This tissue wraps-in and separates muscle fibres, acts as supporting material, and helps movements, protects muscles against shocks and too important tension.

Scientific name of the muscle fibre. Mutiplied thousands of times, it makes up the whole muscle. It is wrapped around by a protective girdle called conjunctive tissue. They are made of fibrils, constituted of thin threads themselves made of proteic molecules. Their size (at adult age) ranges from 10 to 100 angstrom in diameter ( with up to 20cm length). A the origin, during the very first stages of embryo development, muscle fibres develop out of undifferenciated cells calles myoblasts, which merge into one another. After birth these grow in size but not in number. There is a possibility to regenerate them after an injury, out of other undifferenciated cells called "satellite cells". Yet, generally speaking, if the loss of muscle fibre is too important, it is thanks to hypertrophia (increase in size) that compensation occurs.

This refers to the sub-partition of cells. It encloses and separates a volume from the cytoplasm. In certain types of muscle fibres, the endoplasmic reticulum of the "smooth" type used to store calcium is called "sarcoplasmic reticulum" (found in muscle cells). It is in charge of storing and releasing calcium.

They are parallel to one another, and laid in the same direction. A Myofibril is made of a succession of sarcomeres which are the minimal muscular contraction unit. These sarcomeres are laid in chains on the whole length of the fibre.

This refers to the volume situated between Myofibrils and the endoplasmic reticulum in which calcium is released by the sarcoplasmic reticulum wrapped around Myofibrils. Cytosol only contains soluble substances. Water amounts generally to around 85 % of cytosol contents. With its suspended macromolecules in a aqueux and salty environment, it has a viscosity four times more important than that of water and this corresponds to that of a celloïd gel.

Sarcoplasmic reticulum is the name given to the smooth endoplasmic reticulum found in striated skeletal muscle cells. This zone is a store of Ca2+ ions (hence is it called a "calciosome") which are released into the cytoplasm in reaction to a plasma membrane depolarisation, caused by the binding of ACh on muscle cells nicotinic receptors. This increase in cytoplasmic calcium enables the interaction between myosin and actin threads. Calcium is then pumped (thanks to a "pump" using ADP to operate) back to the sarcoplasmic reticulum.

These are organites in charge of breathing: filled with enzimes which transform sugar components and fat into ATP thanks to oxygene. They thus oxydate carbon and glucose to provide energy. It is at that level that carbon oxydation reactions occur which produce ATP. It is a that level that occurs glocose oxydation too. Glucose turns into tiny carbonate molecules called « pyruvate ». Pyruvate is then carried into the mitochondrion matrix, where it is gradually deprived of its carbon and hydrogene components to then create, among many other things, ATP and CO2.

This is the minimal unit involved in muscular contraction. There is not length modification involed during a contraction but a gliding of threads one along the other, which creates a general contraction. The sarcomere's length is reduced by a roughly 20% margin. The speed of contraction is 15 angstrom/second. The more a muscle is divided into sarcomeres, the more it will give the impression of shortening. During the shortening phase of each sarcomere there is no shortening of either thin or thick threads, but a gliding motion leading them to overlap one another. This could be compared to a rowboat. At the core of each sarcomere is found the myosin molecules, each surrounded on both sides by six actin molecules. The myosin molecule is going to connect to actin outstretching its "arms" and draw them inwards. At the very end of the sarcomère (on both sides) is an area called "Z Line" which enables actin molecules to connect, thus ensuring a connexion between each sarcomere with both the following and preceeding one.

The tip of myosin molecules moves forward on a distance approximatively corresponding to the diametre of the actin molecules thread. This bending is made possible by the hydrolysis of an ATP molecule which binds onto the tip of myosin. Each myosin molecule is endowed with a "tip" or "tail" running along its axis and fitted with two globular "heads" (crossbridges). Two globular heads are thus ready for bindings: one for the binding of ATP and the other for the binding onto actin. The crossbridge site is located on each side of the tip of each myosin molecule and draws actin molecules threads inward and rearward, thus shortening the whole sarcomere.

