Creatine kinase high,muscle exercises you can do at home videos,what is the best pre and post workout supplement,pre workout nutrition label worksheet - Good Point

admin | Diet Pills | 19.02.2016
Most students have covered some aspects of muscle contraction in their school biology course, but to varying extents.
Voluntary, skeletal muscles show a repeating, striated pattern under the light microscope and the principal features were named for their optical properties: the "I" bands (for isotropic) have almost the same refractive index in all directions, but "A" bands (for anisotropic) have different refractive indices along and across the fibres. The "A" bands maintain a constant length, but the "I" bands vary in size as the muscle changes length. The "A" bands contains thick filaments composed mainly of the protein myosin, while the "I" band contains thin filaments that are rich in the common cytoskeletal protein actin. Individual myosin molecules resemble two-headed tadpoles: two catalytically active head groups are attached to a long, largely helical tail. All the muscles in the human body show biochemical specialisation which allows them to perform their particular physiological functions. Muscles use a wide variety of fuels, although most muscles have preferred sources of energy. Muscle metabolism accelerates by several orders of magnitude when switching from the resting to the active state. ATP is worth more in the cytosol than it is in the mitochondria, and delivers a bigger bang per molecule.
There is a problem getting "used" ADP back from the myofibrils fast enough without spoiling the high ATP:ADP. The resting concentration of 5'-AMP in the tissues is extremely low, making it an excellent signalling molecule. Creatine is a normal constituent of meat, because domestic animals face exactly the same metabolic challenges that we do. The free cytosolic ADP concentration is normally very low in resting muscle, because ADP is actively taken up by mitochondria in exchange for ATP.
Linear 5' AMP (not 3'5' cyclic AMP) is a major allosteric activator for glycogen phosphorylase and phosphofructokinase, and is also the immediate precursor for the local hormone adenosine, a powerful vasodilator which increases blood flow to rapidly metabolising tissues. Linear 5' AMP is an activator for AMP-activated protein kinase [AMPK] which stimulates glucose uptake by skeletal muscle during exercise and under conditions of metabolic stress. The purine nucleotide cycle is an unusual feature of skeletal muscle, which serves to replenish TCA cycle and glycolytic intermediates when the energy demand is high.
NADH is used by the respiratory chain to generate ATP, but the NADH concentration remains high.
Although oxidative phosphorylation in mitochondria accounts for the bulk of muscular ATP generation, some fibres can generate additional ATP from anaerobic glycolysis from glycogen into lactate.
The Cori cycle poses some interesting regulatory problems, because it requires glycolysis to be activated in exercising muscle, whereas the opposite process, gluconeogenesis, is activated in the liver. In resting cells these interlocking "futile" cycles continue to operate at a slow rate, "wasting" a tolerably small amount of ATP, and basically going nowhere. In all tissues, any threat to the cellular energy supply promptly raises linear 5' AMP and directly switches on glycolysis using phosphofructokinase 1 (PFK1).
This important mitochondrial enzyme is the final "committed" step at the end of the glycolytic pathway. Voluntary muscles contain a variety of fibre types which are specialised for particular tasks. Type 1 or slow oxidative fibres have a slow contraction speed and a low myosin ATPase activity.
These differences are nicely illustrated by the serial sections from rat diaphragm published by Gauthier and Lowey (1979) J. In cardiac muscle and some types of smooth muscle the cells are in electrical contact through communicating gap junctions.
Catecholamine hormones such as adrenalin are released during frightening or stressful situations. Contraction in cardiac muscle is triggered by a wave of membrane depolarisation which spreads from neighbouring cells.
The sodium channel undergoes a second conformational change, as a result of which these channels close spontaneously after a few milliseconds in all excitable tissues. The sodium pump (1) is activated by phosphorylation, which allows it to handle the increased ion traffic across the sarcolemma when cardiac work output rises.
A small protein called phospholamban associated with the sarcoplasmic reticulum calcium pump (9) is phosphorylated, and this accelerates calcium uptake by the S.R. The enzymes triglyceride lipase (14) and glycogen phosphorylase (15) are activated by phosphorylation.
