Effects of Sodium Bicarbonate on High-Intensity Endurance Performance in Cyclists: A Double-Blind, Randomized Cross-Over Trial.

Denne nevner at inntak av natron øker utholdenhet. Her brukte de 0,3g/kg, som blir 24g for en mann på 80kg. Det er ganske mye med tanke på at en teskje er 3g.

http://www.ncbi.nlm.nih.gov/pubmed/25494054/?ncbi_mmode=std

Abstract

BACKGROUND: While the ergogenic effect of sodium bicarbonate (BICA) on short-term, sprint-type performance has been repeatedly demonstrated, little is known about its effectiveness during prolonged high-intensity exercise in well-trained athletes. Therefore, this study aims to examine the influence of BICA on performance during exhaustive, high-intensity endurance cycling.

METHODS: This was a single-center, double-blind, randomized, placebo-controlled cross-over study. Twenty-one well-trained cyclists (mean ± SD: age 24±8 y, BMI 21.3±1.7, VO2peak 67.3±9.8 ml·kg-1·min-1) were randomly allocated to sequences of following interventions: oral ingestion of 0.3 g·kg-1 BICA or 4 g of sodium chloride (placebo), respectively. One h after ingestion subjects exercised for 30 min at 95% of the individual anaerobic threshold (IAT) followed by 110% IAT until exhaustion. Prior to these constant load tests stepwise incremental exercise tests were conducted under both conditions to determine IAT and VO2peak. Analysis of blood gas parameters, blood lactate (BLa) and gas exchange measurements were conducted before, during and after the tests. The main outcome measure was the time to exhaustion in the constant load test.

RESULTS: Cycling time to exhaustion was improved (p<0.05) under BICA (49.5±11.5 min) compared with placebo (45.0±9.5 min). No differences in maximal or sub-maximal measures of performance were observed during stepwise incremental tests. BICA ingestion resulted in an increased pH, bicarbonate concentration and BLa before, throughout and after both exercise testing modes.

CONCLUSION: The results suggest that ingestion of BICA may improve prolonged, high-intensity cycling performance.

CO2-beriket vann til fotbad

Å bade i CO2 beriket vann har vært brukt som medisin i alle år. Hellige og mirkauløse kilder har ofter vært vann med et høyt innhold av karbondioksid. Og det har blitt brukt i spa behandling i århundrer, spesielt i Bulgaria. Man finner Co2-rikt vann spesielt ved sovende og inaktive vulkaner.

CO2 er et veldig lite molekyl som diffunderer lett igjennom huden. I CO2-beriket vann kommer derfor CO2 inn i huden og inn til blodkarene i underhuden, hvor alle sansenerver ligger. Den økte CO2 en gjør at blodkarene rundt nervetrådene og i muskelvevet utvides (vasodilasjon) og at oksygene letter hopper av blodcellene slik at det kan bli brukt til energi i celler som vanligvis har lite tilgang på oksygen.

CO2 beriket vann kan vi lage selv på en svært enkel måte: blande Natron, Sitronsyre og vann. Begge disse stoffene fåes kjøpt på vanlig daglivarebutikk. Vannet begynner å bruse, og dette er CO2.

Studier nevner at man bør ha 900-1200 mg CO2 pr liter vann. Ved å måle pH kan vi regne med at vi har det når pH er nede på 5.

Vi kan se CO2 effekten på huden ved at det kommer tett-i-tett med ørsmå bobler. I f.eks. fotbad vil vi se at når vi tar foten opp fra vannet så er den rød, noe som er et tegn på økt blodsirkulasjon i huden.

For alle med nevropatier, diabetes, sår, nevromer, leggspenninger, restless leg syndrom, som lett blir sliten i bena av å gå, så vil dette være verdt et forsøk.

2-3 ganger i uka pleier å være den vanlige oppskriften. Noen studier har brukt det hver dag i mange uker. Spesielt når det gjelder diabetes sår.

Oppskrift: Bland 1 poseNatron med 2 poser Sitronsyre (blandingsforhold ca. 1:1) og hell innholdet i 5L vann. Det bruser veldig pga reaksjonen som lager CO2. Når du setter føttene nedi skal det komme mange små bobler som dekker huden. Etter 5-10 minutter vil huden som er under vann bli rød. Dette er et tegn på økt blodsirkulasjon.

5-15 minutter etter du er ferdig med fotbadet vil du sannsynligvis kjenne det prikker og strømmer ellers i kroppen også. Vanligvis kjennes det først og fremst i armer og bein, som er de stedene vi lettest kjenner økt blodsirkulasjon.

Her er noen studier som bekrefter effektene av CO2 beriket vann.

Beskriver det meste om balneotherapy, som det også heter. Inkludert kontraindikasjoner(hjerteproblemer og hypercapni som følge av lungeskade): http://www.centro-lavalle.com/edu/wp-content/uploads/2010/05/Carbon_Dioxide_Bath.pdf

Table 4. Major Indicators for CO2 Balneotherapy

1. Hypertension, especially borderline hypertension

2. Arteriolar occlusion, Stages I and II

3. Functional arteriolar blood flow disorders

4. Microcirculatory disorders

5. Functional disorders of the heart

Beskriver alt om hvordan det øker blodsirkulasjon og oksygenmetning: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3169585/?report=classic

Viser at det øker blodsirkulasjonen i huden og oksygenmetningen i muskelvev hos de som lett blir trøtte i beina: http://www.ncbi.nlm.nih.gov/pubmed/9112881/

Viser at det øker blodsirkulasjon og produksjonen av blodkar (angiogenese): http://circ.ahajournals.org/content/111/12/1523.long

Viser at det reparerer sår som ikke vil gro: http://iv.iiarjournals.org/content/24/2/223.long

Viser at det reparerer muskelskade: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3805014/

Viser at det reparerer muskelskade og atrofi (muskelsvikt) etter langtids post-operative sengeliggende: http://www.ncbi.nlm.nih.gov/pubmed/21371433

Viser at det reduserer hjertefrekvens gjennom å dempe sympaticus aktivering (ikke ved å øke parasymptaticus aktivering): http://jap.physiology.org/content/96/1/226

Viser at det øker mitokondrier og fjerner syster: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3499556/

Viser at det øker antioksidant status, reduserer frie radikaler og øker blodsirkulasjon i kapuillærene (mikrosirkulasjon): http://www.ncbi.nlm.nih.gov/pubmed/21248668

Viser at det hjelper til å reparere sår etter operasjon: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3595724/

Dr. Sircus sin forklaring av CO2 medisin som nevner mange måter å gjøre det på: http://drsircus.com/medicine/co2-medicine-bath-bombing-your-way-to-health

Denne artikkelen beskriver mye om historien til CO2-bad. http://ndnr.com/dermatology/cellulite-and-carbon-dioxide-bath/

Mange bilder av diabetes sår (OBS: ikke for sarte sjeler) som blir regenerert i løpet av få uker med 20-30 min fotbad. Disse bruker 900-1000ppm CO2 konsentrasjon. Jeg er usikker på om det er mulig med å blande Sitronsyre og Natron: http://www.iasj.net/iasj?func=fulltext&aId=48581

Denne artikkelen beskriver de fleste sider ved forskjellig bruk av CO2 behandling. God gjennomgang av hvordan blodsirkluasjonen påvirkes. http://www.scuolaeuropeamedicinaestetica.it/public/CARBOXYTHERAPY.pdf

Carbon dioxide and the critically ill—too little of a good thing?

