Skeletal muscle

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Photo of muscle fibers. The black blobs are nuclei.

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Extensor muscle of a grasshopper leg. The muscle has a pennate structure, which can be seen in the "herrring bone" arrangement of the muscle blocks when the femur is viewed from above.

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A skeletal muscle (= voluntary muscle) is a striated muscle that flexes or extends a joint by pulling on bones of the skeleton. (There are a few exceptions. Some muscles do not pull directly on the skeleton, but achieve the same result by pulling something else, like large sheet of tissue.)

Skeletal muscle represents approximately 30 to 40% of the body weight of a healthy 58-kg woman or a 70-kg man. In an adult, the majority of skeletal muscle is found in the legs, with lesser amounts in the head, trunk, and arms. [18]

Skeletal muscle control voluntary movement and are connected to bones by strong fibrous bands of tissue called tendons.

Contents

1   Etymology

The names applied to the various muscles have been derived:

  1. from their situation, as the Tibialis, Radialis, Ulnaris, Peronæus [1]
  2. from their direction, as the Rectus abdominis, Obliqui capitis, Transversus abdominis [1]
  3. from their uses, as Flexors, Extensors, Abductors, etc.; [1]
  4. from their shape, as the Deltoids (shaped like Delta), Rhomboideus; [1]
  5. from the number of their divisions, as the Biceps and Triceps; [1]
  6. from their points of attachment, as the Sternocleidomastoideus, Sternohyoideus, Sternothyreoideus. [1]

2   Function

The function of skeletal muscle is to produce force and motion. They are primarily responsible for maintaining and changing posture, locomotion, as well as movement of internal organs, such as the contraction of the heart and the movement of food through the digestive system via peristalsis.

The function of a muscle depends on its origin and insertion. Muscles act on any joints that they cross. For example, the triceps extend the elbow because they cross the elbow and attach on the forearm.

Muscles provide strength, balance, posture, movement and heat for the body to keep warm.

The action of the muscle deduced from its attachments, or even by pulling on it in the dead subject, is not necessarily its action in the living. By pulling, for example, on the Brachioradialis in the cadaver the hand may be slightly supinated when in the prone position and slightly pronated when in the supine position, but there is no evidence that these actions are performed by the muscle during life. It is impossible for an individual to throw into action any one muscle; in other words, movements, not muscles, are represented in the central nervous system. To carry out a movement a definite combination of muscles is called into play, and the individual has no power either to leave out a muscle from this combination or to add one to it. [1]

3   Substance

3.1   Form

Muscles have many different forms. In the limbs, they are of considerable length, especially the more superficial ones; they surround the bones, and constitute an important protection to the various joints. In the trunk, they are broad, flattened, and expanded, and assist in forming the walls of the trunk cavities. Hence the reason of the terms, long, broad, short, etc., used in the description of a muscle. [1]

In the description of a muscle, the term origin is meant to imply its more fixed or central attachment; and the term insertion the movable point on which the force of the muscle is applied. The origin is absolutely fixed in only a small number of muscles, such as those of the face which are attached by one extremity to immovable bones, and by the other to the movable integument; in the greater number, the muscle can be made to act from either extremity. [1]

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The arrangement of the fibers of certain muscles varies considerably with reference to the tendons to which they are attached.

  1. In some muscles the fibers are parallel and run directly from their origin to their insertion; these are quadrilateral muscles, such as the Thyreohyoideus. [1] A modification of these is found in the fusiform muscles, in which the fibers are not quite parallel, but slightly curved, so that the muscle tapers at either end; in their actions, however, they resemble the quadrilateral muscles. [1]
  2. In other muscles the fibers are convergent; arising by a broad origin, they converge to a narrow or pointed insertion. This arrangement of fibers is found in the triangular muscles, e. g., the Temporalis. In some muscles, which otherwise would belong to the quadrilateral or triangular type, the origin and insertion are not in the same plane, but the plane of the line of origin intersects that of the line of insertion; such is the case in the Pectineus. [1]
  3. In some muscles (e. g., the Peronei) the fibers are oblique and converge, like the plumes of a quill pen, to one side of a tendon which runs the entire length of the muscle; such muscles are termed unipennate. [1] A modification of this condition is found where oblique fibers converge to both sides of a central tendon; these are called bipennate, and an example is afforded in the Rectus femoris. [1] Collectively, these are called pinnate muscles (from Latin pinnatus "feathered, winged").
  4. There are muscles in which the fibers are arranged in curved bundles in one or more planes, as in the Sphincters. [1]

The arrangement of the fibers is of considerable importance in respect to the relative strength and range of movement of the muscle. Those muscles where the fibers are long and few in number have great range of movement, but diminished strength; where, on the other hand, the fibers are short and more numerous, there is great power, but lessened range. [1]

The complex arrangement of muscles is related to muscle function in the live animal. It used to be thought that muscles which contracted to a relatively small fraction of their resting length had fibres parallel to the long axis of the muscle, whereas muscles in which the strength of contraction was more important than the distance over which contraction occurred had fibres with an angular arrangement. Thus, it was thought that muscles might gain strength by leverage, but the contraction distance would be reduced. This was a nice idea, which many of us were taught, but really there is little or no evidence to support it, and a pennate (V-shaped fibre arrangement) structure actually may serve to enhance the overall range of muscle excursion. [8]

3.2   Matter

Most animal muscle is roughly 75% water, 20% protein, and 5% fat, carbohydrates, and assorted proteins. [7]

Skeletal muscle consists of two kinds kinds of tissue: connective tissue and muscle tissue.

3.2.1   Muscle tissue

3.2.1.1   Fasicles

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Skeletal muscle consists of bundles of fibers ("muscle fasicles" from Latin fasces meaning "bundle") of different sizes in different muscles, placed parallel to one another (though they have a tendency to converge toward their tendinous attachments). [1]

Muscle fascicles are visible under a dissecting microscope without magnification when meat is carved. [8]

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The endomysium (black) in a transverse section of meat (the myofibrils are yellow). [8]

Each fascicle consists of muscle fibers, which run parallel with each other. [1] Individual fibers within a fascicle may terminate at a point along the length of the fascicle at a tapered ending anchored in the connective tissue on the surface of an adjacent fiber so that tapered endings transmit their force of contraction to the endomysium or directly to adjacent fibers through fiber to fiber junctions [8]

3.2.1.2   Muscle fibers

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A short part of one muscle fibre which contains many nuclei (the dark blobs). [8]

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Parts of a skeletal muscle fiber.

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A myofiber ("muscle fiber") is a long (commonly less than forty millimeters, approximately the diameter of a golf ball) cylindrical multi-nucleate microscopic cell. [8]

Diameters vary from 0.01mm to 0.1mm (0.1 mm is approximately the diameter of a human hair or the thickness of a piece of paper), assumed to be approximately constant along its length, apart from tapered intafasciular endings. [8] The diameters of fibers increase slowly during the growth of a muscle (radial hypertrophy), but they also increase temporarily when a fibre contracts. Thus, when measuring fibre diameters in a growth study, special care must be taken to avoid or to correct for differences in the degree of muscle contraction. [8]

Muscle volume is almost, although not exactly, constant during contraction. Thus, as fibers shorten in length, their radial dimensions increase. [16]

Like all eukaryotic cells, muscle cells consists of a cell membrane, cytoplasm, and nuclei.

The cell membrane, termed by British physician William Bowman the "sarcolemma" (from Greek sarco "flesh", lemma "sheath"), is a transparent, elastic, and apparently homogeneous membrane of considerable toughness, so that it sometimes remains intact when the inside ruptures. [1] [9]

The cytoplasm (termed sarcoplasm [9]) consists of cytosol, mitochondria, and bundles of one or two thousand myofibrils surrounded by sarcoplasmic reticulum. [9] The SR occupies about 4% of the volume of the cell. [9]

The sarcoplasm contains large amounts of glycosomes (granules of stored glycogen) and significant amounts of myoglobin, an oxygen binding protein. It contains mostly myofibrils, but its contents are otherwise comparable to the cytoplasm of others cells. It has a Golgi apparatus, near the nucleus, mitochondria just on the inside of the cytoplasmic membrane or sarcolemma, as well as a smooth endoplasmic reticulum organized in an extensive network.

The sarcoplasmic reticulum (SR) is a smooth endoplasmic reticulum that stores and pumps calcium ions to regulate the concentration of calcium ions in the cytosol. The sarcoplasmic reticulum keeps the cytosol almost free (about 5 x 10-8 M) of calcium ions in a resting muscle cell, but increases this amount (to about 5 x 10-6 M) when prompted by the transverse tubular or T system, causing the muscle fiber to contract. [9]

Most muscle cells store enough ATP for only a small number of muscle contractions. While muscle cells also store glycogen, most of the energy required for contraction is derived from phosphagens. One such phosphagen is creatine phosphate, which is used to provide ADP with a phosphate group for ATP synthesis in vertebrates.


There are two kinds of muscle fibers: intrafusal muscle fibers and extrafusal muscle fibers. Extrafusal fibers contain myofibrils and are what is usually meant when we talk about muscle fibers.

Extrafusal muscle fibers are innervated by alpha motor neurons. Each alpha motor neuron and the extrafusal muscle fibers innvervated by it make up a motor unit. The connection between the alpha motor neuron and the extrafusal muscle fiber is a neuromuscular junction, where the neuron's signal, the action potential, is transduced to the muscle fiber by the neurotransmitter acetylcholine.

3.2.1.3   Myofibrils

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An intact muscle fiber (bottom of the frame) and a smashed fiber with its fibrils visible (top). [8]

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A mitochondrion (m) and the start of a transverse tubule (t) which we will consider later. If the clear spaces at top right is outside the myofibre, then you can see the membrane around the myofibre, and you can see the transverse tubule is a finger-like inpushing connecting with the space outside the myofibre. [9]

A myofibril is a contractile cylindrical organelle that consists of thousands of repeating units of microscopic protein filaments ("myofilaments") arranged longitudinally in parallel called sarcomeres (Greek sarx "flesh" + meros "part").

Scientists named the parts of a sarcomere for their properties under a polarizing microscope. Striations that appear bright in polarized light are termed anisotropic or A-bands while those that appear dim are termed isotropic or I-bands. [9] Within the A-band is a paler region called the H-zone (from the German "heller", brighter), and within that is a thin M-line (from the German "Mittelscheibe", the disc in the middle of the sarcomere). A thin Z-line (from German Zwischenscheibe, "the disc in between") or disc occurs at the middle of the I band, which delimits the sarcomere. [8] [11]

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The regular longitudinal arrangement of myofilaments cause these striations. A-bands contain thick (10 to 12nm in diameter) filaments made of myosin, crosslinked at the centre by the M-band. I-bands contain thin (5 to 7nm) filaments made of actin. Six thin filaments surround each thick filament, which slides between the thin filaments when the myofibre contracts. [8] [9]

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A transverse section of a pork myofibril (center) by transmission electron microscopy. The myofibril is a little over one micrometre in diameter. The space around the myofibril is greatly enlarged because the myofibril is losing fluid. The arrow shows part of the cytoskeleton resisting the shrinkage of the myofibrils and the loss of fluid from the myofibril.

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Actin molecules in a thin filament are arranged like two strings of pearls twisted around each other: a cross section would reveal two pearls, one from each string, separated by grooves. Other strings of proteins are located in these two grooves. One of these proteins, troponin, responds to the presence of calcium ions and causes the other protein, tropomyosin, to change its depth in the groove. This is the switch that allows myosin heads to row against actin molecules: it is the calcium-activated trigger mechanism for muscle contraction. [8]

The length of the I-band shortens when the muscle contracts, but the length of the A band (1.85 micrometer in mammalian skeletal muscle) remains constant. [8] [9] Since each sarcomere is about 2 micrometers long in resting muscle, its length is shortened by as much as 70% after muscle contraction.

3.2.2   Connective tissue

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Connective tissue of skeletal muscle contains:

  • Layers of connective tissue
  • Tendon, and sometimes aponeurosis

The layers of connective tissue have a major role in protection and covering of muscle fibers, muscle fascicles, and an entire skeletal muscle. Tendons attach the skeletal muscles to bones. Aponeurosis is structurally as tendon that connects the muscles together, or to bone.