The system(s) which terminate CICR are far from clear, There must be some mechanism, since otherwise rising cytosolic calcium would lock the S.R. The repeated entry of external calcium ions during the plateau phase of each cardiac action potential requires a cardio-specific calcium export system to stabilise the internal calcium concentration. Cardiac muscle contracts quite slowly, but it is used continuously and the total energy consumption is high. Each thick filament contains about 250 myosin molecules, with the tails wrapped together along the shaft of the thick filament. Myosin head groups attach temporarily to the actin, after which a conformational change in the myosin drags the filaments in opposite directions.
The eyeballs are steered by extra-ocular muscles when reading: they must contract quickly and precisely, but the muscles in your back and buttocks evolved for continuous heavy lifting where fuel economy is important.
Each fibre is an enormous, multi-nucleate cell, formed by fusing hundreds of myoblasts end-to-end. There are considerable species and anatomical differences, and variations between adjacent cells. In resting muscle, where ATP turnover is very slow, the mitochondria do not use very much oxygen. Many athletes consume additional creatine as a legal dietary supplement, hoping to enhance their muscle performance. The corresponding AMP concentration is vanishingly small, but it rises very rapidly on exercise, as soon as the ADP concentration starts to increase.
AMP is deaminated to yield inosine monophosphate (IMP) which is converted to adenylosuccinate and then back to AMP. You might remember that ammonia is produced by exercising muscles, and has been measured in the sweat of high-class rugby players after an important match.
Both are normally oxidised to carbon dioxide and water, although there is a small contribution from anaerobic glycolysis as described below.
This process is very much less efficient than mitochondrial ATP synthesis, but is important for sprinters and for all competitors in "explosive" athletic events, such as jumps and shot put.
The reduces the concentration of fructose-2,6-bisphosphate, which change inhibits PFK1 and switches on the gluconeogenic pathway via fructose-1,6-bisphosphatase. Moreover, the activity of fructose-1,6-bisphosphatase is much lower in muscle than it is in liver, so muscle can really only do glycolysis, and its capacity for gluconeogenesis is severely limited.
Up to this point it is always possible to get back to glucose, but once through PDH there is no return. This allows fatty acids (which generate ATP, Acetyl CoA and NADH) to inhibit PDH and block the oxidation of carbohydrates when adequate fat supplies are available. Fats are an efficient store of energy, which are much less trouble to carry around than the equivalent quantity of carbohydrate. It is mobilised by adrenalin and glucagon, signalling via calcium ions and 3'5' cyclic AMP, but the total reserve is only sufficient for a few hours use. Also, training (and especially running) makes people feel good, and reduces their chance of suffering a heart attack. It also regulates muscle growth in adults by inhibiting the transformation of stem cells into mature muscle.


It used to be considered a "pro-inflammatory" cytokine that controlled the early "acute phase" response to infection. These cells are specialised for steady, continuous activity and are highly resistant to fatigue.
They are built for aerobic metabolism and can use either glucose or fats as a source of energy.
They have nicotinic acetylcholine receptors, which are ligand-gated sodium channels concentrated in a specialised region of the muscle sarcolemma beneath the axon terminus.
They increase the force and frequency of cardiac contractions by binding to Beta-1 receptors, which are protein molecules protruding from the outer face of the cardiac sarcolemma. Depending on the type of smooth muscle, catecholamines may produce either contraction (alpha receptors linked to intracellular calcium stores), or relaxation (beta receptors linked to adenyl cyclase). In cardiac muscle, but NOT skeletal muscle, slower voltage-gated calcium channels, probably identical with dihydropyridine receptors (5) take over and maintain a positive inward current for several hundred milliseconds (in human ventricle) during the plateau phase of the cardiac action potential.
This allows flexible head groups from the protein myosin in the thick filaments (8) to interact with the protein actin in the thin filaments. Adenyl cyclase manufactures 3'5' cyclic AMP, which is continuously destroyed by a phosphodiesterase enzyme.