Omfattende studie av alle de gode egenskapene ved hyperkapni – høyt CO2 nivå. Nevner mange interessante ting, bl.a. at CO2 indusert acidose gir mye mindre fire radikaler enn om pH senkes av andre faktorer. Bekrefter også at oksygen blir sittende fast på blodcellene ved hypokapni, og at melkesyreproduksjonen begrensens når acidosen er pga CO2 men ikke når den er av andre faktorer.

Spesielt med denne artikkelen er at den beskriver forskjellene på en hyperkapni acidose og acidose av andre faktorer. Hyperkapnisk acidose har beskyttende egenskaper.
http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(99)02388-0/fulltext

Permissive hypercapnia (acceptance of raised concentrations of carbon dioxide in mechanically ventilated patients) may be associated with increased survival as a result of less ventilator-associated lung injury.
Accumulating clinical and basic scientific evidence points to an active role for carbon dioxide in organ injury, in which raised concentrations of carbon dioxide are protective, and low concentrations are injurious.
Although hypercapnic acidosis may indicate tissue dysoxia and predict adverse outcome, it is not necessarily harmful per se. In fact, it may be beneficial. There is increasing evidence that respiratory (and metabolic) acidosis can exert protective effects on tissue injury, and furthermore, that hypocapnia may be deleterious.
If hypoventilation is allowed in an effort to limit lung stretch, carbon dioxide tension increases. Such “permissive hypercapnia” may be associated with increased survival in acute respiratory distress syndrome (ARDS);2 this association is supported by outcome data from a 10-year study.3
Furthermore, hypocapnia shifts the oxyhaemoglobin dissociation curve leftwards, restricting oxygen off-loading at the tissue level; local oxygen delivery may be further impaired by hypocapnia-induced vasoconstriction.
Brain homogenates develop far fewer free radicals and less lipid peroxidation when pH is lowered by carbon dioxide than when it is lowered by hydrochloric acid.19
Finally, greater inhibition of tissue lactate production occurs when lowered pH is due to carbon dioxide than when it is due to hydrochloric acid.20
An association between hypoventilation, hypercapnia, and improved outcome has been established in human beings.2521 In lambs, ischaemic myocardium recovers better in the presence of hypercapnic acidosis than metabolic acidosis.22 Hypercapnic acidosis has also been shown to protect ferret hearts against ischaemia,23 rat brain against ischaemic stroke,16 and rabbit lung against ischaemia-reperfusion injury.24 Hypercapnia attenuates oxygen-induced retinal vascularisation,25 and improves retinal cellular oxygenation in rats.26 “pH-stat” management of blood gases during cardiopulmonary bypass, involving administration of large amounts of additional carbon dioxide for maintenance of temperature-corrected PaCO2, results in better neurological and cardiac outcome.27
Hypercapnia results in a complex interaction between altered cardiac output, hypoxic pulmonary vasoconstriction, and intrapulmonary shunt, with a net increase in PaO2 (figure).28 Because hypercapnia increases cardiac output, oxygen delivery is increased throughout the body.28 Regional, including mesenteric, blood flow is also increased,29 thereby increasing oxygen delivery to organs. Because hypercapnia (and acidosis) shifts the haemoglobin-oxygen dissociation curve rightwards, and may increase packed-cell volume,30 oxygen delivery to tissues is further increased. Acidosis may reduce cellular respiration and oxygen consumption,31 which may further benefit an imbalance between supply and demand, in addition to greater oxygen delivery. One hypothesis32 is that acidosis protects against continued production of further organic acids (by a negative feedback loop) in tissues, providing a mechanism of cellular metabolic shutdown at times of nutrient shortage—eg, ischaemia.
Acidosis attenuates the following inflammatory processes (figure): leucocyte superoxide formation,33 neuronal apoptosis,34phospholipase A2 activity,35 expression of cell adhesion molecules,36 and neutrophil Na+/H+ exchange.37 In addition, xanthine oxidase (which has a key role in reperfusion injury) is inhibited by hypercapnic acidosis.24 Furthermore, hypercapnia upregulates pulmonary nitric oxide38 and neuronal cyclic nucleotide production,39 both of which are protective in organ injury. Oxygen-derived free radicals are central to the pathogenesis of many types of acute lung injury, and in tissue homogenates, hypercapnia attenuates production of free radicals and decreases lipid peroxidation.19 Thus, during inflammatory responses, hypercapnia or acidosis may tilt the balance towards cell salvage at the tissue level.
However, we know from several case series that human beings, and animals, can tolerate exceptionally high concentrations of carbon dioxide, and when adequately ventilated, can recover rapidly and completely. Therefore, high concentrations (if tolerated) may not necessarily cause harm.
From the published studies reviewed, and from the pathological mechanisms assessed, we postulate that changes in carbon dioxide concentration might affect acute inflammation,33—36 tissue ischaemia,16 ischaemia-reperfusion,2024 and other metabolic,1221,32 or developmental14 processes.
We argue that the recent shift in thinking about hypercapnia must now be extended to therapeutic use of carbon dioxide. Our understanding of the biology of disorders in which hypocapnia is a cardinal element would require fundamental reappraisal if hypocapnia is shown to be independently harmful.
In summary, in critically ill patients, future therapeutic goals involving PaCO2 might be expressed as:“keep the PaCO2 high; if necessary, make it high; and above all, prevent it from being low”.