Individual muscles have unique connective tissue infrastructure; muscles responsible for locomotion have a greater collagen content than postural muscles, and the nature of their function contributes to the distribution of collagen within the muscle (e.g., parallel, fusiform, pinnate, etc.). Extending from the tendons, connective tissue is the predominant component of epimysium (surrounding the entire muscle), perimysium (surrounding muscle bundles or fasciculi), and endomysium (surrounding individual muscle fibers). [11]

Collagens are the major protein constituents of endomysial and perimysial connective tissue [11]

Connective tissues are located all around the muscle. [4]

Connective tissue consists of a base substance and two kinds of protein based fiber: collagenous connective tissue and elastic connective tissue. Collagenous connective tissue consists mostly of collagen (hence its name) and provides tensile strength. Elastic connective tissue consists mostly of elastin and provides elasticity. The base substance is called mucopolysaccharide and acts as both a lubricant (allowing the fibers to easily slide over one another), and as a glue (holding the fibers of the tissue together into bundles). The more elastic connective tissue there is around a joint, the greater the range of motion in that joint. Connective tissues are made up of tendons, ligaments, and the fascial sheaths that envelop, or bind down, muscles into separate groups. These fascial sheaths, or fascia, are named according to where they are located in the muscles [4]:

epimysium
The outermost fascial sheath that binds entire fascicles
perimysium
The fascial sheath that binds groups of muscle fibers into individual fasciculi.
endomysium
The innermost fascial sheath that envelops individual muscle fibers.

Connective tissues help provide suppleness and tone to the muscles. [4]

Fasicles are enclosed in a delicate web called the perimysium (Greek for "around muscle") in contradistinction to the sheath of `areolar tissue`_ which covers the entire muscle, the epimysium (Greek for "upon muscle") [1]

The fascicles are bound together by a type of connective tissue called fascia.

Muscles fibers are separated from one another by a delicate connective tissue derived from the perimysium and termed endomysium ("within the muscle"). This does not form the sheath of the fibers, but serves to support the blood vessels and nerves ramifying between them. [1]

3.2.2.1   Tendons

Tendons are what keep our muscles tensioned, they are very important for keeping your skeletal muscles working correctly, since muscles can really only contract on their own. Unlike muscles, however, tendons don't have the same potential to grow stronger over time. Tendons can become tougher and more flexible, but it's a process entirely separate from muscle growth with a considerably lower ceiling for improvement.

This is why athletes dread injuring tendons like their hamstring or Achilles' tendon, its a single point of failure that they can only do so much about (this is why stretching is so important, it's all about keeping the tendons pliable and less prone to tearing).

3.2.3   Proprioceptors

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Proprioceptors (= mechanoreceptors) are nerve endings that relay information about changes in tension, force, and physical displacement of the body (i.e. movement or position) to the central nervous system. [4]

Proprioceptors are found in all nerve endings of the joints, muscles, and tendons. [4]

There are two types of proprioceptors: muscles spindles, which provide information about about changes in muscle length, and Golgi tendon organs, which provide information about changes in muscle tension. [4] A third type of proprioceptor, called a pacinian corpuscle, is located close to the golgi tendon organ and is responsible for detecting changes in movement and pressure within the body. [4]

3.2.3.1   Muscle spindle

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Muscle spindles (= stretch receptors) are skeletal muscle fibers aligned parallel to extrafusal muscle fibers throughout the body of a muscle that detect the amount and rate of change in the length of the muscle.

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Muscle spindles consists of three to ten intrafusal muscle fibers, encapsulated by connective tissue (collagen?). Fluid separates these muscle fibers from the capsule.

Intrafusal fibers have contractile proteins at either end, with a central region that is devoid of contractile proteins. The central region is wrapped by the sensory dendrites of the muscle spindle afferent. When the muscle lengthens and the muscle spindle is stretched, this opens mechanically-gated ion channels in the sensory dendrites, leading to a receptor potential that triggers action potentials in the muscle spindle afferent. [6]

When the extrafusal fibers of a muscle lengthen, so do the intrafusal fibers (muscle spindles). The muscle spindle contains two different types of fibers (or stretch receptors) which are sensitive to the change in muscle length and the rate of change in muscle length. [4]

3.2.3.2   Golgi tendon organ

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Organ of Golgi (neurotendinous spindle) from the human tendo calcaneus.

The Golgi tendon organ (named after Italian physician Camillo Golgi) is a proprioceptive sensory organ that provides information about changes in muscle tension. The Golgi tendon organ is found in series with muscle fibers, located in the tendons that attach muscle to bone.

The sensory dendrites of the Golgi tendon organ afferent are interwoven with collagen fibrils in the tendon. When the muscle contracts, the collagen fibrils are pulled tight, which activates the Golgi tendon organ afferent. ecause changes in muscle tension will provide different degrees of pull on the tendon, the Golgi tendon organ provides information about muscle tension. You might think that muscle stretch would also pull on the tendons and stimulate the Golgi tendon organ afferent. In truth, most of the force of a stretch is absorbed by the muscle itself, so a muscle contraction is a much better stimulus for the Golgi tendon organ. [6]

When this tension exceeds a certain threshold, it triggers the lengthening reaction which inhibits the muscles from contracting and causes them to relax. Other names for this reflex are the inverse myotatic reflex, autogenic inhibition, and the clasped-knife reflex. This basic function of the golgi tendon organ helps to protect the muscles, tendons, and ligaments from injury. The lengthening reaction is possible only because the signaling of golgi tendon organ to the spinal cord is powerful enough to overcome the signaling of the muscle spindles telling the muscle to contract. [4]

Another reason for holding a stretch for a prolonged period of time is to allow this lengthening reaction to occur, thus helping the stretched muscles to relax. It is easier to stretch, or lengthen, a muscle when it is not trying to contract. [4]

3.2.4   Intramuscular fat

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Intramuscular fat (or Intramuscular triglycerides [IMTG]) is located throughout skeletal muscle. It is responsible for the marbling seen in certain cuts of beef.

Intramuscular fat is composed of marbling (fat cells or adipocytes) located between bundles of muscle fibers and fat within muscle cells, which is largely comprised of the lipid in cell membranes and lipid droplets in vesicles [11]

3.2.5   Water

In mammals, the water content of muscle represents about 75% of its weight and it serves as a vehicle for nutrient transportation throughout the body. The water content varies inversely with the fat content, while the protein content is maintained constant within the muscle. [11]

Small amounts of water are in the extracellular space, while about 85% of the water is entrapped within cells. Within muscle cells, water is found within myofibrils, between myofibrils, and between myofibrils and the cell membrane (sarco- lemma) (Offer and Cousins 1992). [11]

4   Mechanics

Salt poured on a deadl eel.

Motor neurons send signals to the muscles to contract. These neurons are controlled by sodium ion and potassium ion channels, which open and close, causing an impulse which stretches muscles. In fresh flesh, the channels and muscles are still intact.

A similar effect will happen if you pour soy salt on a dead squid.

4.1   Muscle contraction

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Muscle contraction is a physiological process in which a muscle fiber generates tension when stimulated by the nervous system. The contraction of a muscle does not necessarily imply that the muscle shortens; it only means that tension has been generated: while under tension, the muscle may lengthen, shorten, or remain the same length, depending on the mass of the external load.

Nerves connect the spinal column to the muscle. The place where the nerve and muscle meet is called the neuromuscular junction. When an electrical signal crosses the neuromuscular junction, it is transmitted deep inside the muscle fibers. Inside the muscle fibers, the signal stimulates the flow of calcium which causes the thick and thin myofilaments to slide across one another. [4]

The sliding filament theory describes a cycle of repetitive events that cause a thin filament to slide over a thick filament and generate tension in the muscle.

  1. An `action potential`_ originating in the central nervous system reaches an `alpha motor neuron`_, which then transmits an action potential down its own axon_.
  2. The action potential propagates by activating voltage-gated sodium channels along the axon toward the neuromuscular junction. When it reaches the junction, it causes a calcium ion influx through the voltage-gated calcium channels.
  3. The Ca2+ influx causes vesicles_ containing the neurotransmitter acetylcholine to fuse with the plasma membrane, releasing acetylcholine out into the extracellular space between the motor neuron terminal and the neuromuscular junction of the skeletal muscle fiber.
  4. The acetylcholine diffuses across the synapse and binds to and activates nicotinic acetylcholine receptors on the neuromuscular junction. Activation of the nicotinic receptor opens its intrinsic sodium/potassium channel, causing sodium to rush in and potassium to trickle out. Because the channel is more permeable to sodium, the charge difference between internal and external surfaces of the muscle fiber membrane becomes less negative, triggering an action potential.
  5. The action potential spreads through the muscle fiber's network of T-tubules, depolarizing the inner portion of the muscle fiber.
  6. The depolarization activates L-type voltage-dependent calcium channels (dihydropyridine receptors) in the T tubule membrane, which are in close proximity to calcium-release channels (ryanodine receptors) in the adjacent sarcoplasmic reticulum.
  7. Activated voltage-gated calcium channels physically interact with calcium-release channels to activate them, causing the sarcoplasmic reticulum to release calcium.
  8. The calcium binds to the troponin C present on the actin-containing thin filaments of the myofibrils. The troponin then allosterically modulates the tropomyosin. Under normal circumstances, the tropomyosin sterically obstructs binding sites for myosin on the thin filament; once calcium binds to the troponin C and causes an allosteric change in the troponin protein, troponin T allows tropomyosin to move, unblocking the binding sites.
  9. Myosin (which has ADP and inorganic phosphate bound to its nucleotide binding pocket and is in a ready state) binds to the newly uncovered binding sites on the thin filament (binding to the thin filament is very tightly coupled to the release of inorganic phosphate). Myosin is now bound to actin in the strong binding state. The release of ADP and inorganic phosphate are tightly coupled to the power stroke (actin acts as a cofactor in the release of inorganic phosphate, expediting the release). This will pull the Z-bands towards each other, thus shortening the sarcomere and the I-band.
  10. ATP binds to myosin, allowing it to release actin and be in the weak binding state (a lack of ATP makes this step impossible, resulting in the rigor state characteristic of rigor mortis). The myosin then hydrolyzes the ATP and uses the energy to move into the "cocked back" conformation. In general, evidence (predicted and in vivo) indicates that each skeletal muscle myosin head moves 10–12 nm each power stroke, however there is also evidence (in vitro) of variations (smaller and larger) that appear specific to the myosin isoform.

Steps 9 and 10 repeat while ATP is available and calcium is freely bound within the thin filaments.

After a muscle contracts, ATP (produced in the muscle cells’ mitochondria) is needed to relax the muscle and return the actin and myosin filaments to their normal positions. When a person (or other animal) dies and the mitochondria are no longer producing ATP, the muscles cannot relax. This stiffening of the muscles is called rigor mortis. [3]

While the above steps are occurring, calcium is actively pumped back into the sarcoplasmic reticulum. When calcium is no longer present on the thin filament, the tropomyosin changes conformation back to its previous state so as to block the binding sites again. The myosin ceases binding to the thin filament, and the contractions cease.

The calcium ions leave the troponin molecule in order to maintain the calcium ion concentration in the sarcoplasm. The active pumping of calcium ions into the sarcoplasmic reticulum creates a deficiency in the fluid around the myofibrils.

This causes the removal of calcium ions from the troponin. Thus, the tropomyosin-troponin complex again covers the binding sites on the actin filaments and contraction ceases.

Movement of Ca++ ions in/out of the muscle cell (fiber) is important in both contraction and relaxation of the muscle, so if a person doesn’t ingest enough calcium, some could be taken out of the bones to supply the muscles with what they need to contract and relax. [3]


[7]

How does muscle turn into meat?

Blood circulation stops after an animal slaughters, and muscles exhaust their oxygen supply. Muscle can no longer use oxygen to generate ATP and turn to anaerobic glycolysis to generate ATP from glycogen_, a sugar stored in muscle. The breakdown of glycogen produces enough energy to contract the muscles, and also produces `lactic acid.`_ With no blood flow to carry the lactic acid away, the acid builds up in the muscle tissue. If the acid content is too high, the meat loses its water-binding ability and becomes pale and watery. If the acid is too low, the meat will be tough and dry.

