ATP - Adenosine Tri-Phosphoric acid[edit | edit code]
ATP formula
ATP
(adenosine triphosphate: adenine bound to three phosphate groups) is a molecule that serves as a source of energy for all processes in the body, including movement. Contraction of the muscle fiber occurs with the simultaneous breakdown of the ATP molecule, resulting in the release of energy that is used to carry out the contraction. In the body, ATP is synthesized from inosine.
ATP must go through several steps to give us energy. First, using a special coenzyme, one of the three phosphates (each of which provides ten calories) is separated, releasing energy and producing adenosine diphosphate (ADP). If more energy is required, the next phosphate is separated, forming adenosine monophosphate (AMP). The main source for the production of ATP is glucose, which in the cell is initially broken down into pyruvate and cytosol.
During rest, the reverse reaction occurs - with the help of ADP, phosphagen and glycogen, the phosphate group reattaches to the molecule, forming ATP. For these purposes, glucose is taken from glycogen reserves. The newly created ATP is ready for its next use. In essence, ATP works like a molecular battery, storing energy when it is not needed and releasing it when it is needed.
ATP structure[edit | edit code]
The ATP molecule consists of three components:
1. Ribose (the same five-carbon sugar that forms the backbone of DNA) 2. Adenine (connected carbon and nitrogen atoms) 3. Triphosphate
The ribose molecule is located in the center of the ATP molecule, the edge of which serves as a base for adenosine. A chain of three phosphates is located on the other side of the ribose molecule. ATP saturates the long, thin fibers containing a protein called myosin, which forms the basis of our muscle cells.
Indications for use of the drug Atf-long
The drug is prescribed in complex treatment:
- IHD, unstable angina, resting and exertional angina;
- post-infarction and myocardial cardiosclerosis; (diffuse and focal cardiosclerosis);
- paroxysmal supraventricular and supraventricular tachycardia and other rhythm disturbances;
- vegetative-vascular dystonia;
- myocardial dystrophy;
- chronic fatigue syndrome;
- hyperuricemia of various origins;
- myocarditis;
- in order to increase tolerance to physical activity.
ATP systems[edit | edit code]
Consistent activation of energy systems during exercise
ATP reserves are sufficient only for the first 2-3 seconds of physical activity, but muscles can only work if ATP is available. For this, there are special systems that constantly synthesize new ATP molecules; they turn on depending on the duration of the load (see figure). These are three main biochemical systems:
1. Phosphagen system (Creatine phosphate) 2. Glycogen and lactic acid system 3. Aerobic respiration
Phosphagen system[edit | edit code]
When the muscles undergo short but intense activity (approximately 8-10 seconds), the phosphagen system is used - ADP combines with creatine phosphate. The phosphagen system ensures that small amounts of ATP are constantly circulating in our muscle cells. Muscle cells also contain a high-energy phosphate, creatine phosphate, which is used to restore ATP levels after short, high-intensity work. The enzyme creatine kinase takes the phosphate group from creatine phosphate and quickly transfers it to ADP to form ATP. So, the muscle cell converts ATP to ADP, and phosphagen quickly reduces ADP to ATP. Creatine phosphate levels begin to decline after just 10 seconds of high-intensity activity. An example of the use of the phosphagen energy system is the 100-meter sprint.
Glycogen and lactic acid system[edit | edit code]
The glycogen-lactic acid system supplies energy to the body more slowly than the phosphagen system and provides enough ATP for about 90 seconds of high-intensity activity. During the process, lactic acid is formed from glucose in muscle cells as a result of anaerobic metabolism.
Given the fact that in the anaerobic state the body does not use oxygen, this system provides short-term energy without activating the cardiorespiratory system in the same way as the aerobic system, but with saving time. Moreover, when muscles work quickly in anaerobic mode, they contract very powerfully, cutting off the supply of oxygen, as the vessels are compressed. This system can also be called anaerobic-respiratory, and a good example of how the body works in this mode is the 400-meter sprint. Typically, athletes are prevented from continuing to work in this manner by muscle soreness resulting from the accumulation of lactic acid in the tissues.
Aerobic respiration[edit | edit code]
If the exercise lasts more than two minutes, the aerobic system comes into play, and the muscles receive ATP first from carbohydrates, then from fats and finally from amino acids (proteins). Protein is used for energy mainly in conditions of hunger (diet in some cases). Aerobic respiration produces the slowest amount of ATP, but produces enough energy to sustain physical activity for several hours. This occurs because glucose breaks down into carbon dioxide and water freely, without being counteracted by, for example, lactic acid, as is the case in anaerobic work.
