accomplish the work in a short period of time. However, the power of this action will be small because the force involved (and therefore the value of w) will be minimal.

(peak tension in an isotonic twitch 그래프 생각... )

With small increments of load, the muscle contraction will still be able to accomplish the work in a short time and the power will increase. However, it will come to a point where the value of the load is high enough that it will begin to take longer and longer to accomplish the work. From this time up the value of power will diminish because it will take longer and longer to accomplish the work. Maximal power is obtained with a load of about 0.3 of the maximal force than can be developed.

-Efficiency is defined as the external work done, divided by the total energy used or consumed to produce that amount of work.

If a muscle produces an external work of 1 mcal/g but consumes 4 mcal/g muscle of ATP, 

then the efficiency of this muscle is 0.25 or 25%.

Clearly, efficiency is zero when the muscle contracts isometrically or when it has no load and contracts isotonically. Efficiency is greatest when the muscle is able to handle the load rather easily, which is when P/Po= 0.3, i.e., 30% of the maximal force that it can produce, and it drops when the load gets relatively heavier or too light. Notice that reducing the load from 80% (P/Po=0.8) to 60% (P/Po=0.6) of maximal force (Po) produced almost triples the efficiency. This is important when considering the performance of the heart as a pump, and the failing heart. The lesson is that when faced with a muscle struggling against a heavy load, an enormous gain in efficiency can be achieved by either modestly decreasing the load, or modestly increasing the contractile force of the muscle. Both methods are used in treating heart failure.

*muscle fatigue

-muscles differ in their ability to resist fatigue, a decline in a muscle's ability to maintain a constant force of contraction in the face of long-term, repetitive stimulation. although fatigue eventually sets in after any kind of muscular activity, it generally occurs more quickly when muscle is stimulated at higher frequencies and when larger forces are generated.

in high-intensity exercise, glycolytic muscle fibers are recruited and, as previously mentioned, have a tendency to generate lactic acid because of their low oxidative capacity. when contractions are strong and sustained, an additional factor can come into play. strong contractions can compress vessels that supply blood to the muscles, which interrupts or reduces the muscles' blood supply; the resulting decrease in oxygen delivery causes muscle cells to produce larger amounts of lactic acid, which by lowering intracellular PH, can alter enzyme activities and interfere in a variety of metabolic processes.

the cause of fatigue in low-intensity exercise, which takes a longer time to develop, is thought to be linked to the depletion of energy reserves, glycogen in particular. full recovery from this type of fatigue requires about 24 hours, whereas recovery from the more rapid-onset type of fatigue requires only minutes or a few hours.

very-high-intensity exercise can induce neuromuscular fatigue, which occurs when motor units are stimulated to contract at high frequencies, as occurs when large forces are generated. when cells are stimulated to contract strongly over long periods, repeated firing of motor neurons can deplete synaptic terminals of acetylcholine, which ultimately causes failure of neuromuscular transmisson.

fatigue also has a psychological component that resists any purely physiological explnation. it is widely accepted state as well as by physical athletes that performance is influenced by mental state as well as physical condition.

Often, the athletes who run the fastest or the longest are the ones with the strongest "will to win". competitors with less desire are more likely to succumb to discouragement when fatigue sets in and muscles begin to ache; as a consequence, they may well put forth less effort.

*long term responses of muscles to exercise

-athletes go into training not simply to hone the skills needed in their particular sport, but also to change the body's physical condition so that it is fitter to perform those skills. such changes involve, among other things, changes in muscles' cellular architecture that result from regular exercise over time. as a result of these changes, the muscles' capacity to generate force and resist fatigue is altered. it is important to choose an exercise regimen that can achieve the desired results. for example,an aspiring marathon runner, who requires great endurance for her sport, should train using long-duration, low intensity exercise such as jogging(aerobic exercise). aerobic exercise increases the oxidative capacity of muscle fiber, thereby increasing their resistance to fatigue. as a result of such training, some fast glycolytic fibers are effectively converted to fast oxidative fibers. changes include increases in the size and number of mitochondria within the fibers, and an increase in the number of capilaries surrounding the fibers. in addition, the average diameter of the fibers decreases, which facilitates the movement of oxygen into the cells but also decreases the cells' force generating capacity.  however, because exercise does not alter the type of myosin present in muscle fibers, slow twitch fibers remain slow and fast twitch fibers remain fast.

in contrast, high intensity exercise decreases the oxidative capacity of muscle fibers and increases their glycolytic capacity, thereby converting a portion of the fast oxidative fibers into fast glycolytic fibers. changes include decreases in the size and number of mitochondria, increases in the concentration of glycolytic enzymes, and increases in average fiber diameter. however, the declining oxidative capacity of these fibers reduces their resistance to fatigue.

As fibers grow, new myofibrils are synthesized, which enables the fibers to generate more force; reflecting the increase in average fiber diameter, entire muscles also become bulkier and more massive. muscle growth is not due to the addition of new fibers because muscle fibers are postmitotic- that is, they cannot divide to form new cells. even though new fibers can be generated from immature precursors called satellite cells, this normally happens only when fibers die and must be replaced.

-a muscle can actively exert force only by contracting, which in the case of skeletal muscle means pulling, not pushing, on a bone. nevertheless, it is clear that you can use muscular force to move the elbow joint, for example, in opposite direction. to flex the forearem, the biceps generates force acively while the triceps relaxes and stretches passively. at times, simultaneous contraction of antagonistic muscle groups is useful. thus when the biceps and triceps are stimulated to contract at the same time, as when you "brace yourself" to receive a package whose weight you are unsure of, the elbow joint stiffens to resist motion, such that the forearem remains stationary.

# 60% of 1RM , 25 rep 이 endurance인 이유??

 weight 를 줄여서 많은 수를 반복시키는 것은 비교적 작은 motor unit의 동원을 develop 시키는 것.

큰 단위의 motor unit보다 작은 motor unit는 흥분하는데 필요한 노력이 더 적다.

즉 어떠한 일을 수행할 때, 최소한의 힘을 사용하는 것이 에너지 효율이 좋다.

만약 그 이상의 힘을 쓴다면 쉽게 지칠 것이다.

그러므로, 오랜 시간을 지치지 않고 뛰게 하고 싶다면 (근지구력) 작은 motor unit가 계속 동원될 수 있게 훈련해야...

(작은 motor unit의 fatigue는 큰 motor unit 의 동원을 야기하고, 이것은 더 많은 에너지가 필요하다...) 

+ 천천히 운동하는 것은 fatigue에 강한 slow twitch filament를 증가시키겠구나...

→결론 : holten 선생님의 경험이다..

+  1 set (25,20,16) 인 이유... : fatigue...

[정혜]

감사합니다

[ChulhwanKim]

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