Lactic acid buildup also releases calcium, which causes muscle contraction. As glycogen supplies are depleted, ATP regeneration stops, and the actin and myosin remain locked in a permanent contraction called rigor mortis. Freezing the carcass too soon after death keeps the proteins all bunched together, resulting in very tough meat. Aging allows enzymes in the muscle cells to break down the overlapping proteins, which makes the meat tender.


When a muscle fibre contracts, the thick filaments slide between the thin filaments so that the I band gets shorter. The length of the A band remains constant. This is called the sliding filament theory of muscle contraction, and was put forward in 1972. If a muscle is at its resting length, the gap between opposing thin filaments at the mid-length of the sarcomere causes a pale H zone in the A band. Although the sliding filament theory now is widely accepted, there remain many unsolved problems in the mechanism of the system. [8]

Contraction is an active process requiring energy, which is provided by the hydrolysis of phosphate from adenosine triphosphate (ATP), although the transduction from chemical to mechanical energy may be delayed until the resulting adenosine diphosphate (ADP) and inorganic phosphate are released by myosin when it recombines with actin. Contraction by filament sliding may be achieved by the rowing action of numerous cross bridges that protrude from the thick filaments and are formed from the heads of myosin molecules whose backbones are bound into the thick filament. However, the conformational change that causes the cross bridge movement does not seem to be a simple angular change of the cross bridge as was originally supposed, and the movement probably originates elsewhere in the molecule, whose structure was first established three-dimensionally in 1993. [8]

Filament sliding and muscle contraction come from the rowing of very large numbers of myosin molecules. Each individual stroke by a myosin molecule head takes about 1 millisecond and produces a 12 nm movement. Although this is a very small distance, many thousands of sarcomeres are arranged in a series, and in a very short time the sum of all these small distances may be measured in centimetres. The myosin head only releases its grip on the actin, and swings back for another power stroke with another actin, if it is recharged with another ATP molecule. Thus, when muscles are converted to meat and no more ATP is available, thick and thin filaments lock together wherever they overlap. This prevents any further filament sliding and the muscle becomes almost inextensible: this condition is called rigor mortis. [8]

When the myosin molecules of the thick filaments are "grabbing and swivelling" their way along the thin filaments, causing the filaments to slide past each other for muscle contraction, they require a constant stream of energy from ATP. Before a myosin molecule of a thick filaments can release itself from an actin molecule of the thin filament, it requires some new ATP. Without ATP, myosin stays locked onto actin, even if the muscle is trying to relax. Thus, when living muscle finally runs out of ATP after slaughter, then rigor mortis develops. [8]

4.2   Movement

Muscles connect with the bones, cartilages, ligaments, and skin, either directly, or through the intervention of fibrous structures called tendons or aponeuroses_. [1] Muscles pull on tendons which are attached to the bone on either side of a joint pivot. [2]

static/images/lever.swf

When one of the muscle contracts, it pulls on its tendon and moves the tibia one way, when the other muscle contracts, it moves the tibia the other way. [2]

Muscles cannot push; they can only pull. Thus, many muscles come in sets of antagonists that do opposite jobs. [3] When muscles cause a limb to move through the joint's range of motion, they usually act in the following cooperating groups [4]:

agonists
These muscles cause the movement to occur. They create the normal range of movement in a joint by contracting. Agonists are also referred to as prime movers since they are the muscles that are primarily responsible for generating the movement.
antagonists
These muscles act in opposition to the movement generated by the agonists and are responsible for returning a limb to its initial position.
synergists
These muscles perform, or assist in performing, the same set of joint motion as the agonists. Synergists are sometimes referred to as neutralizers because they help cancel out, or neutralize, extra motion from the agonists to make sure that the force generated works within the desired plane of motion.
fixators
These muscles provide the necessary support to assist in holding the rest of the body in place while the movement occurs. Fixators are also sometimes called stabilizers.

When an agonist contracts, in order to cause the desired motion, it usually forces the antagonists to relax. This phenomenon is called reciprocal inhibition because the antagonists are inhibited from contracting. [4]

Such inhibition of the antagonistic muscles is not necessarily required. In fact, co-contraction can occur. When you perform a sit-up, one would normally assume that the stomach muscles inhibit the contraction of the muscles in the lumbar, or lower, region of the back. In this particular instance however, the back muscles (spinal erectors) also contract. This is one reason why sit-ups are good for strengthening the back as well as the stomach. [4]

When stretching, it is easier to stretch a muscle that is relaxed than to stretch a muscle that is contracting. By taking advantage of the situations when reciprocal inhibition does occur, you can get a more effective stretch by inducing the antagonists to relax during the stretch due to the contraction of the agonists. You also want to relax any muscles used as synergists by the muscle you are trying to stretch. For example, when you stretch your calf, you want to contract the shin muscles (the antagonists of the calf) by flexing your foot. However, the hamstrings use the calf as a synergist so you want to also relax the hamstrings by contracting the quadricep (i.e., keeping your leg straight). [4]

There are two types of movements: flexion, or contraction of flexor muscles, drawing in of a limb, and extension, produced by contraction of extensor muscles.

Muscles fiber cannot contract partially; they can only contract completely. The central nervous system controls the force of a muscle contraction by recruiting more or less muscle fibers as they are needed. [4]

The muscle fibers constitute the elementary motor elements. [1]

static/images/muscle_mechanics2.gif

In those muscles where the fibers always run in a straight line from origin to insertion in all positions of the joint, a straight line joining the middle of the surface of origin with the middle of the insertion surface will give the direction of the pull. [1]

static/images/muscle_mechanics1.gif

If, however, the muscle or its tendon is bent out of a straight line by a bony process or ligament so that it runs over a pulley-like arrangement, the direction of the muscle pull is naturally bent out of line. The direction of the pull in such cases is from the middle point of insertion to the middle point of the pulley where the muscle or tendon is bent. Muscles or tendons of muscles which pass over more than one joint and pass through more than one pulley may be resolved, so far as the direction of the pull is concerned, into two or more units or single-joint muscles. [1] The direction of the pull is different for each joint and varies for each joint according to the position of the bones. The direction is determined in each case, however, by a straight line between the centers of the pulleys on either side of the joint [1]


[4]

As an example, when you flex your knee, your hamstring contracts, and, to some extent, so does your gastrocnemius (calf) and lower buttocks. Meanwhile, your quadriceps are inhibited (relaxed and lengthened somewhat) so as not to resist the flexion (see section Reciprocal Inhibition). In this example, the hamstring serves as the agonist, or prime mover; the quadricep serves as the antagonist; and the calf and lower buttocks serve as the synergists. Agonists and antagonists are usually located on opposite sides of the affected joint (like your hamstrings and quadriceps, or your triceps and biceps), while synergists are usually located on the same side of the joint near the agonists. Larger muscles often call upon their smaller neighbors to function as synergists.

The following is a list of commonly used agonist/antagonist muscle pairs:

pectorals/latissimus dorsi (pecs and lats) anterior deltoids/posterior deltoids (front and back shoulder) trapezius/deltoids (traps and delts) abdominals/spinal erectors (abs and lower-back) left and right external obliques (sides) quadriceps/hamstrings (quads and hams) shins/calves biceps/triceps forearm flexors/extensors


Lever mechanics determines the amount of force applied to the external environment, specifically the ratio of in-lever to out-lever. For example, moving the insertion point of the biceps more distally on the radius (farther from the joint of rotation) would increase the force generated during flexion (and, as a result, the maximum weight lifted in this movement), but decrease the maximum speed of flexion. Moving the insertion point proximally (closer to the joint of rotation) would result in decreased force but increased velocity. This can be most easily seen by comparing the limb of a mole to a horse - in the former, the insertion point is positioned to maximize force (for digging), while in the latter, the insertion point is positioned to maximize speed (for running

4.3   Kinds of contractions

Voluntary muscular contractions can be further classified according to either length changes or force levels. In spite of the fact that the muscle actually shortens only in concentric contractions, all activations are typically referred to as "contractions".

4.3.1   Isometric contraction

An isometric contraction is a contraction in which no movement takes place, because the load on the muscle exceeds the tension generated by the contracting muscle. This occurs when a muscle attempts to push or pull an immovable object. [4]

In isometric contraction, the muscle remains the same length. An example would be holding an object up without moving it; the muscular force precisely matches the load, which prevents the object from being dropped.

Because isometric exercises are done in one position without movement, they'll improve strength in only one particular position. You'd have to do various isometric exercises through your limb's whole range of motion to improve muscle strength across the range. In addition, since isometric exercises are done in a static position, they won't help improve speed or athletic performance.

4.3.2   Isotonic contraction

An isotonic contraction is a contraction in which movement takes place, because the tension generated by the contracting muscle exceeds the load on the muscle. This occurs when you use your muscles to successfully push or pull an object. [4]

4.3.2.1   Concentric contraction

A concentric contraction or shortening contraction is a type of muscle contraction in which the muscles shorten while generating force. This occurs when the force generated by the muscle exceeds the load opposing its contraction.

In concentric contraction, the force generated is sufficient to overcome the resistance, and the muscle shortens as it contracts. This is what most people think of as a muscle contraction.

4.3.2.2   Eccentric contraction

In eccentric contraction ("negative"), the force generated is insufficient to overcome the external load on the muscle and the muscle fibers lengthen as they contract. An eccentric contraction is used as a means of decelerating a body part or object, or lowering a load gently rather than letting it drop.

4.4   Stretch reflex

When the muscle is stretched, so is the muscle spindle. The muscle spindle records the change in length (and how fast) and sends signals to the spine which convey this information. This triggers the stretch reflex (also called the myotatic reflex) which attempts to resist the change in muscle length by causing the stretched muscle to contract. The more sudden the change in muscle length, the stronger the muscle contractions will be (plyometric, or "jump", training is based on this fact). This basic function of the muscle spindle helps to maintain muscle tone and to protect the body from injury. [4]

One of the reasons for holding a stretch for a prolonged period of time is that as you hold the muscle in a stretched position, the muscle spindle habituates (becomes accustomed to the new length) and reduces its signaling. Gradually, you can train your stretch receptors to allow greater lengthening of the muscles. [4]

Some sources suggest that with extensive training, the stretch reflex of certain muscles can be controlled so that there is little or no reflex contraction in response to a sudden stretch. While this type of control provides the opportunity for the greatest gains in flexibility, it also provides the greatest risk of injury if used improperly. Only consummate professional athletes and dancers at the top of their sport (or art) are believed to actually possess this level of muscular control. [4]


The stretch reflex occurs at the transition between lowering and raising, and many studies have shown that a muscle contracts harder concentrically when this contraction is preceded by a stretch, which is the very thing provided by an eccentric contraction. Demonstrate this to yourself by trying to do a vertical jump without dipping down to start the jump. Or try applying this principle to barbell curls by starting them from the top instead of from the bottom. The down phase, if used skillfully, makes the up phase much easier. [12]

Much of the effect provided by the eccentric/concentric transition comes from the viscoelastic energy stored in the muscles and tendons that are elongating under a loaded trip to the bottom of the range of motion; if there is no loaded trip, there is no energy to store. [12]


[4]

The stretch reflex has both a dynamic component and a static component. The static component of the stretch reflex persists as long as the muscle is being stretched. The dynamic component of the stretch reflex (which can be very powerful) lasts for only a moment and is in response to the initial sudden increase in muscle length. The reason that the stretch reflex has two components is because there are actually two kinds of intrafusal muscle fibers: nuclear chain fibers, which are responsible for the static component; and nuclear bag fibers, which are responsible for the dynamic component.

Nuclear chain fibers are long and thin, and lengthen steadily when stretched. When these fibers are stretched, the stretch reflex nerves increase their firing rates (signaling) as their length steadily increases. This is the static component of the stretch reflex.