Effects of a 4-week training with voluntary hypoventilation carried out at low pulmonary volumes

Spennende studie som viser hvordan lav pustefrekvens i selve trening påvirker restitusjonen etterpå. F.eks. hvordan bikarbonat/natron (HCO3-) påvirker melkesyreterskel. Teknikken bestod i å holde pusten 4 sekunder etter utpust, i bolker a 5minutter i løpet av treningsperioden. Det gir spesielt lite oksygen i blodet, som gir mange positive resultater.

http://www.sciencedirect.com/science/article/pii/S1569904807002327

Helle studien her:  http://www.google.com/url?sa=t&rct=j&q=&esrc=s&source=web&cd=1&ved=0CCsQFjAA&url=http%3A%2F%2Fwww.researchgate.net%2Fpublication%2F5689789_Effects_of_a_4-week_training_with_voluntary_hypoventilation_carried_out_at_low_pulmonary_volumes%2Ffile%2F79e41509ccd387b0f9.pdf&ei=pM58UpS3IIKF4ATU24D4CA&usg=AFQjCNFVh6Yl8e_ScphKf6HTFiLp1CWKsw&sig2=B9Zq9u_LuDDzGru14OKsLQ&bvm=bv.56146854,d.bGE

This study investigated the effects of training with voluntary hypoventilation (VH) at low pulmonary volumes. Two groups of moderately trained runners, one using hypoventilation (HYPO, n = 7) and one control group (CONT, n = 8), were constituted. The training consisted in performing 12 sessions of 55 min within 4 weeks. In each session, HYPO ran 24 min at 70% of maximal O2 consumption (View the MathML source) with a breath holding at functional residual capacity whereas CONT breathed normally. A View the MathML source and a time to exhaustion test (TE) were performed before (PRE) and after (POST) the training period. There was no change in View the MathML source, lactate threshold or TE in both groups at POST vs. PRE. At maximal exercise, blood lactate concentration was lower in CONT after the training period and remained unchanged in HYPO. At 90% of maximal heart rate, in HYPO only, both pH (7.36 ± 0.04 vs. 7.33 ± 0.06; p < 0.05) and bicarbonate concentration (20.4 ± 2.9 mmol L−1 vs. 19.4 ± 3.5; p < 0.05) were higher at POST vs. PRE. The results of this study demonstrate that VH training did not improve endurance performance but could modify the glycolytic metabolism. The reduced exercise-induced blood acidosis in HYPO could be due to an improvement in muscle buffer capacity. This phenomenon may have a significant positive impact on anaerobic performance.

Muscle Pain: Mechanisms and Clinical Significance

En studie til fra Siegfried Mense, om muskelsmerter. Han har ikke fått med seg at trykksensitive nerver kun finnes i huden. Og han har misforstått litt i forskjellene mellom hud-smerter og muskel-smerter siden han sier at hud-smerter ikke kan ha utstrålende effekt. Han har tydeligvis ikke ikke inkludert subcutane nerver i sin vurdering.

Men mye interessant i denne studien likevel. Spesielt vektleggingen av at lav pH er den viktigste bidragsyteren til muskelsmerter.

Han nevner at input fra muskel-nociceptorer har større relevans i ryggmargen enn input fra huden. Derfor er betennelser og lav pH de viktigste drivkreftene i kroniske smerter.

Nevner også at smerter henger sammen, f.eks. at trapezius kan stramme seg for å beskytte brachialis, slik at smerten kjennes i trapezius, mens problemet egentlig sitter i brachialis.

Beskriver også triggerpunkter, men sier at det foreløpig er veldig mange ubesvarte spørsmål om denne teorien.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2696782

Muscle pain is a major medical problem: in, the majority (60% to 85%) of the population has had (nonspecific) back pain of muscular origin at some time or other (lifetime prevalence) (1). Pain evoked by myofascial trigger points has a point prevalence of approximately 30% (2). More than 7% of all women aged 70 to 80 years suffer from the fibromyalgia syndrome (e1). In an Italian study, musculoskeletal pain was found to be the most common reason that patients consulted a doctor (3). Thus, treating physicians should be aware of the mechanisms of muscle pain, insofar as they are currently understood.

Subjective differences between muscle pain and cutaneous pain

Muscle pain Cutaneous pain
Electrical nerve stimulation induces only one pain Electrical nerve stimulation induces a first pain and a second pain
Poorly localizable Well-localized
Tearing, cramping, pressing quality Stabbing, burning, cutting quality
Marked tendency toward referral of pain No tendency toward referral of pain
Affective aspect: difficult to tolerate Affective aspect: easier to tolerate

Muscle pain is produced by the activation of specific receptors (so-called nociceptors): these receptors are specialized for the detection of stimuli that are objectively capable of damaging tissue and that are subjectively perceived as painful. They consist of free nerve endings and are connected to the central nervous system (CNS) by way of unmyelinated (group IV) or thinly myelinated (group III) fibers. They can be sensitized and activated by strong mechanical stimuli, such as trauma or mechanical overloading, as well as by endogenous inflammatory mediators including bradykinin (BK), serotonin, and prostaglandin E2 (PGE2).

Two activating chemical substances are particularly important for the generation of muscle pain: adenosine triphosphate (ATP) and protons (H+ ions).

ATP activates muscle nociceptors mainly by binding to the P2X3 receptor molecule, H+ mainly by binding to the receptor molecules TRPV1 (transient receptor potential vanilloid 1) and ASICs (acid-sensing ion channels) (4).

ATP is found in all cells of the body and is released whenever bodily tissues of any type are injured.

A drop in pH is probably one of the main activators of peripheral nociceptors, as many painful disturbances of muscle are associated with low pH in muscle tissue.

Nerve growth factor (NGF) also has a connection to muscle pain: NGF is synthesized in muscle and activates muscle nociceptors (e2). NGF synthesis is increased when a muscle is inflamed (e3).

Acidic tissue pH is one of the main activating factors leading to muscle pain. Practically all pathological and pathophysiological changes of skeletal muscle are accompanied by a drop in pH, among them

  • chronic ischemic states,
  • tonic contractions or spasms,
  • myofascial trigger points,
  • (occupationally induced) postural abnormalities, and
  • myositides.

The neuropeptides stored in muscle nociceptors are released not only when peripheral stimuli activate the nerve endings, but also when spinal nerves are compressed. In this type of neuropathic pain, action potentials are generated at the site of compression and spread not only centripetally, i.e., toward the central nervous system, but also centrifugally, i.e., toward the nociceptive endings, where they induce the release of vasoactive neuropeptides. In this way, neurogenic inflammation comes about, characterized by hyperemia, edema, and the release of inflammatory mediators (8). The inflammatory mediators sensitize the muscle nociceptors and thereby increase neuropathic pain.

The sensitization of the muscle nociceptors by endogenous mediators such as BK and PGE2 is one of the reasons why patients with muscle lesions suffer from tenderness to pressure on the muscle, and from pain on movement or exercise. It is also the reason why many types of muscle pain respond well to the administration of non-steroidal anti-inflammatory drugs (NSAID), which block prostaglandin synthesis.

An influx of nervous impulses from muscle nociceptors into the spinal cord increases the excitability of posterior horn neurons to a greater extent than one from cutaneous nociceptors (9).

Two main mechanisms underlie the overexcitability of spinal nociceptive neurons:

A structural change of ion channels, rendering them more permeable to Na+ and Ca2+, is the short-term result of an influx of nociceptive impulses into the spinal cord. Among other effects, this causes originally ineffective («silent» or «dormant») synapses to become effective.

