Blodet i din kropp

För att fungera behöver du syre. När du håller andan får du klara dig på det syre du har i kroppen. Ungefär hälften av dina syrereserver finns i lungan - den andra hälften i blodet. En normalvuxen man kanske har 5 liter blod i kroppen. Nu är det inte blodet som är primärintresset för en fridykare utan syret i blodet.
Kroppens celler förbrukar kontinuerligt syrgas och producerar koldioxid som en biprodukt av metabolismen i en process som kallas cellandningen.

Syrets väg
När man tar ett andetag förs luftens syre till lungblåsorna och diffunderar genom dess väggar till lungkapillärerna för att binda sig till de röda blodkropparnas hemoglobin. (
Hemoglobinet är ett äggviteämne som finns i de röda blodkropparna och ger blodet dess rödaktiga färg). Syret färdas sedan i blodet till största del bundet i hemoglobin (som finns i de röda blodkropparna). Syret "släpps av" ute i vävnaderna i kroppen. Blodet transporterar koldioxid (ofta i form av bikarbonat och kolsyra) tillbaka till lungan där det vädras ut.

Syreåtgång
En kropp i vila gör ungefär av med 250ml syre i minuten. Ungefär 30% av det är hjärnans förbrukning. En liter luft innehåller ungefär 200 ml syre.I vila transporterar blodet varje minut en liter syre ut i kroppen, utav detta förbrukas en fjärdedel (0,25 liter). Blodet som återvänder, dvs. venblodet, har då en syremättnad på cirka 75 procent. Hos en vältränad människa kan syreförbrukningen ökas med 15 gånger, det går då åt 3,75 liter syre per minut. Detta kan åstadkommas genom att hjärtat ökar mängden blod den transporterar varje minut med 5 ggr och utnyttjandegraden med 3ggr, dvs. venblodet har en syremättnad omkring 25 procent. Liknande sker vid andhållning, venblodets syremättnad sjunker och tar några minuter att återställa.

Vatten
Hälften av ditt blod utgörs av vatten. Din kropp kropp innehåller ute i vävnaderna ytterligare 40-50 liter vatten. Syre löses inte så lätt i vatten, men 5% av ditt syre finns ändå i det vattnet. När du går under 80% i syrenivåer börjar kroppen använda sig av det syret (taxera). Det tar minst 30 minueter att återställa just den reserven! Viktigt att veta är att blod har ett pH värde (syra-bas värde). Kolsyran som låses i blodet under andhållning gör blodet surt - för en fridykare är detta till viss del positivt då det ökar kroppens förmåga att "ta upp" syre. För mer resonemang kring syre och andhållning fortsätt här, annars läs vidare om blod.

Niacin också kallad Vitamin B3
Denna substans är bra för hjärtat och blodcirkulationen (syresättning) och är kraftigt kärlutvidgande. Kapillärerna är så små att blodceller i bland bara kan passera en och en och ibland kan det bli stopp. Stora organ får sitt blod garanterat via de stora artärerna, men stora delar av kroppen (som huden) får sitt blod (sitt syre och sin energi) från kapillärerna. Niacin eller B-3 vitaminen vidgar dom små kapillärerna. B-3 finns i magert kött. Niacin ökar alltså ämnesomsättningen så det är inget att ta just innan statiskt, men den hjälper dig att syresätta din kropp bättre.
Notera att en effekt som yttrar sig efter att man intagit B3 är en obehaglig brännande känsla i huden i upp till en 1/2 timme efter intagandet. Symtom på överdosering : Mycket stora doser kan medföra skador på bukspottskörtel, lever och gallblåsa. Nikotinamid medför depression hos vissa personer.

Blodtrycket
Är det bra att ha lågt blodtryck som fridykare? Som med så många andra faktorer finns de positiva och negativa effekter av ett specifikt tillstånd.

Fridykargurun Eric Fattah skriver förljande: Low BP:
- Reduces oxygen consumption (extending apnea)
- Increases risk of BO from packing or deep inhales
- Increases susceptibility to dizziness from hyperventilating
- Increases risk of BO at end of apnea

High BP:
- Increases rate of O2 consumption (decreasing apnea length)
- Decreases risk of BO from packing
- Decreases susceptibility to dizziness from hyperventilating
- Decreases risk of BO at end of apnea

However, BP can be manipulated with garlic, onions, cruciferous veggies, licorice, salt, potassium, magnesium, calcium, carbs and water.

The Physiological role of Iron in the body.
Klaas Feenstra

Iron doesn’t have only a vital role as a carrier of oxygen to the tissues from the lungs; it is also important as a transport medium for electrons within cells and as an integrated part of important enzyme reactions in various tissues.
To illustrate this, I will give the figures where the Iron is in a average 75kg Male; there is about 4000mg Iron in the whole body, 73% of that is functional iron, the rest is iron stored in Ferritin and Haemosiderin. The functional Iron can be divided in four groups, respectively Haemoglobin (60%), Myoglobin (9%), Haem and non-haem enzymes (4%) and Transferrin-bound Iron (>1%), all percentage are from the available total iron.