Nuclear bag fibers bulge out at the middle, where they are the most elastic. The stretch-sensing nerve ending for these fibers is wrapped around this middle area, which lengthens rapidly when the fiber is stretched. The outer-middle areas, in contrast, act like they are filled with viscous fluid; they resist fast stretching, then gradually extend under prolonged tension. So, when a fast stretch is demanded of these fibers, the middle takes most of the stretch at first; then, as the outer-middle parts extend, the middle can shorten somewhat. So the nerve that senses stretching in these fibers fires rapidly with the onset of a fast stretch, then slows as the middle section of the fiber is allowed to shorten again. This is the dynamic component of the stretch reflex: a strong signal to contract at the onset of a rapid increase in muscle length, followed by slightly "higher than normal" signaling which gradually decreases as the rate of change of the muscle length decreases.

5   Properties

5.1   Color

The red colour comes from myoglobin, a soluble red pigment found inside muscle fibres. [8]

The more myoglobin, the darker the meat. This explains why turkey comes in red and white.

Turkeys use their legs continuously, which is why thighs and drumsticks are dark meat. Flightless domestic turkeys don’t use their chest muscles much. Their well-rested breasts become our white meat.

Myoglobin contains hemes, pigments responsible for the color of red meat. The color that meat takes is partly determined by the degree of oxidation of the myoglobin. In fresh meat the iron atom is the ferrous state bound to a dioxygen molecule (O2). Meat cooked well done is brown because the iron atom is now in the ferric (+3) oxidation state, having lost an electron. If meat has been exposed to nitrites, it will remain pink because the iron atom is bound to NO, nitric oxide (true of, e.g., corned beef or cured hams). Grilled meats can also take on a pink "smoke ring" that comes from the iron binding to a molecule of carbon monoxide.[9] Raw meat packed in a carbon monoxide atmosphere also shows this same pink "smoke ring" due to the same principles. Notably, the surface of this raw meat also displays the pink color, which is usually associated in consumers' minds with fresh meat. This artificially induced pink color can persist, reportedly up to one year.[10] Hormel and Cargill are both reported to use this meat-packing process, and meat treated this way has been in the consumer market since 2003

5.3   Strength

Strength is the ability of an animal to generate force against an external physical body irrespective of the amount of time it takes to move it. [12] [13] [14] A one rep maximum is used to test maximum muscular strength.

static/images/muscle_physiological_cross_section.gif

A, fusiform; B, unipinnate; C, bipinnate; P.C.S., physiological cross-section.

The strength of a muscle depends upon the number of fibers in what is known as the physiological cross-section, that is, a section which passes through practically all of the fibers. [1] In a muscle with parallel or nearly parallel fibers which have the same direction as the tendon this corresponds to the anatomical cross-section, but in unipinnate and bipinnate muscles the physiological cross-section may be nearly at right angles to the anatomical cross-section. [1] Estimates have been made of the strength of muscles and it is probable that coarse-fibered muscles are somewhat stronger per square centimeter of physiological cross-section than are the fine-fibered muscles. Fick estimates the average strength as about 10 kg. per square cm. This is known as the absolute muscle strength. The total strength of a muscle would be equal to the number of square centimeters in its physiological cross-section x 10 kg. [1]

When muscle fibers are parallel to the direction of the tendon the entire strength of the muscle contraction acts in the direction of the tendon. However, when the muscle fibers are inserted into the tendon at an angle, as in pinnate and bipinnate muscles, the force acting in the direction of the tendon diminishes to nil as the angle approaches 90 degrees (3/4 at 41 degrees, 1/2 at 60 degrees, and 1/3 at 72 degrees). [1]

Three factors determine strength:

  1. Physiological strength (muscle size, cross sectional area, available crossbridging, responses to training). [2]

    A pennate arrangement means that a greater cross-sectional area of muscle can be packed into the femur than would otherwise be possible. [2]

  2. Neurological strength (how strong or weak is the signal that tells the muscle to contract; the intensity of recruitment).

  3. Mechanical strength (muscle's force angle on the lever, moment arm length, joint capabilities).

Only the first two are in a person's control. Therefore, there are two ways to get stronger:

  1. More muscle (more motor units firing)
  2. More efficient CNS (also more motor units firing).

In sports with weight classes it's important to get stronger without putting on mass, to do this they train the CNS to be more efficient ( lots of heavy singles, doubles).


A fundamental property of muscle, which has been known for many years (see Hill, 1950, in the Bibliography), is that if you make a muscle contract so as to get maximum force out of it, then it only contracts very slowly. On the other hand, if you make it contract as quickly as possible, then you don't get much force.

The physical property which relates force and velocity is power (which is force mulitplied by velocity). If you make a muscle contract at a force and speed which maximises power, then it only contracts with a force of about one-third of the maximum that it is capable of producing.

Muscles can produce high force or high speed, but not both. Think of climbing a flight of stairs. If you are carrying a heavy backpack, you stagger up slowly, gasping for breath at every step. If you are not carrrying anything, you bound lightly up, two steps at a time (maybe).

5.5   Length

Once the muscle fiber is at its maximum resting length (all the sarcomeres are fully stretched), additional stretching places force on the surrounding connective tissue. The collagen fibers in the connective tissue align themselves along the same line of force as the tension as the tension increases. Hence when you stretch, the muscle fiber is pulled out to its full length sarcomere by sarcomere, and then the connective tissue takes up the remaining slack. This helps to realign any disorganized fibers in the direction of the tension, which helps to rehabilitate scarred tissue back to health. [4]

5.6   Flexiblity

Flexibility (= mobility) is defined by Gummerson as "the absolute range of movement in a joint or series of joints that is attainable in a momentary effort with the help of a partner or a piece of equipment." [4]

There are different types of flexibility, grouped according to the various types of activities involved in athletic training. The ones which involve motion are called dynamic and the ones which do not are called static. [4]

  • Dynamic flexibility (also called kinetic flexibility) is the ability to perform dynamic (or kinetic) movements of the muscles to bring a limb through its full range of motion in the joints. [4]
  • Static-active flexibility (also called active flexibility) is the ability to assume and maintain extended positions using only the tension of the agonists and synergists while the antagonists are being stretched (see section Cooperating Muscle Groups). For example, lifting the leg and keeping it high without any external support (other than from your own leg muscles). [4]
  • Static-passive flexibility (also called passive flexibility) is the ability to assume extended positions and then maintain them using only your weight, the support of your limbs, or some other apparatus (such as a chair or a barre). Note that the ability to maintain the position does not come solely from your muscles, as it does with static-active flexibility. Being able to perform the splits is an example of static-passive flexibility. [4]

Research has shown that active flexibility is more closely related to the level of sports achievement than is passive flexibility. Active flexibility is harder to develop than passive flexibility (which is what most people think of as "flexibility"); not only does active flexibility require passive flexibility in order to assume an initial extended position, it also requires muscle strength to be able to hold and maintain that position. [4]


[4]

According to Gummerson, flexibility (he uses the term mobility) is affected by the following factors:

Internal influences:

the type of joint (some joints simply aren't meant to be flexible) the internal resistance within a joint bony structures which limit movement the elasticity of muscle tissue (muscle tissue that is scarred due to a previous injury is not very elastic) the elasticity of tendons and ligaments (ligaments do not stretch much and tendons should not stretch at all) the elasticity of skin (skin actually has some degree of elasticity, but not much) the ability of a muscle to relax and contract to achieve the greatest range of movement the temperature of the joint and associated tissues (joints and muscles offer better flexibility at body temperatures that are 1 to 2 degrees higher than normal)

External influences:

the temperature of the place where one is training (a warmer temperature is more conducive to increased flexibility) the time of day (most people are more flexible in the afternoon than in the morning, peaking from about 2:30pm-4pm) the stage in the recovery process of a joint (or muscle) after injury (injured joints and muscles will usually offer a lesser degree of flexibility than healthy ones) age (pre-adolescents are generally more flexible than adults) gender (females are generally more flexible than males) one's ability to perform a particular exercise (practice makes perfect) one's commitment to achieving flexibility the restrictions of any clothing or equipment

According to SynerStretch, the most common factors are: bone structure, muscle mass, excess fatty tissue, and connective tissue (and, of course, physical injury or disability). [4]

The majority of "flexibility" work should involve performing exercises designed to reduce the internal resistance offered by soft connective tissues (see section Connective Tissue). Most stretching exercises attempt to accomplish this goal and can be performed by almost anyone, regardless of age or gender. [4]

The resistance to lengthening that is offered by a muscle is dependent upon its connective tissues: When the muscle elongates, the surrounding connective tissues become more taut (see section Connective Tissue). Also, inactivity of certain muscles or joints can cause chemical changes in connective tissue which restrict flexibility. According to M. Alter, each type of tissue plays a certain role in joint stiffness: "The joint capsule (i.e., the saclike structure that encloses the ends of bones) and ligaments are the most important factors, accounting for 47 percent of the stiffness, followed by the muscle's fascia (41 percent), the tendons (10 percent), and skin (2 percent)". [4]

M. Alter goes on to say that efforts to increase flexibility should be directed at the muscle's fascia however. This is because it has the most elastic tissue, and because ligaments and tendons (since they have less elastic tissue) are not intended to stretched very much at all. Overstretching them may weaken the joint's integrity and cause destabilization (which increases the risk of injury). [4]

When connective tissue is overused, the tissue becomes fatigued and may tear, which also limits flexibility. When connective tissue is unused or under used, it provides significant resistance and limits flexibility. The elastin begins to fray and loses some of its elasticity, and the collagen increases in stiffness and in density. Aging has some of the same effects on connective tissue that lack of use has. [4]

Strength training and flexibility training should go hand in hand. It is a common misconception that there must always be a trade-off between flexibility and strength. Obviously, if you neglect flexibility training altogether in order to train for strength then you are certainly sacrificing flexibility (and vice versa). However, performing exercises for both strength and flexibility need not sacrifice either one. As a matter of fact, flexibility training and strength training can actually enhance one another. [4]

One of the best times to stretch is right after a strength workout such as weightlifting. Static stretching of fatigued muscles (see section Static Stretching) performed immediately following the exercise(s) that caused the fatigue, helps not only to increase flexibility, but also enhances the promotion of muscular development (muscle growth), and will actually help decrease the level of post-exercise soreness. Here's why: After you have used weights (or other means) to overload and fatigue your muscles, your muscles retain a "pump" and are shortened somewhat. This "shortening" is due mostly to the repetition of intense muscle activity that often only takes the muscle through part of its full range of motion. This "pump" makes the muscle appear bigger. The "pumped" muscle is also full of lactic acid and other by-products from exhaustive exercise. If the muscle is not stretched afterward, it will retain this decreased range of motion (it sort of "forgets" how to make itself as long as it could) and the buildup of lactic acid will cause post-exercise soreness. Static stretching of the "pumped" muscle helps it to become "looser", and to "remember" its full range of movement. It also helps to remove lactic acid and other waste-products from the muscle. While it is true that stretching the "pumped" muscle will make it appear visibly smaller, it does not decrease the muscle's size or inhibit muscle growth. It merely reduces the "tightness" (contraction) of the muscles so that they do not "bulge" as much. [4]

Also, strenuous workouts will often cause damage to the muscle's connective tissue. The tissue heals in 1 to 2 days but it is believed that the tissues heal at a shorter length (decreasing muscular development as well as flexibility). To prevent the tissues from healing at a shorter length, physiologists recommend static stretching after strength workouts. [4]

If you are working on increasing (or maintaining) flexibility then it is very important that your strength exercises force your muscles to take the joints through their full range of motion. According to Kurz, Repeating movements that do not employ a full range of motion in the joints (like cycling, certain weightlifting techniques, and pushups) can cause of shortening of the muscles surrounding the joints. This is because the nervous control of length and tension in the muscles are set at what is repeated most strongly and/or most frequently. [4]

Ligaments will tear when stretched more than 6% of their normal length. Tendons are not even supposed to be able to lengthen. [4]

Just as there are different types of flexibility, there are also different types of stretching. Stretches are either dynamic (meaning they involve motion) or static (meaning they involve no motion). Dynamic stretches affect dynamic flexibility and static stretches affect static flexibility (and dynamic flexibility to some degree). [4]

5.6.1   Ballistic stretching

Ballistic stretching uses the momentum of a moving body or a limb in an attempt to force it beyond its normal range of motion. This is stretching, or "warming up", by bouncing into (or out of) a stretched position, using the stretched muscles as a spring which pulls you out of the stretched position. (e.g. bouncing down repeatedly to touch your toes.) This type of stretching is not considered useful and can lead to injury. It does not allow your muscles to adjust to, and relax in, the stretched position. It may instead cause them to tighten up by repeatedly activating the stretch reflex. [4]