ATP is the main energy sponsor of the cell. Or where to get energy? Mitochondrial dysfunction.
Murzaeva Irina Yurievna
Endocrinologist, Preventive Medicine Doctor
October 1, 2018
Today we are introducing ourselves into scientific research. The article will be difficult to read. I simplified the material as much as possible, but it couldn’t be simpler. As always, I was “inspired” to write by everyone’s endless complaint - “weakness, nothing helps, your IVs and pills lasted for 2 weeks...”. Today we will consider the most difficult case of Energy deficiency - Mitochondrial dysfunction . This is still a little-studied and complex part of medical science. Mitochondrial dysfunction can be congenital and, in our case (the case under consideration), acquired.
Energy in our body is presented in the following form - the ATP molecule.
ATP-adenosine triphosphate is the main source of energy for cells in particular and the body as a whole. It is an adenosine ester (purine). In addition, it is a source of synthesis of nucleic acids for the formation of DNA structure! (our genetic code) and an intermediary of the transmission of a hormonal signal into the cell! Conclusion: lack of ATP is fraught with perversion/lack of hormonal response and more. ATP is formed in mitochondria (these are small structural components of any cell, the mitochondrion has its own DNA!, like the cell nucleus!!, it is a highly organized structure). That is why diseases with impaired ATP synthesis are called mitochondrial dysfunction.
The body produces 40 kg of ATP per day. Organs with maximum ATP production: brain 22%, liver 22%, muscles 22%, heart 9%, adipose tissue only 4%, note that the thyroid gland is not even included in this list... The brain and liver are leaders!
Now about the process of energy formation itself . Let's look at the picture.
The process of energy generation can be divided into 3 stages.
Stage 1 is the production of simpler molecules (in the energy production cycle) from carbohydrates (U), fats (F) and food proteins (B). Carbohydrates are broken down into monosaccharides (glucose, fructose), fats into fatty acids, proteins into amino acids. “Splitting” of B, F, U occurs both in an oxygen environment (aerobic) and in an oxygen-free (anaerobic) environment. This is extremely important! Since from anaerobic glycolysis of 1 molecule of glucose - 2 molecules of ATP are formed, from aerobic (oxygen) glycolysis of 1 molecule of glucose - 36 molecules of ATP are formed, from aerobic oxidation of 1 molecule of fatty acid - 146 molecules of ATP, (fats and proteins in an oxygen-free environment do not are broken down!, conclusion - for example, with untreated anemia (O2 deficiency), weight loss is almost impossible). So, the absorption of 1 molecule of glucose requires 6 molecules of O2, and 1 molecule of fatty acids requires 23 molecules of O2. Conclusion - fats are the main source of energy, and everyone needs O2!!!
Stage 2 - formed from all molecules U, F, B - AcetylCoA - intermediate metabolite . The essence of this stage is that the amount of AcetylCoA produced depends on the level of many vitamins and microelements (vitamin C, group B, zinc, copper, iron, etc.). Why is it so important for energy production to replenish the deficiency of these elements!
Stage 3 - this same AcetylCoA enters 2 main biochemical pathways for the production of ATP - this is the Krebs cycle (citric acid) and the oxidative phosphorylation cycle (electron transfer, “respiratory chain”;), NAD- and NADH+ are formed. The connection between these two waste cycles is “a bottleneck”, a “weak spot” in the formation of ATP. And it depends on the pH of the cell environment - with the development of cellular hypoxia = cellular acidosis and the process of ATP formation worsens - the body drowns in excess NADH, and NADH is associated with “oxygen leakage from the cell” (I will not decipher the mechanism) and the formation of active ( aggressive) forms of oxygen (free radicals) - and these are damaging agents for cells when formed in excess.
Metabolic acidosis is a consequence of primary O2 deficiency in the body (acidosis itself becomes the cause of secondary O2 deficiency - oxygen leakage). Acidosis is expressed by the accumulation of an intermediate metabolic product - lactate, an excess of H+ (hydrogen ion), mitochondria “begin to suffocate and grow old and die”! And with the aging of mitochondria, the body ages, which is why some diseases become so younger - atherosclerosis, Alzheimer's disease, diabetes mellitus (yes, this is a mitochondrial disease), cancer, arterial hypertension, AIT, chronic fatigue syndrome, even UC and Crohn's disease (as one of the theories), etc.