Iron metabolism exist of two loops, one external and one internal, respectively the iron in the red blood cells which normally die and are replaced after 120 days and where Iron is re-used through macrophages and transferrin transport. Iron is lost by cell losses, including bleeding and the continue process of replacing the surfaces of the body.

On a average level, 18+ males need a median absorbed dose of 1.05 mg/day, 18+ females need a median absorbed dose of 1.46 mg/day.

Iron Absorption
There are two kinds of iron in the diet with respect to the mechanism of absorption – haem iron and non-haem iron, utilising two separate types of receptor on the mucosal cells.

The amount of uptake is dependent of Dietary factors, summarising:

Haem iron absorption
- Amount of haem iron present in meat
- Content of calcium in meal. Calcium inhibits iron uptake
- Food preparation (time, temperature), Higher temperature and longer time degrades haem iron into non-haem iron

Non-haem iron absorption
- Iron status in subjects (Iron deficit subjects will uptake more Iron a normal subject)
- Amount of bio available non-heam iron (adjustment for fortification and contamination iron)
- Balance between dietary factors enhancing and inhibiting iron absorption

Factors enhancing iron absorption
- Ascorbic Acid
- Meat, Fish, Seafood (Iron supplements intake with Meat, Fish and Seafood, is by an unknown process better absorbed than without)
- Certain organic acids

Factors inhibiting iron absorption
- Phylates (Bran, Bread, Oats, can be partially counteracted by Ascorbic Acid)
- Iron-binding phenolic compounds (tea, coffee, cocoa, spinach, several herbs and spices)
- Calcium (Milk, cheese etc.)
- Soy protein

It could be concluded that concerning iron absorption is dependant of the overall diet. For example, it is none that especially in developing countries, drinking tea with main meals is probably an important factor contributing to a high prevalence and severity of Iron deficiency.

Iron Deficiency and Iron-Deficiency Anaemia

These concepts are often incorrectly used as synonyms. Commonly, iron deficiency refers to the lack of iron available in the body, or available by absorption. In Iron-Deficiency Anaemia, there is not enough Iron available for the red bloodcells, for example due to a transferrin related problem. It can be caused by Iron Deficiency, but it doesn't have to. Measuring Hb/Ht doesn't really give a clear figure what the amount of ferrine in the body is, and if it is the cause to an anaemia.

Causes of iron deficiency

The most common cause of iron deficiency is a nutritional deficiency. Nutritional iron deficiency implies that the diet cannot cover physiological iron requirements. World-wide, this is the most common cause of iron deficiency, although there are also pathological causes as, but not limited to hookworm, gluten enteropathy or in patients who undergone gastric surgery.

Deleterious effects of iron deficiency

In summary, the effects of iron deficiency are larger then only the well-known anaemia. There is also an relationship between iron deficiency and brain function and the immunological response of the T-lymphocytes can become impaired (phagocytosis and killing of bacteria).

Treatment

The cause of an iron-deficiency anaemia may be purely nutritional, i.e. the diet cannot cover the physiological losses of the subject. To treat a patient with a moderate iron-deficiency anaemia only by improving the diet would take a very long time, probably several years. A good diet is important for the prevention of iron deficiency but is not sufficient for the treatment of an existing iron-deficiency anaemia. Oral iron therapy is usually very effective if well absorbed iron tablets are given at sufficient dosage for a sufficiently long time.

Motivating the patient, by explaining why and how the tablets should be taken, is essential for an effective treatment. Sometimes a therapeutic failure is caused by the poor properties of the iron tablets. The coating of iron tablets must be sufficiently good to prevent oxidation of the ferrous iron to ferric, but at the same time not too resistant to allow the tablets to disintegrate and be dissolved in the gastrointestinal tract.

Parental iron preparations an also be used. Because of their potentially more sever side-effects and risks, they should only be used in patients who cannot absorb iron because of malabsorption, in patients with inflammatory intestinal disorders and in patiens with more marked side-effects from oral iron, such as consistent nausea and epigastric pain which cannot be ameliorated by reducing the dose of oral iron.

On overdose of iron:

Unbelievable or not, even iron can lethal in to high dosages. The acute lethal dose in adults is at 180-300 mg iron per kg body weight. You can’t live without Iron, but too much can kill you in a very nasty way.

As a Final note; This reply on the topic should not be used as a blueprint for treatment of anaemia. If you are anaemic and have problems with it, the person you should see is your General Practitioner, who can a. treat you better than with the most iron tablets found in the average store, and b. can exclude any pathological cause to anaemia.

Sources:
JS Garrow, WPT James and A Ralph. Human Nutrition and Dietetics, 10th edition, published by Churchill Livingstone, London pg. 177-192
CH, Farmacotherapeutisch Komas 2002 pg. 213-218
RS Cotran, V Kumar and T Collins. Robbins Pathologic Basis of Disease, 6th edition, published by W.B. Saunders Company, London, pg. 627-630