5.6.2   Dynamic stretching

Dynamic stretching, according to Kurz, "involves moving parts of your body and gradually increasing reach, speed of movement, or both." Do not confuse dynamic stretching with ballistic stretching! Dynamic stretching consists of controlled leg and arm swings that take you (gently!) to the limits of your range of motion. Ballistic stretches involve trying to force a part of the body beyond its range of motion. In dynamic stretches, there are no bounces or "jerky" movements. An example of dynamic stretching would be slow, controlled leg swings, arm swings, or torso twists. [4]

Dynamic stretching improves dynamic flexibility and is quite useful as part of your warm-up for an active or aerobic workout (such as a dance or martial-arts class). [4]

According to Kurz, dynamic stretching exercises should be performed in sets of 8-12 repetitions. Be sure to stop when and if you feel tired. Tired muscles have less elasticity which decreases the range of motion used in your movements. Continuing to exercise when you are tired serves only to reset the nervous control of your muscle length at the reduced range of motion used in the exercise (and will cause a loss of flexibility). Once you attain a maximal range of motion for a joint in any direction you should stop doing that movement during that workout. Tired and overworked muscles won't attain a full range of motion and the muscle's kinesthetic memory will remember the repeated shorted range of motion, which you will then have to overcome before you can make further progress. [4]

5.6.3   Active stretching

Active stretching is also referred to as static-active stretching. An active stretch is one where you assume a position and then hold it there with no assistance other than using the strength of your agonist muscles (see section Cooperating Muscle Groups). For example, bringing your leg up high and then holding it there without anything (other than your leg muscles themselves) to keep the leg in that extended position. The tension of the agonists in an active stretch helps to relax the muscles being stretched (the antagonists) by reciprocal inhibition. [4]

Active stretching increases active flexibility and strengthens the agonistic muscles. Active stretches are usually quite difficult to hold and maintain for more than 10 seconds and rarely need to be held any longer than 15 seconds. [4]

Many of the movements (or stretches) found in various forms of yoga are active stretches. [4]

5.6.4   Passive stretching

Passive stretching is also referred to as relaxed stretching, and as static-passive stretching. A passive stretch is one where you assume a position and hold it with some other part of your body, or with the assistance of a partner or some other apparatus. For example, bringing your leg up high and then holding it there with your hand. The splits is an example of a passive stretch (in this case the floor is the "apparatus" that you use to maintain your extended position). [4]

Slow, relaxed stretching is useful in relieving spasms in muscles that are healing after an injury. Obviously, you should check with your doctor first to see if it is okay to attempt to stretch the injured muscles. [4]

5.6.5   Static stretching

Many people use the term "passive stretching" and "static stretching" interchangeably. However, there are a number of people who make a distinction between the two. According to M. Alter, Static stretching consists of stretching a muscle (or group of muscles) to its farthest point and then maintaining or holding that position, whereas Passive stretching consists of a relaxed person who is relaxed (passive) while some external force (either a person or an apparatus) brings the joint through its range of motion. [4]

Notice that the definition of passive stretching given in the previous section encompasses both of the above definitions. Throughout this document, when the term static stretching or passive stretching is used, its intended meaning is the definition of passive stretching as described in the previous section. You should be aware of these alternative meanings, however, when looking at other references on stretching. [4]

5.7   Density

The density of mammalian skeletal muscle tissue is about 1.06 kg/liter.

5.8   Energy consumption

Muscular activity accounts for much of the body's energy consumption. All muscle cells produce adenosine triphosphate (ATP) molecules which are used to power the movement of the myosin heads. Muscles have a short-term store of energy in the form of creatine phosphate which is generated from ATP and can regenerate ATP when needed with creatine kinase. Muscles also keep a storage form of glucose in the form of glycogen. Glycogen can be rapidly converted to glucose when energy is required for sustained, powerful contractions. Within the voluntary skeletal muscles, the glucose molecule can be metabolized anaerobically in a process called glycolysis which produces two ATP and two lactic acid molecules in the process (note that in aerobic conditions, lactate is not formed; instead pyruvate is formed and transmitted through the citric acid cycle).

6   Classification

6.1   Abductor

An abductor is a muscle that moves a body part away from the midline of the body.

6.2   Adductor

An adductor is a muscle which moves a body part toward the midline of the body

6.3   Extensor

An extensor is a muscle that straightens a joint

6.4   Flexor

A flexor is a muscle that bends a joint.


Muscle fiber specialization has occurred in different muscles to match metabolic properties with required functions. Muscle fiber types can be generally classified as white or αW (fast contraction speed, low metabolic oxidative capacity, and high metabolic glycolytic capacity), red or βR (slow contraction speed, high metabolic oxidative metabolism, and low metabolic glycolytic capacity), and intermediate or αR (fast contraction speed, intermediate or high metabolic oxidative metabolism, and high metabolic glycolytic capacity). Many other types have been described based on their histochemical staining patterns, leading to the theory that the metabolic capacity of fibers is a continuous variable and their differentiation is a dynamic process. [11]

These three muscle fiber types (Types 1, 2A, and 2B) are contained in all muscles in varying amounts. Muscles that need to be contracted much of the time (like the heart) have a greater number of Type 1 (slow) fibers. When a muscle first starts to contract, it is primarily Type 1 fibers that are initially activated, then Type 2A and Type 2B fibers are activated (if needed) in that order. The fact that muscle fibers are recruited in this sequence is what provides the ability to execute brain commands with such fine-tuned tuned muscle responses. It also makes the Type 2B fibers difficult to train because they are not activated until most of the Type 1 and Type 2A fibers have been recruited. [4]

HFLTA states that the the best way to remember the difference between muscles with predominantly slow-twitch fibers and muscles with predominantly fast-twitch fibers is to think of "white meat" and "dark meat". Dark meat is dark because it has a greater number of slow-twitch muscle fibers and hence a greater number of mitochondria, which are dark. White meat consists mostly of muscle fibers which are at rest much of the time but are frequently called on to engage in brief bouts of intense activity. This muscle tissue can contract quickly but is fast to fatigue and slow to recover. White meat is lighter in color than dark meat because it contains fewer mitochondria. [4]

6.5   Slow twitch (Type I, red)

Type I, slow twitch, or "red" muscle, is dense with capillaries and is rich in mitochondria and myoglobin, giving the muscle tissue its characteristic red color. It can carry more oxygen and sustain aerobic activity using fats or carbohydrates as fuel. Slow twitch fibers contract for long periods of time but with little force.

Slow-twitch fibers contract slowly, but they also fatigue slowly. [4]

The main reason the slow-twitch fibers are slow to fatigue is that they contain more mitochondria than fast-twitch fibers and hence are able to produce more energy. Slow-twitch fibers are also smaller in diameter than fast-twitch fibers and have increased capillary blood flow around them. Because they have a smaller diameter and an increased blood flow, the slow-twitch fibers are able to deliver more oxygen and remove more waste products from the muscle fibers (which decreases their "fatigability"). [4]

6.6   Fast twitch (Type II, white)

Type II, fast twitch muscle, has three major subtypes (IIa, IIx, and IIb) that vary in both contractile speed and force generated. Fast twitch fibers contract quickly and powerfully but fatigue rapidly, sustaining only short, anaerobic bursts of activity before muscle contraction becomes painful. They contribute most to muscle strength and have greater potential for increase in mass. Type IIb is anaerobic, glycolytic, "white" muscle that is least dense in mitochondria and myoglobin. In small animals (e.g., rodents) this is the major fast muscle type, explaining the pale color of their flesh.

Fast-twitch fibers contract quickly.

They come in two varieties: Type 2A muscle fibers which fatigue at an intermediate rate, and Type 2B muscle fibers which fatigue quickly. [4]

7   Motion

7.1   Radial growth of muscle fibers

static/images/arnold_education_of_a_bodybuilder.jpg

Arnold Schwarzenegger on the cover of his biography.

Bodybuilders generally have a triangular shaped physique.

[15]

Muscles grow radially because of myofibre hypertrophy (the constituent myofibres grow radially) and myofibrilliar hyperplasia (the number of myofibrils in myofibres increases).

Measurement of radial growth is difficult for several reasons: Myofibres are prismatic rather cylindrical (they have flat sides where they are pressed together), myofibres are often tapered (their diameters may decrease towards one or both ends of the myofibre), and because myofibre diameters increase when a myofibres contracts.

static/images/muscle_radial_hypertrophy.gif
static/images/muscle_fiber_split.gif

New myofilaments are added around the outside of the myofibril. This increases the length of the diffusion pathway for calcium ions as they turn contraction on and off, which causes mechanical stress in the myofibril - the outside contracts and relaxes before the central axis. Calcium ions building up in the interior of the myofibril activate enzymes (calpains) which release thin myofilaments from their Z-lines. Contraction causes the weakened myofibril to split. But, the myofibril is very long, and a split at one point may not match up to a split at another point. We end up with a complex structure. Where once there was a single myofibril seen in transverse section, we now see many myofibrils in transverse section - but following them along the myofibril we find they are all linked. Thus, we have not really formed any new myofibrils, just increased their size and complexity. [15]

The radial growth of muscle fibers is associated with an increase in the apparent number of myofibrils seen in cross section. Ribosomes within the myofilament lattice can presumably synthesize new myofibrillar proteins. As new myofilaments are added and the myofibril increases in diameter, myofibrils may split longitudinally, but seldom are the splits continuous along the complete length of a muscle fiber. Thus, what looks like one myofibril in a plane above the split may appear as two myofibrils in a lower plane. Spitting may occur first at Z lines (i.e., between sarcomeres), where peripheral thin filaments tend to pull at an angle during contractio.Splitting starts in the center of an I band and then spreads to the A band and the periphery of the myofibril, although this is only characteristic of chronic stretching. [16]

As the myofibre grows radially, it adds new nuclei. It is important to remember when we look at transverse sections of myofibres - the number of nuclei seen under the sarcolemma (the cell membrane) depends on the thickness of the transverse section relative to the length of the nuclei. If the nuclei are long and thin, then they are more likely to be seen in transverse section than short, thick nuclei. The thicker a transverse section, the more nuclei will be seen. Even taking this into account, however, there is no doubt the number of nuclei increases as myofibres undergo radial hypertrophy. Where do the extra nuclei come from? This was a puzzle for a hundred years. New nuclei are normally obtained from mitosis (cell division), and mitosis is normally detectable when chromosomes separate at metaphase - looking rather like bunches of bananas. But, in a hundred years, nobody ever saw any metaphase chromosomes in a myofibre.

Myofibre nuclei have the following features. (1) No clear zone separates them from myofibrils. (2) They are more basophilic (stained by basic dyes for light microscopy) than fibroblast nuclei. (3) The nucleolus (containing RNA) is well defined and large. (4) The outer chromatin (the granular pattern of stained DNA) is tightly distributed along the nuclear membrane. (5) The internal cromatin is evenly dispersed.

Myofibre nuclei contain DNA combined with histones and other structural proteins to form chromatin. When DNA is used for protein synthesis, the chromatin is dispersed, only binds weakly to histological stains, and is called euchromatin. In non‑dividing cells, chromatin may form darkly stained irregular clumps called chromatin particles. Nuclei also contain RNA and darkly stained clumps of RNA form nucleoli. The number of nucleoli may vary between animal species. Condensed regions of darkly stained chromosomes sometimes persist between cell divisions and are called heterochromatin. In the mononucleated cells of the body, such as those of the skin or liver, darkly stained chromosomes composed of inactive DNA are seen when cells divide. But, as explained below, the situation in multinucleated myofibres is more complex, and distinct chromosomes are not seen by light microscopy within myofibres.

True myofibre nuclei are located within the sarcoplasm. Although the nuclei of satellite cells are seen by light microscopy within the sarcoplasm, electron microscopy shows satellite cells are located in depressions in the myofibre surface. Thus, the nucleus of a satellite cell is separated from the sarcoplasm of its myofibre by a satellite cell membrane and a myofibre membrane.