A change of gene transcription in the neuronal nucleus, leading to a modification of synthetic processes, causes new ion channels to be synthesized and incorporated into the nerve cell membrane. The long-term result of central sensitization is a nociceptive cell whose membrane contains a higher density of ion channels that are also more permeable to ions. This explains the hyperexcitability of the cell. Glial cells, too, particularly microglia, can contribute to the sensitization of central neurons by secreting substances such as tumor necrosis factor a (TNF-a) (8).

The increased excitability of spinal neurons and the spread of excitation within the CNS are the first steps in the process of chronification of muscle pain. The endpoint of chronification consists of structural remodeling processes in the CNS that open up new pathways for nociceptive information and cause pain to persist over the long term. Patients with chronic muscle pain are difficult to treat, because the functional and structural changes in the CNS need time to regress. The fact that not all muscle pain becomes chronic implies that chronification requires not only the mechanisms just discussed, but also other ones, e.g., a genetic predisposition.

Pain arising in muscle is more likely to be referred pain than pain arising in the skin. Referred pain is pain that is felt not (only) at its site of origin, but at another site some distance away. A possible mechanism of referred pain is the spread, within the spinal cord, of excitation due to the muscle lesion (9) (figures 2 and ​and3).3). As soon as the excitation reaches sensory posterior horn neurons that innervate an area beyond the site of the original muscle lesion, the patient feels referred pain in that area, even though none of the nociceptors in it are activated (13).


An example is shown in figure 3: a stimulus delivered to the myofascial trigger point (MTrP) in the soleus muscle causes only mild local pain, while the patient feels more severe (referred) pain in the sacroiliac joint. No conclusive answers are yet available to the questions of why muscle pain is more likely than cutaneous pain to be referred, why it is usually not referred to both proximal and distal sites, and why pain referral is often discontinuous. There is, however, a well-known discontinuity of spinal topography between the C4 and T2 dermatomes.

The main reason why pain arises in muscle spasm is muscle ischemia, which leads to a drop in pH and the release of pain-producing substances such as bradykinin, ATP, and H+.

The vicious-circle concept of muscle spasm – muscle pain causes spasm, which causes more pain, etc. – should now be considered obsolete. Most studies have shown that muscle pain lowers the excitability of the α-motor neurons innervating the painful muscle (14) (a «pain adaptation» model) (15).

Muscle spasm can be precipitated by, among other things, pain in another muscle. Thus, a spasm-like increase EMG activity in the trapezius muscle has been described in response to painful stimulation of the biceps brachii muscle (16). Another source of muscle spasms is pathological changes in a neighboring joint. These sources of pain must be deliberately sought.

In a widespread hypothesis on the origin of MTrP’s (19), it is supposed that a muscular lesion damages the neuromuscular endplate so that it secretes an excessive amount of acetylcholine. The ensuing depolarization of the muscle cell membrane produces a contraction knot that compresses the neighboring capillaries, causing local ischemia. Ischemia, in turn, leads to the release of substances into the tissue that sensitize nociceptors, accounting for the tenderness of MTrP’s to pressure. Substances of this type have been found to be present within the MTrP’s of these patients (20). This supposed mechanism leaves many questions unanswered but is currently the only comprehensive hypothesis on the origin of MTrP’s.

Patients with MTrP’s often have pain in three locations:

  • at the site of the MTrP itself,
  • at the origin or insertion of the affected muscle, because of pulling by the muscle fibers that have been stretched by the contraction knots,
  • and referred pain outside the MTrP (figure 3).

Because the MTrP is cut off from its blood supply by compression of the local microcirculation, oral NSAID’s are not very effective against TrP pain.

Functional Anatomy of Muscle – Muscle, Nociceptors and Afferent Fibers

Svært mye interessant om nervesystemets rolle i muskler og smerte.

Spesielt at det er ingen frie nerveender i muskelcellene, men bare i blodkarene i musklene. Derfor reagerer vi med smerte på betennelser og lav pH i blodet, mens trykksensitiviteten kun sitter i huden.

Den nevner at pH sensibiliteten er den viktigste smertebidraget fordi pH synker i de fleste patologiske tilstander, f.eks. hard trening eller skade.

Den nevner at det er mer SP (Substans P, som er relatert til smerte) i huden enn i muskler.

Nevner at frie nerveender ikke går til kapillærer eller muskelceller, bare til arterioler og venuler.

Nevner også innervering av bindevev, og at dette feltet foreløpig er lite studert og oversett. Spesielt viser de til at Toracolumbar Facia (i korsryggen) har størst innervasjon av C-fiber nociceptorer(som inneholder SP) under huden, og litt i multifidene.

En nociceptor er ikke bare en passiv mottaker av impulser, men er også en aktiv deltaker i vevets tilstand når det gjelder betennelser og blodsirkulasjon for de sender nevropetider ut fra doresalhornet til vevet (antidromiske impulser). Altså motsatt vei av reseptor-signalretningen.

CGRP virker vasodilerende, mens SP gjør at blodkarveggenes permeabilitet øker. Når permeabiliteten øker siver det ut proteiner og stoffer som egentlig ikke skal være i vevet, og da økes betennelser og immunsystemets aktivitet. Så det er SP vi ønsker å dempe først og fremst.

http://www.google.com/url?sa=t&rct=j&q=&esrc=s&source=web&cd=1&cad=rja&ved=0CCsQFjAA&url=http%3A%2F%2Fwww.springer.com%2Fcda%2Fcontent%2Fdocument%2Fcda_downloaddocument%2F9783540850205-c1.pdf%3FSGWID%3D0-0-45-935848-p173845615&ei=_GJEUqyUOevn4QSBl4HQDg&usg=AFQjCNEpyWrolHywvUNyw_Cwa8yWTiEUnw&sig2=OJLZ3XrnTalCUUqE-uhCeQ&bvm=bv.53217764,d.bGE

The predominant location of free nerve endings supplied by group IV fibers was the adventitia of arterioles and venules. Surprisingly, muscle fibers themselves did not receive direct innervation by free nerve endings. Group III afferents generated not only free nerve endings but also paciniform corpuscles, whereas group IV fibers terminated exclusively in free nerve endings.The high sensitivity of the free nerve endings to chemical stimuli, particularly to those accompanying inflammatory lesions or disturbances of the microcirculation, may be related to their location on or in the walls of the blood vessels. The finding that the muscle fibers proper are not supplied by free nerve endings (Reinert et al. 1998) may relate to the clinical experience that muscle cell death is usually not painful, at least not if it occurs slowly, as for instance during muscular dystrophy, polymyositis, or dermatomyositis. A different situation is tearing of a muscle fiber bundle, which can be extremely painful. In this condi- tion, many muscle cells are destroyed simultaneously and release their contents (e.g., K+ ions and ATP) in the interstitial space, from where they can diffuse to the next nociceptive endings.
In skeletal muscle, the free nerve endings appear to be distributed quite evenly in the proximodistal direction. At least, in a quantitative evaluation of the inner- vation density by neuropeptide-(SP- and CGRP-) containing fibers, no difference between the proximal and distal portions of the rat gastrocnemius–soleus (GS) muscle was found (Reinert et al. 1998). Therefore, a higher innervation density at the transition zone between muscle and tendon is not a probable explanation for the frequent pain in this region.