How does the citric acid cycle (Krebs cycle), for example, relate to obesity? - active intake of fatty acids from food leads to depletion of carnitine transport (everyone knows for comparison Carnitine for sports nutrition) systems (fatty acid transporters, there are few of them anyway) and a decrease in the activity of the “respiratory chain”, tissue sensitivity to insulin decreases - The well-known insulin resistance develops! The outcome is metabolic sadness - metabolic syndrome.
Accordingly: the reasons for the decrease in ATP synthesis are, first of all, O2 deficiency ! (as happens in big cities, where there is little greenery!!, gas pollution - the product of gasoline combustion is not O2, but CO2!!!!, people do not leave the premises, move little - “small vessels are closed to access of O2”, the causes may be respiratory diseases and cardiovascular pathologies), acidosis = “acidification of the body” (accumulation of lactate, excess H+), polydeficiency of vitamins and microelements to improve the absorption of fat, vitamins, and uranium. To treat O2 deficiency, a device was even invented - based on interval hypoxic training. This is a new era in the treatment of many pathologies.
How to suspect mitochondrial problems? They are difficult both to understand and to diagnose.
Among the “simple tests” that can be collected by any laboratory - a decrease in blood pH, O2, an increase in: lactate, CRP, fibrinogen, cholesterol, LDL, triglycerides, homocysteine, uric acid (clinically - increased blood pressure, increased heart rate at rest, shortness of breath at rest), decrease in ferritin, from rare cases - decrease in glutathione, blood vitamins, decrease in Q10, disturbance in the antioxidant system (in the blood).
Among the rarer, but still available tests (more specific) are organic acids in urine (thanks to this analysis, you can determine approximately at what level the disorder is occurring and how to correct it). If the pathology is so difficult to detect, “how to treat it?”, ask You
It is possible to treat.
First of all, we change our lifestyle - improve the delivery of O2!, quit smoking! we breathe more often in the park and not only.. We treat and put into remission chronic respiratory diseases, replenish the deficiency of vitamins and minerals!, add antioxidants, vascular drugs (!) it is very important to improve the cows (weakness is always accompanied by absent-mindedness, decreased memory and attention - that’s right , maximum vascular network in the brain!!), less often we add “energy drinks” - succinic acid, Q10, carnitine, NADH, etc. I’m not talking here about congenital mitochondrial dysfunctions - this is a consequence of a genetic breakdown, and we are now talking more about acquired causes . We will wait for new scientific materials on this topic...
Special instructions for the use of the drug Atf-long
When AV blockade is combined with other rhythm disturbances, the drug is not prescribed. With prolonged use of ATP-Long, it is necessary to monitor the level of potassium and magnesium in the blood. It is undesirable to use in cases of severe arterial hypotension. Prescribe with caution if you are prone to bronchospasms. ATP-Long should not be used simultaneously with cardiac glycosides due to the increased risk of AV block. Please note that the tablets contain small amounts of sucrose and lactose. During treatment with ATP-Long, it is necessary to limit the consumption of products containing caffeine (coffee, tea, cola drinks). Use during pregnancy and lactation. There are no clinical data on the safety and effectiveness of the drug during pregnancy and lactation, therefore its use by women during pregnancy is contraindicated. If it is necessary to use the drug during breastfeeding, breastfeeding should be stopped for the period of treatment. Children . Not used to treat children. The ability to influence the reaction rate when driving a vehicle or working with other mechanisms. There is no data on the ability of the drug ATP-Long to influence the reaction rate when driving vehicles or other mechanisms.
Interactions of the drug Atf-long
ATP-Long cannot be used simultaneously with cardiac glycosides due to the increased risk of AV block. When used simultaneously with potassium-sparing diuretics, potassium preparations and ACE inhibitors, the risk of developing hyperkalemia increases, and with Magnerot and other magnesium preparations - hypermagnesemia. Dipyridamole enhances the therapeutic effect of the drug ATP-Long, and xanthinol nicotinate, caffeine, theophylline, aminophylline reduce it. ATP-Long can enhance the antianginal effect of β-adrenergic receptor blockers and nitrates.
