Overview
Excretion
Bicarbonate is removed from the kidney using various transport mechanisms: Cl - dependent (AO1-3, or anion exchange), NA + - dependent (NBC1, 3, and 4 + NBC2 - this is a splice variant of NBC3; NDCBE1 and AE4) and SLC26A-dependent SLC26A4, PAT-1 / SLC26A6 and SLC26A7). AO receptors “change” bicarbonate to chloride in a 1: 1 ratio, while sodium (Na +) -dependent carriers transport bicarbonate through membranes by an electrogenic (NBC1, NBC4) or electro-neutral route (NBC3) in a ratio of 2 or 3: 1 ( bicarbonate: sodium). 6) SLC26A-class regulates Cl- / basic conversions, acting in some cases on bicarbonate. Most of these receptors are concentrated in the kidneys (NBC1, or kNBC1), mainly in the proximal tortuous renal tubule. The excretion of bicarbonate from the kidneys is regulated by various receptors, mainly with the involvement of ions, which either replace bicarbonate, or help transport it through membranes. In acute metabolic / respiratory alkalosis, as you know, the excretion of potassium from the body (which stops with acidosis) is accelerated, 7) moreover, excretion together with urine of sodium, potassium and chloride is interconnected (sodium promotes excretion of potassium, potassium-sodium, etc.). 8) According to clinical studies of the state of alkalosis in general, against this background, potassium excretion from the body (with urine) is intensified (over several days), which is directly associated with sodium loss. In a clinic, the elimination of potassium from the body along with urine can be triggered by the intake of sodium bicarbonate, and in a state of alkalosis, people lose a total of 300-500mEq potassium. Scientists have proven that oral administration of a standard dosage of sodium bicarbonate (300 mg / kg) causes the rapid elimination of a large amount of sodium together from the body (24 +/- 2% of an oral dose of sodium, or 82 mg / kg) for 210 minutes; the same is true for potassium bicarbonate, but to a lesser extent (although 26 +/- 5% of the potassium taken is also excreted in the urine). In healthy people, excretion of sodium bicarbonate from the kidneys practically does not affect calcium homeostasis in healthy people, while potassium bicarbonate contributes to a (insignificant) calcium retention in the body. 9) It is likely that increased excretion of bicarbonate from the body after taking it is due to the fact that sodium and bicarbonate transporters are paired with each other (since the for example of bicarbonate in the body is regulated, and the excess is immediately excreted along with urine, along with which about a quarter of the dose of sodium ) Rapid elimination of sodium from the body is usually accompanied by the same loss of potassium, but since potassium is not taken together with sodium bicarbonate (oral), it is not a fact that the abuse of sodium bicarbonate in the background of a diet low in potassium increases the risk of developing potassium deficiency in the body.
Neurology
Memory and cognitive function
Acid-sensitive channels of neurons, as you know, are to one degree or another responsible for synoptic plasticity, learning ability, memory, pain and neuro-degeneration 10), and the activity of neurons, as you know, helps to reduce the pH level (increased acidity) in the head the brain. The acid in the brain acts on acid-sensitive receptors, thereby modulating the activity of neurons. Gaviscon you know, physical exercises contribute to the activation of neurotrophic factors of the brain (such as UFHM), which, according to scientists, stimulate cognitive function against the background of physical activity 11) both in healthy people and in people with cognitive disorders or spinal injury. As you know, high-intensity training acts as a neuroendocrine regulator of acidity in the body (reacting with prolactin and growth hormone), and yet, sodium bicarbonate, lowering the acidity level, does not have the slightest effect on UFHM, the level of which increases sharply when physical activity. 12) An increased concentration of neuro-trophic factors in the brain is not related to serum acidity, and to date, scientists have no reason to believe that taking dietary supplements - “buffers” (such as sodium bicarbonate) leads to a decrease in the amount of these factors in the brain.
Bioenergy
Against the background of physical activity, our body produces more energy (which, as a rule, is replenished by taking glucose during rest, generic when lactate (“fuel”) enters the brain, glucose starts to oxidize more slowly 13)), which is not associated with metabolic acidosissince scientists have found that food sodium bicarbonate (supplement) does not affect these parameters. It was previously believed that an increase in the level of bicarbonate in the blood prevents lactate from penetrating the blood-brain barrier (since, with an increase in the level of H + ions, transport enzymes become more active 14). Despite the fact that, purely theoretically, the intake of food bicarbonate during training can contribute to the “conservation” of the percentage of glucose to lactate (as a rule, during intense physical exertion, often glucose is converted to lactate), this is not confirmed in practice.
Circulation
As you know, against the background of metabolic acidosis, blood flow to the brain is hampered, due to the sensitivity of blood vessels to hydrogen ions, 15) as a result of which increased acidity (not related to the level of carbon dioxide in the blood with hypercapnia and normocapnia) leads to the expansion of blood vessels, against the background of the production of nitric oxide and the activation of calcium channels. The above mechanism, according to scientists, is associated with the fact that against the background of chronic (mild) acidosis, the blood supply to the brain is disturbed, which normalizes (in young people with a slight metabolic acidosis) by intravenous infusion of sodium bicarbonate, while the rate of oxygen saturation of the blood does not change. Scientists are still arguing whether sodium bicarbonate helps in the fight against the effects of metabolic acidosis or not, because it is likely that the mild metabolic acidosis that many people eat now is not a cause for concern, but this, unfortunately, is not proven.