The actin molecule is a globular molecule which combines to others to make up a chain. This chain has a coiling pattern, and constitutes what is known as a "thin" thread. Each actin molecule owns a binding site for myosin. A thin thread owns thus many binding sites. An actin molecules thread homes two other ones: the tropomyosin molecule which coils around it (and, by doing so, physically inhibits the actin's binding sites) and troponin molecules (of globular shape) acing as connexion between actin and tropomyosin For muscle contraction to begin, the troponin molecule coiled around actin must move and thus drag the tropomyosin molecule away from the binding sites on which myosin will bind. For troponin molecules to move calcium has to fix itself onto them. When this is done, the overall shape of troponin molecules is modified and this one alters its position, hence dragging tropomyosin along, which in turns uninhibits the actin binding site, in turn enabling myosin to get in contact with it. When calcium leaves troponin molecules, they get back to their original location and "push" tropomyosin back in front of binding sites, and thus prevents muscular contraction to take place.

Globular in shape, it is both fixed to tropomyosin (coiled around actin, and right on its binding sites) and to actin. Troponin molecules function as ball-bearings bearing on a larger "cable" (tropomyosin" to make it move on actin. Tropomyosin is usually coiled over most of the actin's binding sites, thus making impossible any contact from myosin's crossbridging sites to actin, and thus preventing muscular contraction to occur. Troponin is thus the molecule which, thanks to its movements, indirectly uninhibits or inhibits the actin 's binding sites by altering the position of the coil of tropomyosin. We are here facing a proces similar to that of a latch. When a set of calcium ions fix themselves onto troponin the latter rotates (such as the cylinder of a lock) and this movement drags tropomyosin away (such as a latch that once kept the door closed), and then uninhibits the binding site for myosin's molecules' crossbridging.

This is a long coiled molecule acting as a muscular contraction lock. This molecule is coiled around the thin thread molecule, and is moved away by the motions of another molecule to which it is bound. Tropomyosin can also be considered as the biological equivalent of a plug-mask or a latch, or more simply, a bit of plastic put on a magnet to prevent connection.

This is the name given to the end part of myosin molecules, involved in a binding-deconnecting cycle with actin binding sites, leading to the shortening of sarcomeres and thus to the creation of power. This crossbridging site needs ATP to function, and uses it to find the energy required to move and fetch the actin 's binding site, then uses another ATP molecule again to unhook from it. This is what is known as the crossbridging cycle : the process is as follows: binding of myosin's crossbridging site onto actin's binding sites, rearward movement, unhooking of the crossbridging site, followed by a forward movement from it to fetch another actin's binding site, etc.

This is the area where connection between myosin's molecules' crossbridging sites and actin occurs. It is at that level that myosin binds to actin to then draw it rearward, thus shortening the sarcomere and creating a pull-force. These actin's binding sites are generally inhibited by a molecule called tropomyosin, coiled around actin, which makes muscular contraction impossible as long as it has not withdrawn.

This refers to the division of myofibre corresponding to the sarcomere.

This refers to the central zone of sarcomeres :This is the area where one can only find myosin, the area towards which actin threads will be drawn during muscular contraction. Each myosin molecule is surrounded by actin molecules, and when these are drawn inwards by the action of myosin this movement occurs in the direction of myosin's center, or "H-line".

This is the opposite zone to that of the "H-line", that is to say the area where only actin molecules are to be found, at the end of sarcomeres; it is at that level that inward movements begin.

This is the area between two sarcomeres : it is at that level that muscle stretching occurs. When a muscle stretches because of a weight beyond its contractile power, sarcomeres do not stretch, but the only "elastic" zone does, and it is that between them, called "Z-line".

Calcium is a fundamental ion for cell functionning. It is indirectly responsible for the "opening" of the actin molecules binding site, enabling myosin molecules to bind to them. This opening happens when calcium fixes itself onto troponin and, by doing so, alters its general shape, in turn forcing troponin to settle back, which in turn again trigers a change in tropomyosin molecules position, that previously inhibited that actin's binding site. Calcium is released from stores located around Myofibrils (sarcoplasmic reticulum). It gets fixed on troponin thanks to electrical phenomena.