The existence of satellite cells became accepted in 1961, although they had been seen a hundred years earlier - but no one believed it. Pericytes are mesodermal cells found around very small blood vessels. They contain actomyosin and are probably capable of contraction and phagocytosis.

The features of satellite cells are: (1) They are indented into a myofibre surface, although sometimes they bulge outwards. (2) They have variable amounts of basophilic cytoplasm - usually very little. (3) Their outer chromatin is heavily and unevenly deposited along the nuclear membrane. (4) Their internal chromatin is scattered in clumps. (5) Their nucleolus is small and usually masked by internal chromatin - because mitosis is still possible. (6) Sometimes the nuclei are uniformly stained dark. (7) Most of them have a clear space of 0.5 to 0.2 micrometres separating them from the myofibrils - this is where the two membranes are located.

Muscle nuclei increase in number during postnatal development but the relative magnitude of the increase varies from muscle to muscle. Before the existence of satellite cells was proved by electron microscopy, it was rather difficult to explain how muscle nuclei were able to increase in number without any evidence, by light microscopy, of mitosis in myofibre nuclei. Myofibre nuclei are able to withstand longitudinal compression during muscle contraction by means of concertina‑like wrinkles in their nuclear membrane and, for many years, histologists regarded wrinkled muscle nuclei as evidence of an unusual type of nuclear division. They were wrong! New nuclei added during the postnatal growth of myofibres come from the daughter cells of satellite cell mitosis. Like myoblasts, satellite cells are part of the myogenic cell lineage from somitic mesoderm - essentially - they are premyoblasts which have been trapped on the myofibre surface by the development of the endomysium (the connective tissues around each myofibre). Mitosis in satellite cells has been seen by electron microscopy and the synthesis of DNA by satellite cell nuclei has been proved by radioautography (tritiated thymidine used in the synthesis of new DNA is detected by its radioactivity). If a myofibre is damaged by disease, its myofibrils are removed by phagocytic cells - then a new myofibre may be formed from satellite cells within the old endomysial tube. There is some evidence satellite cells can move around on the myofibre surface. Can you think how this might be exploited agriculturally? On a proportional basis, there are more nuclei in red muscles than in white muscles, and nuclei are more frequent at the ends of myofibres than at their midlength. Younger animals have proportionally more satellite cells than older animals. The main two functions of satellite cells are to provide nuclei for growing myofibres and a source of myoblasts for postnatal muscle regeneration. These two functions may be independently regulated by factors such as insulin and IGF (insulin-like growth factor) controlling the growth function, and fibroblast growth factor controlling the regenerative function .

Why were mitotic chromosomes never observed inside myofibres ? You would expect them if satellite cells look like other nuclei inside the myofibre. The answer - satellite cells are too small to allow the chromosomes to separate sufficiently to be seen clearly by light microscopy.

7.2   Gain

The ability to gain muscle also varies person to person, based mainly upon genes dictating the amounts of hormones secreted, but also on sex, age, health of the person, and adequate nutrients in the diet.


[5]

The exact mechanism by which exercise enhances strength remains unclear, but its basic principles are understood. Overall, two processes appear to be involved: hypertrophy, or the enlargement of cells, and neural adaptations that enhance nerve-muscle interaction. Muscle cells subjected to regular bouts of exercise followed by periods of rest with sufficient dietary protein undergo hypertrophy as a response to the stress of training. (This should not be confused with short-term swelling due to water intake.) Enhanced muscle protein synthesis and incorporation of these proteins into cells cause hypertrophy. Because there are more potential power strokes associated with increased actin and myosin concentrations, the muscle can exhibit greater strength. Hypertrophy is aided by certain hormones and has a very strong genetic component as well.

The neural basis of muscle strength enhancement primarily involves the ability to recruit more muscle cells--and thus more power strokes--in a simultaneous manner, a process referred to as synchronous activation. This is in contradistinction to the firing pattern seen in untrained muscle, where the cells take turns firing in an asynchronous manner. Training also decreases inhibitory neural feedback, a natural response of the central nervous system to feedback signals arising from the muscle. Such inhibition keeps the muscle from overworking and possibly ripping itself apart as it creates a level of force to which it is not accustomed. This neural adaptation generates significant strength gains with minimal hypertrophy and is responsible for much of the strength gains seen in women and adolescents who exercise. It also utilizes nerve and muscle cells already present and accounts for most of the strength increases recorded in the initial stages of all strength training, because hypertrophy is a much slower process, depending, as it does, on the creation of new muscle proteins. Thus, overall, the stress of repeated bouts of exercise yield neural as well as muscular enhancements to increase muscle strength.

7.3   Atrophy

Muscle atrophy is defined as a decrease in the mass of the muscle; it can be a partial or complete wasting away of muscle, and is most commonly experienced when persons suffer temporary disabling circumstances such as being restricted in movement and/or confined to bed as when hospitalized. When a muscle atrophies, this leads to muscle weakness, since the ability to exert force is related to mass.

The similar in effect neurogenic atrophy is muscle atrophy that results from damage to the nerve that stimulates the muscle causing a shriveling about otherwise healthy limbs. Also, time in a circa zero g environment without exercise will lead to atrophy. This is partially due to the smaller amount of exertion needed to move about, and that muscles are not used to maintain posture


Myostatin is the hormone that break down muscle tissue. In some animals, fasting inhibits the action of myostatin

Is there any reason why body builders and athletes don't take myostatin inhibitors then?

It's easy to inhibit things in a mouse-model because you can (fairly) easily knockout specific genes. In humans there needs to be an effective pharmacological inhibitor, which currently doesn't really exist to my knowledge. This is correct. The reason why no humans are using a myostatin inhibitor is because they don't exist. Humans do exist that naturally don't produce Myostatin, but from what I have read in research so far, they aren't inhibiting their own myostatin, they just aren't producing, so we have to either find a way to block myostatin production, or effect.

Theory is that muscle uses a lot of energy just to keep on your body and since early humans didn't have such abundant food it wasn't possible for them to eat enough to keep all this muscle so it was selectively advantageous to inhibit muscle growth at a certain point. Early humans relied on stamina hunting rather than using their strength to overpower their prey. Additionally the lack of myostatin actually causes your heart to grow too large and reduces life expectancy. No sources since this is all from memory years ago.

7.4   Genetics

Needs support, but sounds right.

Your ability, or lack thereof, to produce force and build muscle is almost entirely based on the genetics you were born with, and your testosterone level, which is also genetically predetermined. Being predisposed to putting on huge quantities of muscle mass is pretty uncommon in females – and really, in males too – and if you have these genetics, you know it already. Like most women, you don't have enough testosterone to get huge.

7.5   Nutrition

Adequate nutrition is important to build strength. General guidelines:

  1. Eat copius amount of protein. A good rule of thumb is 1 to 1.5 grams of protein per lb of body weight. Err on the side or more rather than less.

    Not all protein is equal. Protein from animal sources (meat, milk, eggs, cheese, and whey protein) are superior to non-animal sources by virtue of a superior amino acid profile. Many people find whey protein powder to be helpful in fulfilling their protein requirements.

8   Soreness

The cause of soreness remains poorly understood despite wide study. It is thought to be the result of inflammation in the basic contractile unit of the muscle fiber and the fact it responds well to anti-inflammatory therapy tends to support this theory. What is certain is that `lactic acid`_ (a transient byproduct of muscle contraction) has nothing to do with it. [12]

Soreness is usually produced when the body does something to which it is not adapted. For example, after your first workout or when you change a workout program. [12]

The onset of the perception of soreness is normally delayed anywhere from 12 to 48 hours, depending on the age and conditional level of the athlete, the nature of the exercise being done, and the volume and intensity of the exercise. For this reason, the exercise literature refers to it as delayed-onset muscle soreness ("DOM"). [12]

The part of the rep that causes most of the soreness is the eccentric or "negative" phase of the contract, where the muscle in lengthening under the load rather than shortening. This is probably because of the way the component of the contractile mechanism in the muscle fibers are stressed as they stretch apart under a load. [12]

This explain why some exercises produce more soreness than others. Exercises without a significant eccentric component, like the power clean, in which the weight is dropped rather than actively lowered, will not produce nearly the soreness that the squat will. Squats, benches, presses, deadlifts, and many assistance and ancillary exercises have both an eccentric and concentric component, where the muscles involved both length and shorted under the load. Some sports activities, like cycling, are entirely concentric, since all aspects of pedaling involving the shortening of the muscles involved. You can therefore train such exercises without causing much, if any, soreness. Since soreness is an inflammatory process, the harder an athlete can train without producing high amounts of muscle inflammation and the attendant unfriendly hormonal responses, the better that is for recovery. Exercise methods that produce high levels of soreness as a constant feature of the program - due to random exercise selection that precludes adaptation to the stress - can contribute to long-term systemic inflammation, the kind that produces poor health instead of fitness and strength. Soreness is an unavoidable part of training, but it should not be sought after as a primary objective and worn as a badge of honor for its own sake. [12]

9   Energy

Mitochondria generate the energy which produces the calcium flow in the muscle fibers. [4]

Different types of muscle fibers have different amounts of mitochondria. Muscle fibers with more mitochondria can produce more energy. [4]

10   Consumption

The meat sold in shops is derived from skeletal muscle. [8]

The muscle fibres found in most commercial cuts of meat seldom run the complete length of the muscle in which they are located. [8]

There are important differences between muscle as a functional tissue in the live animal and the final meat that is consumed. These include the onset of rigor mortis, the proteolytic postmortem processes, and the effect of cooking (e.g., the effect of heat on muscle proteins). [11]

In general, as muscle is converted into meat, oxygen is no longer available for cells, producing a shift from aerobic to anaerobic metabolism. The increase in lactic acid reduces muscle pH from ~7.1 to ~5.6. The depletion in energy and the inability of ATP-dependent calcium, sodium, and potassium pumps to function lead to a rise in intracellular ionic strength [11]


Cannibalism is detrimental to the body because it exposes the consumer to more diseases. Viruses tend to be specific to a species, and it is rare for them to jump. So if you are eating beef meat contaminated with some virus that is affecting the cow, chances are you won't catch it. But if you are eating human flesh, that is contaminated with HIV, you now have a very good chance of contracting it. This also means that eating an ape species is less risky than eating a human, but more so than eating a cow.

10.1   Safety

Humans can eat meat raw. It is perfectly safe if we were to eat it immediately after a kill like predators in the wild do. But that is not how we do meat. We eat meat that is days, weeks, or even months old by the time it gets to us. As such it has had ample time to grow bacteria and fungus levels to the point of toxicity.

Also animals do get sick from parasites or bacteria/fungus from raw meat/spoiled meat all the time. We just do not care or notice.

Cooking food kills most bacteria, fungus, and parasites, and denatures many toxins. That makes it safe to eat longer after it would have been dangerous raw. It also partially breaks down the food making it easier to digest, meaning we spend less energy extracting nutrients and get more of the nutrients out of the food.

Everyone makes good points here but there's also the fact that predators eat the animal as soon as they catch or kill it which doesn't give much time for bacteria to develop on the meat. Our food has usually been dead for days or longer so the risk for germs to grow on it is larger.

Chicken meat is porous and so bacteria can penetrate into the meat from the surface. Steaks are not so this is why it's ok to eat a raw steak, but not raw ground beef.

Ground beef removes that seal and mixes it and all of the surface bacteria together. This is why you're supposed to only eat well-done ground beef. Most of the bacteria is on the outside of the steak, which is cooked. Hamburger meat gets churned about so the bacteria is mixed around, and needs to be fully cooked.

We can and do eat meat raw (Sushi), the thing about mass produced meat is that if even a single chicken is sick then the rest of the meat get this bacteria during processing. If you kill an animal and it didn't have a disease (salmonella, e-coli, trichinella) then you'd be perfectly fine to eat the meat raw. However, you can kill those bacterias (also it tastes a lot better) at 145 degrees. Thus, cooking.


Why is it okay to eat raw fish?

Parasites and bacteria in raw animal meat are different than ones you'd fine raw fish.

The way animals are slaughtered also has to do with the health risks. Parasites and bacteria tend to come from an animal's gut, not it's muscle. If your butcher nick's open an animal's intestines, any harmful microorganisms released could contaminate all the meat the butcher is preparing.