Panic syndrome
there came to the conclusion that when performing a chess test with illumination, in people with panic syndrome, the level of lactate in the head increased sharply (which can not be said about the control group of subjects), and, according to some reports, there is some correlation between panic disorders and changes in the level of acidity : baseline (in particular, the balance between CO2 and bicarbonate), 16) including indicators after a panic attack (when bio-markers of acidity return to normal), and basic metabolism (bicarbonate, hydrogen ions and pH). In addition, the cerebellar tonsil (the area of the brain responsible for fear, panic, and human emotions) responds to the stimulating effect of acids through the ASIC1a receptor, which is present in large quantities in the cerebellar tonsil and, in particular, the areas responsible Gaviscon fear. The inhalation of carbon dioxide (CO2) during the experimental test also causes panic attacks associated with a lack of air (when more carbon dioxide than oxygen enters the lungs), and people with panic syndrome are more likely to respond to CO2 tests than healthy people. Acute alkalosis (a condition opposite to acidosis, when the pH level rises sharply, which leads to a decrease in acidity) also causes panic attacks in experimental animals; both sodium bicarbonate and sodium lactate, when administered intravenously to people with panic syndrome, exacerbate panic syndrome. 17) People with panic syndrome, as a rule, are more susceptible to the action of acids, the basic balance of which is formed when their signals pass through acid-sensitive receptors. Nevertheless, panic attacks in such people occur both with low and high acidity, and in this case, sodium bicarbonate is unlikely to help them (it will rather aggravate the problem).
Neuro transmission during physical activity
Scientists claim that the production of β-endorphin during physical exertion (we are talking only about high-intensity training, where the maximum initial speed VO2 max is more than 60%) is due to the state of muscle acidosis, since the active production of β-endorphin is closely associated with a decrease in pH, while oral administration sodium bicarbonate (300 mg / kg), which helps to increase the pH to (or more) 7.4, actively blocks the release of β-endorphin. 18) Due to the slowdown of oxidative processes during active training (due to which β-endorphin is produced), acidic “buffers” like sodium bicarbonate effectively inhibit the production of β-endorphin. And although the intake of acids (either acetazole amide, or the inhalation of 4% CO2) in order to lower serum pH, as scientists note, stimulates the production of adrenaline (against the background of intense physical exertion), alkalosis (with hyperventilation of the lungs) does not affect the concentration of adrenaline in serum. Studies in which bicarbonate is used specifically to increase the pH level (300 mg / kg 90 minutes before the cycling test, which did not affect the endurance of the participants) did not bring the expected “fruits”, since the level of adrenaline in the serum of the participants did not change, however, scientists noted a prescription decrease in plasma adrenaline (by 34%) and norepinephrine (by 30%); 19) this difference is not related to the different physical activity and performance of these people, as evidenced by another experiment, element participants of which were injected with bicarbonate intravenously (again in order to normalize the pH), as a result of which they increased productivity and endurance, however, the serum concentration of catecholamines bicarbonate had no effect. As we can see, today there is no consensus on how sodium bicarbonate affects the production of adrenaline during physical exertion. Some scientists believe that the effect in this case is zero, while others believe that bicarbonate interferes with the synthesis of adrenaline in this case.
Cardiovascular health
Suction
An experiment with menopausal women who were given mineral water with / without the addition of bicarbonate (approx. 1,000 mmol per 500 ml of water) with a standard diet led to a decrease in infant lipidemia within 7 hours (peak value decreased by 13.2%and the area infant the pharmacokinetic curve “concentration-time” - by 15.5%), while the level of cholesterol in the blood of these women remained virtually unchanged. In another experiment, scientists noted the ability of bicarbonate to inhibit lipid absorption, which was not confirmed in the future, as it was not possible to establish the cause of such a reaction.
Cholesterol and lipoproteins
As you know, against the background of metabolic acidosis, LDL begins to oxidize actively, which is associated with a shortened latent phase of oxidation, which theoretically can lead to the development of atherosclerosis. 20) At the moment, there is no data on whether bicarbonate intake is fraught with atherosclerosis for people with metabolic acidosis. Thus, purely theoretically, sodium bicarbonate causes LDL oxidation in people with metabolic acidosis (that is, in the elderly or in people with impaired renal function), which is not proven due to the lack of research.
Arterial pressure
SLC4A5 (NBC4) sodium bicarbonate transporter polymorphisms are somehow related to hypertension 21), especially single-nucleotide polymorphisms (SNPs) of the rs7571842 and rs10177833 transporters and, to a lesser extent, the SNK GRK4 transporter. SLC4A5-carrier regulates intracellular pH and helps the passage of bicarbonate through the cell membrane, and disruption of their normal functioning (at the genetic level) leads to the phenomenon of “salt-sensitive hypertension”. Carriers of sodium bicarbonate are genetically different from each other, which is often associated with high blood pressure, but all this has nothing to do with oral administration of bicarbonate. An experiment with elderly people (with normal blood pressure), which at one time limited salt intake and then suddenly started drinking sodium bicarbonate (dissolved in mineral water) every day for 4 weeks, led to a decrease in blood pressure (by 5.7 +/- 6.4 mm Hg), which scientists attribute not so much to bicarbonate intake as to a low-salt diet (by 7.0 +/- 7.2 mm Hg), while the effect of bicarbonate in this case can most likely be Emod neutral (no less about sodium citrate, which nullifies the benefits of a low-salt diet). According to few data, taking sodium bicarbonate with a low-salt diet has a neutral effect, without increasing blood pressure.
Chronic obstructive pulmonary disease
Chronic obstructive pulmonary disease (COPD) is a heart disease in which a person quickly gets tired and is generally contraindicated in physical activity; an experiment with people with severe COPD who were given a standard dosage of sodium bicarbonate (300 mg / kg) to increase their endurance and activity, in fact, did not lead to anything. 22) According to limited data, the intake of sodium bicarbonate by people with COPD has no effect on their stamina, performance and physical activity in general.
Glucose Metabolism Reactions
Insulin resistance