Lactic acid is the by-product of muscle glycogene consumption. Glycolysis (sugar muscle consumption to create energy) can either be done in a sufficient/non-sufficient oxygene environment (aerobic/anaerobic environment). In the case of aerobic glycolysis this consumption of sugar occurs at the level of mythochondrions, which will completely consume lactic acid indirectly produced. In the case of an effort without enough oxygene provided, sugar consumption occurs into the cytoplasm and lactic acid can not be eliminated thanks to perspiration.

When an ATP molecule is hydrolysed (dissolved into water) it "breaks apart" into an ADP element on the one hand and into a Phophate element on the other hand, and releases energy. The coupling back of these two elements makes the regeneration of ATP possible, but it will require the same amount of energy to do so.

Molecule with very energetic atomic links. This is a very energetic phosphate compound. This molecule is used to produce energy. Its breaking up by water (hydrolysis) releases energy (around 30kj/mol), and its synthesis consumes the same amount of energy. ATP Hydrolysis gives an ADP molecule and a phosphate compound.

Neurotranmeter.

Action of water cutting molecules and releasing chemical energy (in the case of ATP hydrolysis). The basic idea is to disrupt molecules to release energy.

occurs when a compound such as ADP becomes ATP. This is the reverse phenomenum of hydrolysis. Energy is here used to merge instead of disrupting.

When ATP loses an electron, captured by another molecule.

Either loss of electrons (becomes positive) or electron addition (becomes negative).

Transmitting the message of Calcium release. These are nerve cells the axons of which divide into branches connecting to a maximum of myofibrils. The more axons within myofibres receiving calcium release messages, the more sarcomeres contractions will occur, and so the most powerful will contraction be.

This is the unprotected end of motor neuron (unprotected by any girdle), the one in charge of transmitting information via a neurotransmeter. As an electric cable, it corresponds to the end part, where the wires are left unprotected for connection.

The Motorneuron + myofibre unit is refered to as a « motor end plate ». This is the zone on which connection between the nervous system and the muscular system occurs. At the level of myofibres, in the groves of the plasma membrane surface (protecting Myofibrilles) we can find a « motor end plate » where motor axons bind. At the level of axons ends are vesicles releasing a neurotransmetter (Ach). When the action potential binds to the motor end plate it depolarises the plasma membrane thus opening the ducts releasing calcium. These ducts are said to be "potential-dependant", because they need an action potential to move. This calcium hence released will enable the release of a neurotransmetter called Ach binding onto the motor end plate and transmitting an action potential again. The motor end plate carries an enzyme (choline) which will use the connection to go up the axon end and be used to create another Ach. As a home electric connection, this would correspond to the electric "contact" parts.

This is the name given to the MotorNeuron--myofibre system: since each motor-neuron is connected to a muscle fibre, the complete muscular contraction is the fruit of the simultaneous action of these independant networks of connection: many motor-nerons will simultaneously stimulate the myofibre to which they are linked and the sum-total of these stimulation-contraction phases of each single motor-unit will create power. Compated to an internal combustion engine, the motor unit would roughly correspond to the combustion chambre - sparking plug unit; the sparking plug is the motor-neuron bringing up information, and the myofibre would be the combustion chamber where chemical reactions occurs, leading to the creation of power. The simultaneous involvement of each plug-chamber system (motor unit) creates our movements.

This is what is usually refered to as "nerve influx", which is in fact made up of a series of action potentials. This corresponds to a change in cell polarity. These are ions (potassium, sodium) which are at the origin of such electric potential difference between the inside and the outside of a cell. The action potential is made up of a series of events: first occurs a short-lived and local depolarisation, followed by an increase in internal membrane potential, and finally by a repolarisation of the internal membrane. An action potential lasts between 2 and 3 milliseconds.