11   Questions

12   Further reading

http://www.aps.uoguelph.ca/~swatland/Lectures.html

Specifically:

http://www.aps.uoguelph.ca/~swatland/HTML10234/LEC7/LEC7.html http://www.aps.uoguelph.ca/~swatland/HTML10234/LEC8/LEC8.html http://www.aps.uoguelph.ca/~swatland/HTML10234/LEC9/LEC9.html

13   References

[1](1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20, 21, 22, 23, 24, 25, 26, 27, 28, 29, 30) Henry Gray. Anatomy of the Human Body: Myology. http://www.bartleby.com/107/102.html
[2](1, 2, 3, 4) W. J. Heitler. January 2007. How the legs work. http://www.st-andrews.ac.uk/~wjh/jumping/legwrk.htm
[3](1, 2, 3) J. Stein Carter. Jan 22 2014. Muscles. http://biology.clc.uc.edu/courses/bio105/muscles.htm
[4](1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20, 21, 22, 23, 24, 25, 26, 27, 28, 29, 30, 31, 32, 33, 34, 35, 36, 37, 38, 39, 40, 41, 42, 43, 44, 45, 46, 47, 48, 49, 50, 51, 52, 53, 54, 55, 56, 57, 58, 59, 60, 61) Brad D. Appleton. 1993 - 1996. STRETCHING AND FLEXIBILITY. http://web.mit.edu/tkd/stretch/stretching_toc.html
[5]October 27, 2003. How does exercise make your muscles stronger? http://www.scientificamerican.com/article/how-does-exercise-make-yo/
[6](1, 2) Proprioceptors. http://courses.washington.edu/conj/bess/spindle/proprioceptors.html
[7](1, 2) What is Meat? https://www.exploratorium.edu/cooking/meat/INT-what-is-meat.html
[8](1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20) Howard Swatland. Structure of meat. http://www.aps.uoguelph.ca/~swatland/ch5_0.htm http://www.aps.uoguelph.ca/~swatland/ch5_1.htm
[9](1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11) Howard Swatland. Myofibrils. http://www.aps.uoguelph.ca/~swatland/HTML10234/LEC10/LEC10.html http://www.aps.uoguelph.ca/~swatland/HTML10234/LEC11/LEC11.html
[11](1, 2, 3, 4, 5, 6, 7, 8, 9) M. Juarez, N. Aldai, O. Lopez, M. E. R. Dugan, B. Uttaro, and J.L.Aaaulhus. Beef Texture and Juiciness.
[12](1, 2, 3, 4, 5, 6, 7, 8) Rippetoe 2005. Starting Strength: Basic Barbell Training.
[13]Rippetoe Kilgore 2006. Practical programming for strength training.
[14]October 2002. What is fitness? http://library.crossfit.com/free/pdf/CFJ_Trial_04_2012.pdf
[15](1, 2) Howard Swatland. Radial Growth of Muscle Fibres. http://www.aps.uoguelph.ca/~swatland/HTML10234/LEC23/LEC23.html
[16](1, 2, 3) Howard Swatland. Radial Growth http://www.aps.uoguelph.ca/~swatland/ch7_3.htm
[17]Howard Swatland. 16: Fibrous connective tissues. http://www.aps.uoguelph.ca/~swatland/HTML10234/LEC16/LEC16.html
[18]Henry C. Lukaski. Human Body Composition. Chapter 14: Assessing Muscle Mass.

[4]

Warming up is quite literally the process of "warming up" (i.e., raising your core body temperature). A proper warm-up should raise your body temperature by one or two degrees Celsius (1.4 to 2.8 degrees Fahrenheit) and is divided into three phases: general warm-up, stretching, and sport-specific activity.

It is important that you perform the general warm-up before you stretch because ?. It is not a good idea to attempt to stretch before your muscles are warm (something which the general warm-up accomplishes).

Warming up can do more than just loosen stiff muscles; when done properly, it can actually improve performance. On the other hand, an improper warm-up, or no warm-up at all, can greatly increase your risk of injury from engaging in athletic activities.

It is important to note that active stretches and isometric stretches should not be part of your warm-up because they are often counterproductive. The goals of the warm-up are (according to Kurz): "an increased awareness, improved coordination, improved elasticity and contractibility of muscles, and a greater efficiency of the respiratory and cardiovascular systems." Active stretches and isometric stretches do not help achieve these goals because they are likely to cause the stretched muscles to be too tired to properly perform the athletic activity for which you are preparing your body.

The general warm-up consists of: joint rotations and aerobic activity. These two activities should be performed in order.

The general warm-up should begin with joint-rotations, starting either from your toes and working your way up, or from your fingers and working your way down. This facilitates joint motion by lubricating the entire joint with synovial fluid. Such lubrication permits your joints to function more easily when called upon to participate in your athletic activity. You should perform slow circular movements, both clockwise and counter-clockwise, until the joint seems to move smoothly.

After you have performed the joint rotations, you should engage in at least five minutes of aerobic activity such as jogging, jumping rope, or any other activity that will cause a similar increase in your cardiovascular output (i.e., get your blood pumping). The purpose of this is to raise your core body temperature and get your blood flowing. Increased blood flow in the muscles improves muscle performance and flexibility and reduces the likelihood of injury.

The stretching phase of your warmup should consist of two parts: static stretching and dynamic stretching. It is important that static stretches be performed before any dynamic stretches in your warm-up. Dynamic stretching can often result in overstretching, which damages the muscles.

Stretching is not a legitimate means of cooling down. It is only part of the process. After you have completed your workout, the best way to reduce muscle fatigue and soreness (caused by the production of lactic acid from your maximal or near-maximal muscle exertion) is to perform a light warm-down. This warm-down is similar to the second half of your warm-up (but in the reverse order). The warm-down consists of sport-specific activity, dynamic stretching, and static stretching.

Many people are unaware of the beneficial role that massage can play in both strength training and flexibility training. Massaging a muscle, or group of muscles, immediately prior to performing stretching or strength exercises for those muscles, has some of the following benefits: increased blood flow The massaging of the muscles helps to warm-up those muscles, increasing their blood flow and improving their circulation. relaxation of the massaged muscles The massaged muscles are more relaxed. This is particularly helpful when you are about to stretch those muscles. It can also help relieve painful muscle cramps. removal of metabolic waste The massaging action, and the improved circulation and blood flow which results, helps to remove waste products, such as lactic acid, from the muscles. This is useful for relieving post-exercise soreness. Because of these benefits, you may wish to make massage a regular part of your stretching program: immediately before each stretch you perform, massage the muscles you are about to stretch.

According to SynerStretch, there are three factors to consider when determining the effectiveness of a particular stretching exercise:

isolation leverage risk

Ideally, a particular stretch should work only the muscles you are trying to stretch. Isolating the muscles worked by a given stretch means that you do not have to worry about having to overcome the resistance offered by more than one group of muscles. In general, the fewer muscles you try to stretch at once, the better. For example, you are better off trying to stretch one hamstring at a time than both hamstrings at once. By isolating the muscle you are stretching, you experience resistance from fewer muscle groups, which gives you greater control over the stretch and allows you to more easily change its intensity. As it turns out, the splits is not one of the best stretching exercises. Not only does it stretch several different muscle groups all at once, it also stretches them in both legs at once.

Having leverage during a stretch means having sufficient control over how intense the stretch becomes, and how fast. If you have good leverage, not only are you better able to achieve the desired intensity of the stretch, but you do not need to apply as much force to your outstretched limb in order to effectively increase the intensity of the stretch. This gives you greater control.

According to SynerStretch, the best stretches (those which are most effective) provide the greatest mechanical advantage over the stretched muscle. By using good leverage, it becomes easier to overcome the resistance of inflexible muscles (the same is true of isolation). Many stretching exercises (good and bad) can be made easier and more effective simply by adjusting them to provide greater leverage.

Although a stretch may be very effective in terms of providing the athlete with ample leverage and isolation, the potential risk of injury from performing the stretch must be taken into consideration. Once again, SynerStretch says it best: Even an exercise offering great leverage and great isolation may still be a poor choice to perform. Some exercises can simply cause too much stress to the joints (which may result in injury). They may involve rotations that strain tendons or ligaments, or put pressure on the disks of the back, or contain some other twist or turn that may cause injury to seemingly unrelated parts of the body.


The protein calsequestrin binds and stores calcium ions within the sarcoplasmic reticulum. [9] Calsequestrin concentration is higher in fast‑contracting than in slow-contracting myofibres. [9]



Animals are born with a certain number of muscle fibers in each muscle.

[16]

The ends of muscle fibers are rounded if they insert into tendons but tapered if they insert intrafascicularly beneath the endomysium of another fiber.

As a muscle fiber accumulates contractile proteins during growth, it also increases its sarcoplasmic volume sarcoplasm and number of mitochondria. Mitochondria are very abundant in the sarcoplasm of fibers from young animals but the proliferation of mitochondria may lag behind the increase in sarcoplasmic volume which occurs with fiber growth. This is most evident in white fibers. Mitochondria appear to proliferate by fission after each mitochondrion has been internally subdivided by the formation of a septum.

The cross sectional areas of muscle fibers are increased if the fibers are cut obliquely rather than in exact cross section. Oblique sections may be caused by poor alignment of the tissue on the microtome chuck but, even in correctly aligned tissue, they may occur if some fibers of the sample are contracted more than others. Fibers with a lesser degree of contraction may be thrown into sinuous folds that give rise to oblique sections at intervals along the fiber length. If fibers are cylindrical, this is not a problem since the minimum diameter gives the true diameter. But if fibers tend are polygonal, minimum diameters may underestimate true mean diameters.


Think of the length of any major muscle in a calf or piglet, then think of the length of the same muscle in a commercial beef or pork carcass. There has been a major increase in length. Thus, longitudinal growth of whole muscles makes a major contribution to meat production in all our meat animals.

the longitudinal growth of individual muscles is achieved by the longitudinal growth of individual myofibres, which is complicated by the angular insertion of myofibres in most muscle.

Only a few muscle like the Sartorius in the hindlimb have parallel myofibres. In most muscles, the myofibres are arranged at angles to modify the effects of individual myofibre contraction. If a myofibre contracts over a greater distance than the length of the whole muscle, then leverage is obtained and the force of contraction is magnified at the expense of distance. Often distance and force are unchanged but the angular arrangement of myofibres allows more myofibres to be connected to the tendon than would be possible if the myofibres were all parallel.

Longitudinal growth originates from the formation of new sarcomeres at the ends of myofibres. The addition of new sarcomeres is regulated. Sarcomere length and the degree of overlap of thick and thin filaments must be maintained at an optimum for efficient muscle contraction

Regulation may be mediated by the protein dystrophin as a mechanochemical transducer. However, the system must be very complex, because sarcomere length shortening during contraction differs between muscles and is related to the angular changes of nearby skeletal joints. Myofibrils insert obliquely at their ends. This enables new myofilaments to be added without interfering with the mechanical continuity of the myofibrils at their attachment to the cell membrane. The ratio of muscle belly length to free tendon length remains approximately constant during growth.

An increase in the girth of a deep muscle (usually from the radial hypertrophy of myofibres) causes overlying superficial muscles to bulge outwards. Thus, the dominant pattern of cellular growth in the superficial muscle may be longitudinal growth, since its length from origin to insertion is increased in a curvilinear manner as the deep muscle bulges outwards.

The longitudinal growth of muscles follows that of the skeleton. Thus, bone length is related to meat yield.

About every 20 minutes, a new sarcomere is added to the length of myofibres in pigs growing to market weight. In muscles with relays of intrafascicularly terminating fibers along their length, or relays of fasciculi along their length, the number of points at which longitudinal growth occurs is increased. If two growth points, one at each end of a myofibre, can add a sarcomere every 20 minutes, then the formation of each sarcomere must take about 40 minutes

he number of myofibres appearing at the midlength of a muscle may be less than the real number of myofibres in the muscle. Myofibres can terminate intrafascicularly along the length of a muscle. When they grow in length, they cause an increase in the apparent number of myofibres (but there has been no change in the real number!).


[17]

static/images/tissue_fibrous_connective.gif

Fibrous connective tissue. It has three essential features: (1) cells (stained with methylene blue), (2) fibres (stained pink with eosin), and (3) matrix (in the spaces between the cells and the fibres).