However, in the same study the nerve fiber density in the peritendineum (the connective tissue around a tendon) of the rat calcaneal tendon was found to be several times higher than that in the GS muscle. In contrast, the collagen fiber bundles of the tendon tissue proper were almost free of free nerve endings. The high fiber density in the peritendineum may explain the high prevalence of tenderness or pain in the tissue around the tendon and the insertion site. The scarcity of nerve endings in the center of the tendon may relate to the clinical observation that (incomplete) ruptures of the tendon may occur without pain.

Judging from their respon- siveness to pain-producing agents, the following receptor molecules are likely to be relevant for muscle pain and tenderness (Mense and Meyer 1985; Caterina and David 1999; McCleskey and Gold 1999; Mense 2007):

  • Bradykinin (BKN) receptors (B1 and B2). BKN is cleaved from blood plasma proteins when a blood vessel breaks or increases its permeability so that plasma proteins enter the interstitial space. In intact tissue, BKN excites nerve endings by the activation of the BKN receptor molecule B2, whereas under pathological conditions (e.g., inflammation) the receptor B1 is the predominant one (Perkins and Kelly 1993; for a review of receptor molecules mediating the effects of classic inflammatory (pain-producing or algesic) substances, see Kumazawa 1996).
  • Serotonin receptors (particularly 5-HT3). Serotonin (5-hydroxytryptamin, 5-HT) is released from blood platelets during blood clotting. The stimulating effects of serotonin on nociceptive terminals in the body periphery are predomi- nantly mediated by the 5-HT3 receptor (at present, more than 15 different 5-HT receptors are known in the CNS). The serotonin concentrations released in the tissue are usually not sufficient to excite nociceptors directly, but they can sen- sitize them, i.e., make them more sensitive to other pain-producing agents such as BKN.
  • Prostaglandins, particularly prostaglandin E2 (PGE2). Prostaglandins (PGs) are released in a pathologically altered muscle by the enzymatic action of cycloox- igenases. PGE2 binds to a G protein-coupled prostanoid receptor (EP2) in the membrane of the nociceptive ending. Similarly to serotonin, PGE2 sensitizes nociceptors rather than exciting them under (patho)physiological circumstances (Mense 1981).
  • Acid-sensing ion channels (ASICs). ASICs constitute a family of receptor molecules that are sensitive to a drop in pH and open at various pH values. The channel proteins react already to small pH changes, for instance from pH 7.4 to 7.1. This receptor family (for instance ASIC1 and ASIC3) is particularly impor- tant for muscle pain, because almost all pathologic changes in muscle are accom- panied by a drop in tissue pH, e.g., exhausting exercise, ischemia, and inflammation (Immke and McCleskey 2003). In these conditions, the pH of the muscle tissue can drop to 5–6. The proton-sensitive nociceptors may also be of importance for the induction of chronic muscle pain. Repeated intramuscular injections of acidic solutions have been reported to induce a long-lasting hyper- algesia (Sluka et al. 2001).
  • P2X3 receptors. This receptor is a subtype of the purinergic receptors that are activated by ATP and its derivatives (Burnstock 2007; Ding et al. 2000). ATP is the energy-carrying molecule in all cells of the body; accordingly, it is present in every tissue cell. It is released from all tissues during trauma and other pathologic changes that are associated with cell death. For this reason, ATP has been considered a general signal substance for tissue trauma and pain (Cook and McCleskey 2002). ATP is particularly important for muscle pain, because it is present in muscle cells in high concentration (Stewart et al. 1994). When injected into human muscle, ATP causes pain (Mo ̈rk et al. 2003).
  • Transient receptor potential receptor subtype 1 (TRPV1) formerly called VR1. This receptor is one of the most important molecules for the induction of pain. The natural stimulant for the TRPV1 receptor is Capsaicin, the active ingredient of chilli peppers (Caterina and Julius 2001). The receptor is also sensitive to an increase in H+-concentration and to heat, with a threshold of approximately 39C. Its endoge- nous ligands are H+-ions.
  • Other TRP receptors. TRPV4 is a mechanosensitive ion channel that is sensitive to both weak and strong (noxious) intensities of local pressure (Liedtke 2005). It may be the receptor for mediating pain evoked by pinching and squeezing.
  • Tyrosine kinase A (TrkA) receptor. The ligand of this receptor is NGF (Caterina and David 1999). NGF is well-known for its sensitizing action on nociceptors in the body periphery and neurons in the CNS; it is synthesized in muscle, and its synthesis is increased during pathophysiological changes of the muscle (e.g., inflammation, Menetrey et al. 2000; Pezet and McMahon 2006).
  • Glutamate receptors. There is evidence indicating that the NMDA receptor (one of the receptors for glutamate) is present on nociceptive endings in masticatory muscles. Injections of glutamate into the masseter muscle in human subjects induced a reduction in pressure pain threshold which was attenuated by coinjection with ketamine, an NMDA receptor antagonist (Cairns et al. 2006).
Substances exciting muscle nociceptors independent of membrane receptors.
  • Hypertonic saline: injections of NaCl solutions (4.5–6.0%) have long been and still are used to elicit pain from deep somatic tissues (Kellgren 1938; for review, see Graven-Nielsen 2006).
  • Potassium ions: The most likely explanation for the excitatory action of high concentrations of extracellular potassium ions is a depolarization of the membrane potential due to a reduction of the inside–outside potassium gradient (usually the potassium concentration inside the axon is much higher).

DRG cells projecting in a cutaneous nerve have been reported to contain SP, CGRP, and somatostatin (SOM).

In comparison to skin nerves, muscle nerves appear to contain less SP. This finding makes sense, because the vasodilatation and plasma extrava- sation caused by the release of SP and CGRP from free nerve endings (see below) would be dangerous for skeletal muscles, since many of them are surrounded by a tight fascia. Therefore, an SP-induced muscle edema would result in a high increase in interstitial pressure, and could cause muscle necrosis.

In a study on functionally identified DRG cells employing a combination of electrophysiological and immunohistochemical techniques, Lawson et al.(1997) reported that cells terminating in cutaneous nociceptive endings showed a strong tendency to express SP, particularly if they had a slow conduction velocity or a small soma in the DRG. 

The peptides are synthesized in the somas of the DRG or in ganglion cells of cranial nerves. They are transported to both the central and the peripheral terminal of the primary afferent unit.