Cardiac and skeletal ryanodine receptors probably differ in their precise intracellular location. The transmembrane protein triadin might provide a link to either measure or modulate calcium binding to the low-affinity binding protein calsequestrin in the lumen of the S.R.
This is achieved by the electrical exchange of one intracellular Ca++ ion for three extracellular Na+ ions in cardiac muscle. This specifically increases the force of cardiac (but not skeletal muscle) contraction by interfering with the cardiac Ca++ export system. Fuel economy is very important, not only for minimising food requirements, but also for reducing unwanted heat production.
It is totally specialised for energy production, and achieves the highest sustained metabolic rates (and the highest arterio-venous oxygen extractions) of any tissue in the body. These tissues are degraded in an orderly fashion, and release mainly alanine and glutamine into the blood. If this material is completely unfamiliar then you must study the muscle chapters in a basic biochemistry or physiology textbook, to ensure that you are up to speed with the other members of the class. In relaxed muscles the sarcomeres are about 2 microns long, but some of the bands move closer together as the muscle shortens.
Sarcomeres are symmetrical structures, and many thousands are aligned end to end along the length of the muscle. The head groups are exposed on the surface, where they can interact with actin in the thin filaments in the presence of calcium ions released from the sarcoplasmic reticulum. Binding a fresh molecule of ATP releases the myosin from the actin, so that the cycle can be repeated many times during a single muscle twitch.
They show a striated pattern, reflecting the regular arrangement of sarcomeres within each cell. Smooth muscle is found in the blood vessels, gut, skin, eye pupils, urinary and reproductive tracts. These mechanisms are essential for survival: if they were not present then large amounts of food energy would be wasted, animals would over-heat, and the heart could not pump sufficient blood to fully perfuse every muscle capillary bed at maximal rates. Vertebrate blood flow is regulated by oxygen demand to supply just enough oxygen to meet each cell's needs, with hardly any left over to damage the fabric of the muscle.
The pre-capillary sphincters contract, and blood flow shuts down to a basal level that supplies just sufficient oxygen for cellular needs. At the same time, ADP is actively taken up by the mitochondria, keeping the cytosolic [ADP] very low. ATP is normally present in large amounts, and subcellular diffusion of ATP is not an issue, but there is a serious problem "recycling the empties" quickly enough because the intracellular concentration of ADP is (and must be) very low.
This means that (at normal cellular energy levels) the ratio between creatine and creatine phosphate is nearly 1:1 so that there are plenty of empty bottles (creatine) to bring the "spent" ATP back from the myofibrils, without needing to transport any ADP.
However, there is normally plenty of creatine around anyway, and it is far from clear that this supplementation does any good. This makes cytosolic 5' AMP an exquisitely sensitive indicator of the cellular energy supply in all types of muscle, and indeed in all other tissues as well. Try not to confuse AMPK with protein kinase A (which responds to 3'5' cyclic AMP) since their functions are entirely different.
The net effect is an AMP-dependent conversion of aspartate to fumarate and ammonia whenever the mechanical work load increases. Fats are the most economical fuel source, but limitations on fat delivery rates means that carbohydrates must be used at higher work outputs. Most muscles cannot process the resulting lactate, which must be returned to the liver where it is recycled into glucose.
Conversely, when [ATP] is high and there are adequate levels of TCA cycle intermediates, a rise in [citrate] switches glycolysis off again.
These adaptations allow adrenalin to drive glucose production in the liver, without compromising the ability of skeletal muscle to break down glucose during exercise.
Nevertheless the enzyme is always available to meet a sudden increase in metabolic demand, which is often signalled by a sharp rise in the intracellular calcium concentration.
Unfortunately fats do not easily cross the blood-brain barrier, and can only be delivered to muscle tissues at a limited rate.
Some plants store oils in their seeds or in their fruit, but store carbohydrate in their roots and tubers. Adipocytes provide the major energy store in humans, but muscle proteins are also degraded when food intake is inadequate.
In practice food withdrawal may not be complete, and reduced physical activity lowers the fasting energy requirements.