Fibrous connective tissue hold the myofibers in meat together.

Some muscles have extremely strong connective tissue to prevent the myofibres being damaged as the muscle contracts. Muscle with an angular arrangement of myofibres gain leverage when they contract. The length of the contraction is reduced but the strength is increased. The myofibres must be anchored in strong connective tissue. The strongest connective tissues are found in the distal muscles of the limbs and in the neck.

Muscles with a high connective tissue content must be cooked with moist heat (stewed not barbecued or roasted). Connective tissues tend to be stronger in large animals (eg., beef) than in small animals (eg., lamb). Connective tissues tend to be stronger in old animals (eg., mature beef) than in young animals (eg., veal).

This explains why stewing beef (neck and distal limb muscles) is less expensive than steak or roasts. This also explains why beef carcasses are graded by animal age. Grade A beef is from youthful animals (up to about 18 months of age).

The fibrous connective tissues in meat form a continuous mesh from the microscopic strands of endomysium around individual myofibres, to the thick layers of perimysium around bundles of myofibres (fasciculi), all being gathered and connected to the very thick epimysium on the surfaces of individual muscles.

The endomysium, perimysium and epimysium contain two types of protein fibres, collagen and elastin.


Elastin is the type of connective tissue that will never breakdown, causing an inedible skin on your meat. In the industry we call it silverskin.

http://www.justcook.ca/how-to-cook-a-piece-of-meat/


The silverskin must be removed. When subjected to the heat of the oven, sauté pan or grill, it shrinks and will cause the filet to curl. It is also tough and inedible. Because the silverskin is tough and sinewy it is fairly easy to remove.

Silverskin is the thin (but tough), white, silvery looking connective tissue on the underside of every rack of ribs. The reasons for removing it are quite simple: it makes the ribs easier to cut/eat, and, once it is removed it allows any rub you are using to flavor/penetrate the meat. It is quite easy to remove, especially if your ribs are at room temperature, and I like to let my ribs sit out on the counter for about an hour before doing it. Silverskin is also found on other cuts of meat, like tenderloin of beef, lamb and pork.

the tough connective tissue surrounding muscle, the pearlescent membrane found on certain cuts of meat that is removed before cooking to prevent curling; also called elastin

Further reading:


Push your core out when lifting. Essentially why a lifting belt provides a benefit for heavier lifts, it allows you to have something to push against.


Milo. Knowing the importance of not wasting anything, Milo fashioned the animal’s hide into a crude belt of sorts which he wore in his Olympic endeavours.

The second mythical story comes from the Norse God, now of Marvel fame, Thor. Aside from his legendary Hammer, another weapon in the Viking’s repertoire was his trusty belt, megingjörð. According to Norse legend, when megingjörð was combined with Thor’s hammer and iron gloves, the belt doubles his already legendary strength.

it was Olympic events where weightlifting belts undoubtedly gained the most popularity. Indeed the first official international contest between weightlifters, namely the 1896 Olympic Games, saw some competitors don their belts in search of better lifts. Though not all lifters wore them, many did

As weightlifting’s importance grew, so too did the prevalence of weightlifting belts amongst the general training populace.


http://www.exrx.net/WeightExercises/Hamstrings/BBGoodMorning.html


http://sfcustomchiro.com/blog/

Foam rolling should form an integral part of everyone’s home care routine. Foam rollers - lightweight cylinders made of high- or low- density foam - facilitate self-massage and myofascial release, which in turn boosts circulation and helps us to maintain healthy, flexible tissue. And succinctly put, healthy tissue means less chance of developing dysfunction. Foam rolling is a practical, effective way to support and enhance preventative chiropractic treatment.

Because foam rolling increases circulation, it serves as a great pre-workout warm up, and, equally, a beneficial post-workout recovery aid. Whereas stretching before a workout can blunt our muscles’ ability to generate force, foam-rolling brings a much needed surge of oxygen to targeted areas. One study found that participants who foam-rolled were “less sore” after a “devastating” workout that included several sets of squats. Over time, the study projected, that same reduced feeling of fatigue would allow participants to extend their workout time and volume, leading to chronic performance enhancements


How long should you wait between sets? Should you try to spend only a few seconds between sets to fully work the muscle and increase the "burn", or should you wait longer until your muscles have fully recovered from the last set?

The "best" amount of time to rest between sets, like most things in bodybuilding, depends on what specific goal you're training for.

Fleck, S. Bridging the gap: interval training physiological basis. NSCA J. 5: 40, 57-62, 1983. http://journals.lww.com/nsca-scj/Citation/1983/10000/Interval__Physiological_basis_.8.aspx

Comment:

Basically at 30 seconds you're burning through your ATP-PC reserves and using some glycolytic metabolism to provide extra energy. The ATP-PC system takes around 90 seconds to get back to 90% power, IIRC. So the glycolytic system is supplementing it and allowing you to do work. Note you don't have full power using this system, which is why for pure strength training you take longer breaks. Here[3] is an article which goes in depth about the various metabolisms.

Strength is the ability to generate force against resistance, irrespective of the movement produced by doing so.

It is currently fashionable to characterize certain types of training as "functional" and other types of training as something else.

Power is force applied to a resistance that cause the object providing the resistance to accelerate. Force applied to a stationary force plate is a measurably quantity, but not power.

In the weight room, if the weight on the bar stays the same, the faster the bar moves, the more power that has been applied to it. If the weight gets lighter, it's obviously easier to move faster, so power would depend on how much faster it gets moved. As the weight decreases, power actually goes down in humans, due to the inability of a human to continue to make it go faster and faster the lighter it gets. Same with a heavier weight, but as the weight increases to the power where it's too heavy to lift at all, power decreases all the way to zero, since movement is required power. At 1RM, force is very high while power is very very low. Powerlifting really is misnamed.

In all of sport, the highest power outputs ever measured occur during the second pull of the snatch.

Strength contributes to power by providing the force involved in the acceleration. Strength improvement will improve power, although there are other facts involved that depends on the nervous system of the individual.

The squat, press, deadlift and bench press incorporate the isometric and dynamic components of the quick lifts -- the snatch and the clean and jerk -- because they are multijoint movements that involve lots of muscles doing lots of things during the movement. The slow lifts can all be done fast themselves and can therefore be used to develop power as well as strength. In contrast, the quick lifts cannot be done slow, and are always used to train power.

The media have managed to equate fitness with aerobic exercise. The cruel fact is that strength training contributes mightily to endurance/aerobic training, and endurance training contributes essentially nothing to strength training.

Increased strength reduces the fraction of one's strength used during aerobic activity to pedal or run.

Although squats and all other slow lifts are dependent upon the phosphocreative/gylcolitic energy regime, they have the ability to positively influence activities that primarily oxidative in nature.

Aerobic training produces endurance adaptations at the cellular level, changes that are actually detrimental to strenght.

Why do we squat, press and deadlift? Because they work all the muscles and joints in the body, they simulate normal human movement patterns, and they produce strength appropriate to all uses for which the muscles and joints will be put. They can be trained fast or slow, done with a minimum of equipment, and form important components of the quick lifts. They are very hard; they produce psychological toughness when done correctly.

The bench press is inferior to the press as an overall exercise, but it does allow for the development of greater upper body strength than the press since the position on the bench is supported.

THE SQUAT

The squat is the way that evolution has adapted the bipedal human body to lower itself to the ground. It is the position in which half the population of South Asia spend the afternoon.

The squat produces bigger muscles, better nervous control over those bigger muscles, denser bones, tougher tendons and ligaments, the cardiac and pulmonary capacity to function under the circumstance of loaded squatting, and the psychological skills necessary to do them. Deadlifts come close, but don't quite stimulate the systemic response that deep squats produce possibly because the range of motion is not as great, or possibly because their lack of strecth-reflex activation outs out a key component of the stress.

Some people will will take a stance that is too narrow, and will need to be wider than they want to be. This stance is the best for allowing the hips to do their job of lowering and raising; it is not designed to isolate anything but rather to distribute the force evenly between the hips and knees so that everything contributes its anatomically predetermined share of the work to the job.

... Come out of the bottom position and pay attention to what you don the way up. The trick is to keep the chest up while this happens. Keeping the ches tup and lifting the chest are two different things. The former involves maintaining the angle and position of the back while hip drive occurs, while the latter involves changing that angle and position. Attempting to increase the angle of the back by lifting the chest while coming up will you forward, off your heels on to your toes and kill your hip drives, in addition to exposing your spine to changing leverages under load as its angle increases. The back will become vertical when it is supposed to at the end of the movement;

Any forward knee movement will diminish hamstring tension and make the stretch-reflex enchanced hamstring contraction much less powerful. If the heels are not planted firmly, some of the force geneated against the tibia gets absord as the heels get pushed down instead of pulling the pelvis into extension. In the squat, the tibia is the anchor for the hamstring and it can't anchor anything if it's distal end at the heel is quash shy.

THE BENCH PRESS


Your muscle cells contract via units called sarcomeres, made up of the proteins myosin and actin. Myosin fibers bind to the actin and cause the sarcomeres to contract when calcium is introduced into the unit. ATP is a fun little energy molecule and it is required for the myosin heads to release actin, allowing the muscles to relax. When someone dies, the body can no longer produce ATP and, additionally, calcium floods into the sarcomere due to cellular breakdown. So, after death, calcium triggers the contraction of sarcomeres and thus muscles, and there is no more ATP to separate the myosin/actin and allow them to relax. This effect is temporary because as your cells die/decay, proteins (such as myosin/actin) are broken down.


Being injury free and being consistent are the two biggest keys to long term success.

Focus on BRO EXCERSISES every once and a while. You know... atleast make it look like you workout. Leg Press Bicep Curl - You're arms will thank you in the long run Tricep Pulls

I wish I had started by building a bigger and wider base by keeping intensity low and exercise selection high, instead of diving in to high intensity, low volume and high specificity programs. Sure I wouldn't have gotten as strong in my first 3 months, but id sure as shit be a lot stronger and less beat up now.


More motor unit brain rallies to achieve task. Arm muscles won't be strong enough; appeals to other muscles. Leveraged resources you already have, other muscles. Muscle fibers during stress expose microscopic damage. In response, injured cells release ctyokines, inflammatory molecules, that active immunse system to repair injury. The greater the damage, the more your body will need to repair itself. The cycle eventallly makes muscle bigger and stronger. Body has already adapted to everyday activities and don't generate stress.

Cells need to be expose to higher workloads than they are used. If you don't continusoly expose them to resistance, they will shrink (atrophy).

Exposing muscle to high degree of tension while muscle is lengthening generates codnition for new growth. Muscles relies on more than activity to growth: hormones and rest. Protien preserves muscle mass in the form of amino acids. This repair process mainly occurs while sleeping. Gender and age and genetics affect this.


For the last 6 months or so I have been focusing on nothing but losing the belly fat and getting six pack abs. At first I also thought that if I reduced calories my muscle mass would waste away, but after quite a bit of research found this was not really the case.

The trick comes in not really focusing on the calories but instead on the types of food. If you determined that your resting metabolic rate was say 2000 calories (i.e you needed to take in in 2000 calories just to maintain your weight), then to lose weight you'd need to reduce your intake to just 1800 calories (or expend more energy through exercise so that you're using say 2200 calories).

Now, if that 1800 calories came from only sugary/refined foods, then your body would lack essential nutrients and basically start feeding on itself to get those nutrients. If however, those 1800 calories came from high quality 'whole' protein sources, then the body would have the essential nutrients it needs to maintain and even build muscle while at the same time burning fat for energy.

My advise to you would be to find out what exactly your metabolic type is (simply do a google search) and eat the right foods (in the right amounts) for your type. Complement this with strength training i.e squats, deadlifts and bench presses together with high intensity interval training i.e alternating between sprinting and jogging. This will give you firm muscle tone while at the same time burning away that belly fat.


Adding fibres. i.e. adding cells is hyperplasia and it's currently unknown if this occurs naturally in adult humans. Most visible growth can be attributed to hypertrophy, where the cells grow bigger.


Eugen Sandow was a German bodybuilder. He is an example of what bodybuilding looks like before the availability of steroids.