In a quantitative evaluation of neuropeptide-containing free nerve endings and preterminal axons (both characterized by varicosities) in the GS muscle of the rat, most endings were found around small blood vessels (arterioles or venules), whereas capillaries and the muscle cells proper were not contacted by these end- ings.

Efferent or motor fibers conduct action potentials from the CNS to the periphery; their soma is located in the spinal cord or brainstem and the fibers leave the CNS via the ventral root or cranial nerve motor roots. An exception are postganglionic sympathetic fibers whose cell bodies are mostly located in the sympathetic trunk (e.g., vasomotor fibers that constrict blood vessels).

The nerve to a locomotor muscle in the cat (the lateral GS) is composed of approximately one-third myelinated (720) and two-thirds unmyelinated (2,480) fibers (Table 2.2; Mitchell and Schmidt 1983; Stacey 1969). Nearly one quarter of the myelinated (group III) fibers had nociceptive properties in neurophysio- logical experiments (Mense and Meyer 1985). Of the unmyelinated fibers, 50% are sensory (group IV), and of these, approximately 55% have been found to be nociceptive in the rat (Hoheisel et al. 2005).

Data obtained from one muscle nerve cannot be transferred directly to other muscle nerves, because considerable differences exist between different muscles. For instance, neck muscle nerves of the cat contain unusually high numbers of sensory group III receptors (Abrahams et al. 1984). One possible explanation for these differences is that the muscles have different functions and environmental conditions: in contrast to the neck muscles, which must register the orientation of the head in relation to the body in fine detail, the locomotor hindlimb muscles often have to contract with maximal strength and under ischemic conditions.

In addition to nociceptors, there are other muscle receptors whose function is essential for the understanding of muscle pain:

  • Muscle spindles are complex receptive structures that consist of several specialized muscle fibers (the so-called intrafusal muscle fibers; the name is derived from their location inside the spindle-shaped connective tissue sheath. Accordingly, all the “normal” muscle fibers outside the spindle are “extrafusal” fibers). Muscle spindles measure the length and the rate of length changes of the muscle, i.e., their discharge rate increases with increasing muscle length and with increasing velocity of the length change.
  • Golgi (tendon) organs measure the tension of the muscle. They are arranged in series with the extrafusal muscle fibers; their location is the transition zone between muscle and tendon. The supplying fiber is the Ib afferent, whose structure is identical to the Ia fiber (thick myelin sheath and high conduction velocity). The receptor has a much simpler structure than the muscle spindle; it consists of receptive endings that are interwoven between the collagen fiber bundles of the tendon.
  • Muscle spindles and Golgi organs are proprioceptors, i.e., they measure the internal state of the body.
  • Pacinian corpuscles (PC) and paciniform corpuscles. These receptors do not respond to static pressure; they require dynamically changing mechanical stimuli, and are best excited by vibrations of relatively high frequency (close to 300 Hz; Kandel et al. 2000). The receptive ending is formed like a rod, and covered by several concentric membranes which give the receptor an onion-like appearance in cross-sections.

At present, little information is available about the innervation of fascia. This is an important gap in our knowledge, because fascia is an important component of the musculoskeletal system and likely to contribute to many forms of pain that are subsumed under the label “muscle” pain. One example is low back pain: The thoracolumbar fascia (TF) plays an essential role in body posture and trunk move- ments (Bogduk and Macintosh 1984). It is not only a passive transmitter of mechanical forces of the low back and abdominal muscles but also contractile by itself (Schleip et al. 2005).

In the connective tissue around the superficial lamina of the TF we found many CGRP- and SP-containing free nerve endings. The majority of the fibers were located in the subcutaneous layer, as well as between the fascia and the surface of the multifidus muscle (Fig. 2.8). The SP-positive endings are of particular interest, because they are thought to be nociceptors.
The loose connective tissue around the TF is probably deformed during any trunk movement, and therefore the free nerve endings are strategically situated to sense any disorders in these movements. It is conceivable that overload of the fascia puts mechanical stress and irritation on the endings, and thus may contribute to low back pain.
SP then releases histamine from mast cells, and together with CGRP these agents cause vasodilatation and an increase in vascular permeability of the blood vessels around the active ending. The result is a shift of blood plasma from the intravascular to the interstitial space. Outside the blood vessel, BKN is cleaved from the plasma protein kallidin, serotonin (5-HT) is set free from platelets, and PGs (particularly PGE2) from endothelial and other tissue cells. All these substances sensitize nociceptors. Thus, the main tissue alteration induced by a nondestructive noxious mechanical stimulus is a localized region of vasodilatation, edema, and sensitized nociceptors.
A nociceptor is not a passive sensor of tissue-threatening stimuli; it actively influences the microcirculation and chemical composition of the intersti- tial space around it.
If a noxious stimulus activates only one part of the ending, the action potentials originating in that region of the ending can invade antidromically (against the normal direction of propagation) those branches of the ending that were not excited by the stimulus. These antidromic action potentials release neuropeptides from the unstimulated branches. The whole process is called the axon reflex.  It is assumed to be the reason for the visible wheal and flare around a cutaneous lesion.

The vascular permeability is increased mainly by SP (and by the neurokinins A and B; Gamse and Saria 1985), whereas CGRP is assumed to act primarily as a vasodilator. There is evidence showing that CGRP enhances the plasma extravasation induced by SP and neurokinins A and B, but reduces the vasodilatory action of SP by desensitizing muscle arterioles to the peptide (O ̈ hle ́n et al. 1988).

The area of wheal and flare after a localized damage to the skin – for instance around a needle prick – could be an indicator of the extent of the excited nocicep- tive ending.

The size of the receptive fields (RFs) of cutaneous polymodal nociceptors was found to be less than 2 mm in cat (Bessou and Perl 1969) and 6–32 mm in rabbit (Kenins 1988). A receptive field is that region of the body from which a receptive ending (or a central sensory neuron) can be excited. The above figures are larger than the reported length of the branches of a nociceptor ending (a few hundred mm; Stacey 1969).

The release of SP, CGRP, neurokinin A, and other agents from nociceptors is the central factor in the cascade of events that lead to neurogenic inflammation in the periphery (Lembeck and Holzer 1979). Neurogenic inflammation is characterized by tissue edema and infiltration by immune cells, i.e., it exhibits the major histo- logical signs of a (sterile) inflammation. It develops whenever action potentials are generated not at the receptive ending but somewhere along the course of primary afferent units (spinal nerve or dorsal root). The action potentials propagate both to the CNS (causing pain) and to the peripheral ending (causing release of neuropep- tides and neurogenic inflammation). The published data indicate that vasodilatation can be elicited by antidromic stimulation of both Ad- and C fibers, but increase in vascular permeability and plasma extravasation by stimulation of C fibers only.