The explanation for both effects probably involves cytokines - small protein hormones produced by most cells, including muscle, that affect other tissues in the body.
Muscle myostatin gene expression is transiently reduced by resistance training, permitting an increase in muscle mass, but myostatin production subsequently recovers so there is a limit to the growth than can be achieved.
Nowadays it is seen to have a more subtle role, modulating the immune response, and preventing over-reaction by the immune system.
The pattern of gene expression within each voluntary muscle cell is governed by the firing pattern of its single motor neurone.
These are general purpose muscle fibres which give the edge in athletic performance, but they are more expensive to operate than type 1. In the figure above, the left hand section was stained for the mitochondrial enzyme succinate dehydrogenase, the centre panel shows direct immunofluorescence against "fast" type myosin, and the right hand section was stained for alkali-stable ATPase activity (i.e.
These ion channels respond to acetylcholine (secreted from the nerve) by depolarising the muscle sarcolemma near the motor end plate. This starts with the spontaneous depolarisation of the specialised pacemaker cells in the sino-atrial node, spreads via the atria to the atrio-ventricular node and thence to the conducting fibres in the Bundle of His (in the intraventricular septum) and the Purkinje system. These activate G-proteins within the membrane, which in turn activate the enzyme adenyl cyclase on the inner face of the sarcolemma. This relaxation is apparently mediated by the cyclic AMP-dependent phosphorylation and inactivation of the enzyme myosin light chain kinase, which plays a central role in smooth muscle contraction.
The cell membrane (sarcolemma) is usually more permeable to potassium ions than to sodium ions, and this gives rise to a membrane potential of about 80mV (inside negative) in relaxed muscle. As in nerves and skeletal muscle, the membrane potential in cardiac muscle is eventually restored to its resting value by a delayed efflux of positive potassium ions from the cells.
About 10% of the calcium needed to activate cardiac contraction enters during each beat from the ECF.


A change in myosin conformation causes the thick and thin filaments to slide against each other and hydrolyse ATP, which provides the energy for contraction. The steady-state concentration of cyclic AMP depends on the balance between synthesis and degradation.
They eventually increase the supply of ATP and provide the energy for the anticipated extra work. The different skeletal muscle fibre types are described above: in general the routine tasks are handled by slowly contracting, economical fibres with an fat-based aerobic metabolism, and the more expensive high-speed fibres using carbohydrate fuels are only recruited when the occasion demands. These amino acids help to maintain blood glucose during fasting through gluconeogenesis in liver, kidney and gut. Three cytoplasmic isoenzymes have been identified in human tissues: the MM type from SKELETAL MUSCLE, the MB type from myocardial tissue and the BB type from nervous tissue as well as a mitochondrial isoenzyme. They differ substantially in subcellular structure from vertebrate muscles, they have a different system for oxygen and substrate delivery and a different energy-yielding metabolism. The system only works because of highly selective delivery of resources exactly where they are needed. This restriction may limit the availability of substrates other than oxygen (for example, glucose and free fatty acids) to the muscle tissue.
AMPK protects cells from stresses causing ATP depletion by switching off ATP-consuming biosynthetic pathways, whereas PKA is part of a hormonal second messenger system, and is discussed in relation to the Cori cycle below. The process can be used repeatedly because the aspartate pool is many times larger than the pool of TCA intermediates and is constantly replenished from the blood or the internal muscle protein stores. This circulation of glucose from liver to muscle with lactate moving in the reverse direction, is known as the Cori cycle after the young husband and wife team who first discovered it over eighty years ago.
It is therefore necessary to maintain a residual carbohydrate supply so that the brain can continue to function, and muscles can cope with a maximal energy demand. Most amino acids [except for leucine and lysine] are glycogenic: their carbon skeletons can be converted (at least partially) into glucose via Krebs cycle intermediates.
Human beings have evolved to withstand a bad winter in a primitive hunter-gatherer society.
Large muscles might seem attractive, but there is good evidence that the amount of muscle on a "normal" animal is almost ideal, and that increases in muscle mass lead to reductions in overall biological fitness. Recent work has shown that skeletal muscle is a major source of IL6 and that exercise massively increases IL6 output. Motor neurones branch within their target muscle and thereby control several muscle fibres, called a motor unit.
These are large cells with a poor surface to volume ratio and their limited capillary supply slows the delivery of oxygen and removal of waste products.
The depolarisation triggers voltage-gated sodium channels which spread the excitation over the remainder of the cell. These cells finally activate the bulk of the ventricular muscle in the chamber walls, in each case through direct electrical contacts. Adenyl cyclase produces 3'5' cyclic AMP, which is an important second messenger controlling numerous intra-cellular activities.
Vascular smooth muscle redistributes the blood supply during exercise, and visceral smooth muscle empties the gut in stressful or frightening situations.
Calcium ions are also removed from the cytosol into the ECF by an ATP-driven calcium pump (2) in all tissues. Movement and ATP hydrolysis continue until the calcium ions are removed from the cytosol at the end of each contraction. They are also expressed in brain, egg cells and many other tissues, where they regulate calcium release from the smooth endoplasmic reticulum. Smooth muscle is particularly economical because it has a low myosin: actin ratio, a low ATPase activity and a much lower contraction speed. Skeletal muscles lack a urea cycle, but they are able to transaminate most amino acids and degrade their carbon skeletons as far as Krebs cycle intermediates, such as succinyl-CoA and fumarate. Insects also severely restrict oxygen delivery, using muscular sphincters at the openings of their respiratory trachea.
Fatty acids cannot be converted into glucose, but triglyceride droplets contain 6% by weight glycerol, which the liver converts into sugar phosphates. This may be important, because depression, type 2 diabetes and cardiovascular disease are now considered to have low-grade inflammatory components.
The high precision eye muscles have only a few fibres in each motor unit, but the muscles in your back have thousands. Notice the differences in the fibre diameters, which correlates with their requirements for efficient gas and substrate exchange. Cyclic AMP activates protein kinase A which phosphorylates many intracellular enzymes, temporarily modifying their properties. In contrast to all this, the force of contraction in voluntary muscle is unaffected by circulating hormones. The remainder is released from the sarcoplasmic reticulum through a channel known as the ryanodine receptor (6). Most of the calcium ions are returned to the sarcoplasmic reticulum by a calcium pump (9) but about 10% leave the cell via proteins (2) and (3) described above. This enzyme phosphorylates several of the proteins involved in the contraction process, and temporarily alters their properties until a protein phosphatase restores the status quo ante by removing the phosphate group.
It is ideal for sphincters and slow squeezes, and is used for these tasks in preference to striated fibres. There is a high capillary density and the cells are small, with a high surface to volume ratio. Surplus cycle intermediates are converted via an allosteric NAD-linked "malic" enzyme into pyruvate, which is transaminated to yield alanine.
People who take regular exercise may keep their immune systems in better balance, and thereby reduce their risk of mental illness and cardiovascular disease. Ryanodine receptors are widely distributed in the body, and are present in non-muscle tissues such as brain.
Calcium ions are stored within the sarcoplasmic reticulum loosely bound to a protein, calsequestrin (10). They are blocked by the important drugs verapamil and nifedipine, which reduce the force of cardiac contraction, while maintaining an adequate cardiac output by relaxing vascular smooth muscle and reducing the peripheral vascular resistance. The tissue is rich in myoglobin (for oxygen transport) and creatine + creatine phosphate (for energy transport). Some amino acids such as serine are deaminated to pyruvate and ammonia, which is de-toxified yielding glutamine. The calcium concentration inside resting cells is low, but rises sharply during contractions.
The organ shows a distinct preference for free fatty acids, ketone bodies and lactate; but requires insulin for efficient glucose uptake and utilisation. In this way surplus nitrogen is exported from the muscles to the liver, kidney and gut for further processing. The operation of the ryanodine receptor depends in a mysterious way on the flow of calcium ions through the dihydropyridine receptors in cardiac muscle, but not in other muscle types.



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