Neuropathies and radiculopathies and other pathological conditions that are asso- ciated with antidromic activity in sensory nerve fibers are examples of such events (Marchand et al. 2005). Neurogenic inflammation is likely to increase the dysesthe- sia and pain of patients suffering from neuropathies.

Inflammatory disorders are usually accompanied by sensitization of peri- pheral nociceptors, which is one source of inflammatory pain (for details, see Chap. 3). 

Om Natron

Natron, norges billigste kosttilskudd, fåes kjøpt i butikken som helt rent natriumbikarbonat. Bikarbonat er et av de viktigste mineralene i kroppen fordi det hjelper oss å holde en stor pH-buffer kapasitet. Blodets pH holdes innenfor en liten ramme på 7,35-7,45. Hvis pH kommer langt nok utenfor denne rammen kan det være livsfarlig og vi kan gå i koma eller få permanente skader. Med stor nok buffer kan vi tåle store svigninger uten at det trenger å gå på bekostning av andre funksjoner i kroppen. Jeg anbefaler vanligvis 1 ts 2-4x daglig, som er 10-20g, i perioder når man trenger det.

Maten vi spiser og vår moderne livsstil gir kroppen en stor syre-utforing og mange mennesker går rundt med en mild acidose. Det gjelder spesielt om man har et kosthold med mye korn og lite grønnsaker. Bikarbonatinnholdet i blodet går ned, nyrene kompenserer og sjelettet utskiller mineraler. Natron fyller opp bikarbonatlagrene igjen slik at kroppen ikke trenger å kompensere med andre funksjoner.

I denne studien fra 2010 blir kostens påvirkning på surhetsgraden i kroppen gjennomgått. Den nevner bl.a. hvordan selv en mild acidose gjør at muskelene blir insulinresistente. http://www.ncbi.nlm.nih.gov/pubmed/21481501

En studie fra 2001 så på forskjellen mellom et syrefremmende kosthold og et basefremmende kosthold. Selv blodets pH ble minimalt endret, men det gikk på bekostning av andre funksjoner. Ved et surt kosthold henter kroppen basedannende mineraler fra skjelettet. Kalsiumutskillelsen økte med 74% hos de sure og kan være et bidrag til osteoporose. Den basiske gruppen fikk bl.a. bikarbonat å drikke.  http://www.ncbi.nlm.nih.gov/pubmed/11446566

Svært interessant studie fra 2009 som viser hvordan bikarbonat øker mitokondrienes aktivitet og respirasjon hos mus fordi H+ i musklene dempes. Musene fikk 0,05g/kg bikarbonat og kom opp i en pH på 7,5 som holdt seg der i mer en enn time etterpå. http://ajpendo.physiology.org/content/299/2/E225

Studie fra 1991 som viser at bikarbonat er essensielt for DNA aktivitet, gjort på in vitro (på celler). pH er optimal mellom 7,5-8. http://www.ncbi.nlm.nih.gov/pubmed/1890072 

Studie fra 1990 som viser at natriumklorid (salt) øker kalsium utskillelse, mens natriumbikarbonat (natron) gjør det ikke. Denne studien viser også at tilførsel av bikarbonat faktisk senker blodtrykk etter bare 7 dager. http://www.ncbi.nlm.nih.gov/pubmed/2168457

Denne studien fra 1996 viser også at natriumklorid demper den negative effekten av for mye salt i maten. Det senker blodtrykket. http://www.ncbi.nlm.nih.gov/pubmed/12013486

Denne studien viser at det er klorid-delen av salt, ikke natrium-delen, som skaper høyt blodtrykk og problemene vi hører om ang for mye salt i maten. Natrium som kommer fra natriumbikarbonat regnes som helt ufarlig. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2927202/

Studie fra 2012 som viser at å drikke bikarbonat minker faren for hjerte/kar problemer hos unge mennesker med høyt kolesterol. Etter 4 uker sank totalt kolesterol med 6%, LDL med 10%, men CRP og andre faktorer ble ikke påvirket. http://www.ncbi.nlm.nih.gov/pubmed/19954956

TRENING

Bikarbonat brukes til å øke prestasjon og utholdenhet i trening, spesielt i kort-distanse og høy-intensitet øvelser. I intense aktiviteter synker pH i blod, og dette gjør at kroppen må hyperventilere for å fjerne CO2 raskt nok og holde blodet i riktig pH-ramme. Man tilfører bikarbonat for å gi kroppen større bufferkapasitet også under trening.

En studie fra 2010 gjenomgikk hvilke doser og til hvilke tider det bør inntas før treningen. De kom frem til at om man tar 0,2g/kg bør man ta det 40-50min før, og om man tar 0,3g/kg bør man ta det 60min før. http://www.ncbi.nlm.nih.gov/pubmed/20040895

En studie fra 2009 viste at 0,3g/kg ga en mye raske innhenting av pustefrekvens og CO2 etter høy-intensitet trening. Deltakerne fikk 6 doser med 10min mellomrom (fikk pH opp i 7,51) og utførte treningen 1t etter det igjen. De nevner at ved høyere bikarbonat konsentrasjoner konsumeres mer H+ og dermed også produserer mer CO2. http://www.biomed.cas.cz/physiolres/pdf/58/58_537.pdf

En studie fra 2004 så på hvordan bikarbonat påvirker muskel-pH under og etter gjentatte sprinter. pH ble 7,50, men i musklene var det ingen forskjell hverken i pH, melkesyre eller bufferkapsitet. Likevel presterte deltakerene med bikarbonat bedre i sprint 3, 4 og 5 enn kontrollgruppen. Etter trening hadde bikarbonatgruppen mye mer laktat i musklene, noe som innebærer at anaerobisk energi blir lettere tilgjengelig når blodet er mer basisk. Dette forklarerer større utholdenhet. http://www.ncbi.nlm.nih.gov/pubmed/15126714

I en studie fra 2011 ble det vist at det er ingen sammenheng mellom bikarbonat inntak og melkesyre i musklene under høy-intensitet intervaller. http://www.ncbi.nlm.nih.gov/pubmed/21197542

En studie fra 2011 undersøkte hvordan de vanlige høye dosene som anbefales for atleter (0,3g/kg) påvirker mage/tarm symptomer. For noen kan det gi diare. Studien viste at pH ble høyest og mage/tarm problemer minst når det inntas sammen med mat. Og symptomene var værst 90 minutter etter inntak. De konkluderer med at det bør inntas 2-2,5t før trening om man vil unngå mage/tarm symptomer. http://www.ncbi.nlm.nih.gov/pubmed/21719899

En studie fra 2013 viste at ved bikarbonat doser på 0,3g/kg kan det blir mage/tarm symptomer. 91% fikk diarre, 64% ble oppblåst og tørste, 45% ble kvalme. http://www.ncbi.nlm.nih.gov/m/pubmed/23746564

En ny studie fra 2013 undersøkte hvordan bikarbonat inntak flere dager før en treningsøkt kunne forbedre prestasjon og dempe acidose. De to 0,3g/kg i 5 dager. Tid før utmattelse(Tlim) økte med 23%. Bikarbonat økte også plasmavolum. Av den grunn økte ikke pH selv om bikarbonatinntaket økte. Derfor konkluderer forskerne her med at det holder å ta det dagen i forveien. Eller det viser oss at vi ikke trenger å være redd for en akkumulering av bikarbonat ved langvarig inntak. De viser også til at bikarbonat inntak bidrar til å begrense syre-overskudd i musklene ved at basisk blod trekker H+ ut. Dette øker laktat-aktivitet og dermed utholdenheten. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3623762/

En studie fra 2011 nevner at pre-alkalisering med bikarbonat før trening minker effekten av Heat-Shock protiner, altså demper stressreaksjonen etter trening. http://www.ncbi.nlm.nih.gov/pubmed/21498114

En studie fra 2013 nevner at oksidativt stress etter trening minker med inntak av bikarbonat, men at årsaken ikke kommer av økt antioksidantaktivitet, men av økt TBARS og Monicyte expressend heat-shock protein. http://www.ncbi.nlm.nih.gov/pubmed/22610152

Studie fra 2012 som viser at kronisk tilførsel av bikarbonat fungerer like bra som akutt. http://www.ncbi.nlm.nih.gov/m/pubmed/23001395

Studie fra 2013 som viser at bikarbonat oksygenmetningen høy under trening. http://www.ncbi.nlm.nih.gov/m/pubmed/23903526

Studie fra 2008 som nevner at en pre-alkalisering bedrer restitusjonen etter trening, både ved aktiv og ved passiv restitusjon. http://www.ncbi.nlm.nih.gov/m/pubmed/18004683

En studie fra 2011 mener at bikarbonat har ingen effekt på trening. http://www.ncbi.nlm.nih.gov/m/pubmed/21465247

Meta-analyse så på 58 studier, fra 2010 som mener man kan ta 0,3-0,5g/kg for å øke prestansjon med 1,7%. http://www.ncbi.nlm.nih.gov/pubmed/21923200

Studie fra 1999 som forteller at ved sykkelritt opp til 60 minutter vil bikarbonat gjøre at man får større utholdenhet, utmattelse utsettes. http://www.ncbi.nlm.nih.gov/m/pubmed/10367725/

Nettside som forteller om bivirkninger m.m. relatert til bikarbonat mot sure oppstøt. http://www.nlm.nih.gov/medlineplus/druginfo/meds/a682001.html

MEDISIN

En studie fra 2000 nevner at det kan brukes for å dempe metabolsk acidemia, men ikke til å fjerne melkesyre. http://www.ncbi.nlm.nih.gov/pubmed/10631227

I medisin kan det brukes i akutt behandling av f.eks. sjokk hvor kroppen går inn i alvorlig acidose, under 7,15. http://www.ncbi.nlm.nih.gov/pubmed/18614899

En studie fra 2013 nevner at bikarbonatinntak demper nyresteinproduksjon etter bare 3 dager, når det gjelder citrat-relaterte steiner. Men pasienter med rene urinsyresteiner vil nok ikke ha like god effekt. http://www.ncbi.nlm.nih.gov/pubmed/23602798

En studie fra 2013 bekrefter at bikarbonat er nyttig for å forhindre komplikasjoner ved nyresvikt. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3729547/

KREFT

Kreftsvulster har en pH på 6,5-6,8, mens normalt vev har en pH på 7,35-7,45. Det sure mijøet i kreftsvulster gjør at de blir mer resistente mot medisiner.

En studie fra 2010 undersøkte muligheten for å endre pH rundt kreftsvulster for å hemme veksten og spredningen. Nevner at inntak av bikarbonat hos mus gjør dette. http://www.ncbi.nlm.nih.gov/pubmed/21155627

En studie fra 2011 nevner at bikarbonat i kreftbehandling er upålitelig. Av en eller annen grunn klarte ikke forskerene å oppnå alkalose i musene. Selve kreftsvulsten blie ikke særlig påvirket, men spredning ble dempet og overlevelse økte for musene i denne studien. http://www.ncbi.nlm.nih.gov/pubmed/21663677

Denne studien fra 2009 nevner at bikarbonat inntak øker pH i kreftceller og hemmer spredning hos mus. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2834485/

Studie fra 2013 nevner at bikarbonatinntak øker pH i kreftcellen, som igjen øker opptaket av askorbinsyre og dermed hemmes HIF-1 og kreftens evne til overlevelse. http://www.ncbi.nlm.nih.gov/pubmed/23916956

Studie fra 2013 som viser hvordan bikarbonat og en systemisk høy pH hindrer kreftspredning. http://www.ncbi.nlm.nih.gov/m/pubmed/23936808

ARTIKLER

http://suppversity.blogspot.no/2011/11/baking-soda-for-stressed-white-blood.html

http://www.collective-evolution.com/2012/05/06/baking-soda-is-proving-to-be-an-effective-treatment-for-cancer/

http://articles.mercola.com/sites/articles/archive/2012/08/27/baking-soda-natural-remedy.aspx

http://en.wikipedia.org/wiki/Sodium_bicarbonate

Full gjennomgang av natriumbikarbonats toksisitet her: http://www.inchem.org/documents/sids/sids/sodbicarb.pdf 

«The uptake of sodium, via exposure to sodium bicarbonate, is much less than the uptake of sodium via food. Therefore, sodium bicarbonate is not expected to be systemically available in the body. Furthermore it should be realised that an oral uptake of sodium bicarbonate will result in a neutralisation in the stomach due to the gastric acid. » …viser desverre ikke til noe referanse for dette utsagnet.

Natrium er ca. 1/4 av natriumbikarbonat (NaHCO3), så når vi spiser 4g Natron, får vi i oss ca.1g natrium. Maksimumsgrensen for natrium er 5g, som innbærer 20g Natron. http://www.helsekostopplysningen.no/Innhold/Kost–Kosttilskudd/Vitamniner-og-mineraler/Mineraler-og-sporstoffer-/Natrium-Na–Engelsk-Sodium-/

Denne fra 1984 nevner at natriumbikarbonat (baking soda) kjøpt i butikken er bare 3% av prisen av det vi får kjøpt på apotek, men like trygt og effektivt. http://www.ncbi.nlm.nih.gov/pubmed/6319065

Om man har lite magesyre fra før av kan det gir ubehag når man spiser natron og får enda mindre magesyre. En enkel måte å teste dette på er å ta 1ts natron i et halvt glass før mat om morgenen. Om du raper innen 5 min så har du nok magesyre. Bikarbonatet reagerer med magesyren og gir kullsyre. Og derfor raper du. Med lite magesyre blir det ikke laget nok kullsyre til å stimulere raping.