Coral Calcium

I just got done reading the “Reader Mail” of this weeks issue. I am not looking to start and argument but I think that showing a different view point on Coral Calcuim is in order. I worked with several Nutritional Biochemists and the basis of all their nutritional programs was Coral Calcuim. Not for the calcuim itself, hell they even told me there was a better way of getting it, but because it alkalizes the blood.
If the body gets too acidic then the uptake of nutrition and the function of the entire body is slowed down. To relate that to all T-Men/Women, it means fewer gains.
I used the Coral during my employment these unique individuals and found that my recovery times shortened, my energy had increased and I slept very well.
Now I am not saying this is great, but from what I have seen with the patients at the clinic and with using it myself it has benifits.

 Just thought everyone should know.

Take Care,
Travis Gordon

"Not for the calcuim itself, hell they even told me there was a better way of getting it, but because it alkalizes the blood.
If the body gets too acidic then the uptake of nutrition and the function of the entire body is slowed down. "

Quackery alert…

BTW, have you heard of the placebo effect?

-Zulu

Calcium carbonate is not very efficient in alkalizing your body PH. Calcium, magnesium, potassium or sodium in either the citrate (preferable) or bicarbonate forms will work quite well.

Restless, that didn’t make much sense…firstly carbonate will become bicarbonate at physiological pH. Carbonate alkilizes your body by becoming bicarbonate.

CO2 <=> HC03(-) <=> H2CO3

2ndly, citrate is an acid with pKa’s of 3.13, 4.76, and 6.40…which means it stays acidic (ie. gives up protons) at physiological pH’s (7.2-7.4). So these citrates will make blood pH more acidic.

Also, it’s well known the best method of calcium supplementation is Calcium Carbonate (ie. TUMS). In fact, that’s what doctors often perscribe for patients with osteoperosis.

Alkalizing your body PH is BS though.

-Zulu

To step in, I’m very skeptical of supplements, but the coral calcium seemed to help with some chronic inflammation in my left shoulder. Within 5-6 days os starting it, the pain was gone. I have access to ART, but not often enough, microcurrent, interferential stimulation, Wobenzyme(zilch in results, I think it’s a waste of money), and of course rehab exercises, ice etc. The studies can say what they like, but it helped me. Curing cancer, I’m skeptical. Good source of calcium, probably.
A few pts. that tried it gave me some positive feedback also.
Here are a few other things that don’t work according to studies: myostat, chiropractic, the atkins’ diet, bands, weight training for athletes, stretching, etc. Try it with an open mind, it helped me.

ND, you made a great point. Though, I heard that the Cal carbinate is a rather large molecule and it takes longer for uptake? I have heard that as an alternative to that Calcium Hydroxyapitae is perfered because of the smaller molecule and the tendancy to breakdown quickly and easily for absorption.

Irondoc, I am glad to see that someone has give this a shot. Your point about what WAS considered to be non-accepted and is now common place holds true to alot of things. Nutrition and trainning alike!

Keeping in mind that most “popular” science and medical publications are influenced by those in power (AMA and Pharmacutical Companies) and are thus showing mostly one point of view. Especially when it comes to alternative practices (nutrition and complimentary medicine).

The comment about Coral Calcuim not curing cancer is true. Although, since caner thrives in an anaerobic enviornment(this was proven in 1932 by German researcher Otto Warburg, who won the Nobel Prize for this research) and since Coral Calcuim and other foods/supplements that alkalize the blood help to oxygenate the blood and tissues, it kind of goes without saying that this would be a good ADDITION to ones diet for fight/prevent cancer. No one thing is a end-all-be-all. Its a matter of getting the body balanced via nutrition, physical activies, emotion, and the clearing of physical truma that will facilitate healing.

I ask if the online administrators could chime in on this. Having the opinion of the T-Mag staff and the guest writers would be great.

P.S.
I am not trying to argue on the subject. I just think that both sides should be equally represented.

Travis Gordon

Calcium Carbonate (CaCO3) is actually not a molecule at all. It ionizes when dissolved in solution into C03(2-) + Ca2+…which then reaches equilibrium with CO2 and HCO3, and H2CO3 rapidly.
Calcium Hydroxyapitae also ionizes, but hydroxyapitae is a much larger ion and likely requires active transport to cross the membrane. Ca2+ and CO3(2-) and it’s equilibria partners are readily controlled via numerous ion channels and exchangers! (Ahhh…home!)

Travis, it’s not just IronDoc that has has a positive experience with Coral Calcium. Mike Mahler has also, if I remember correctly. It’s been discussed here on the forum numerous times.

Everything I read is that calcium is calcium and that some forms are just more bioavailable than others. However, anecdotally, there are strong advocates in athletic and powerlifting circles, as well as many in the general population.

I think it wise to look at all angles on something such as this. Believe me, if I had cancer, I would try everything, including cranking up the coral calcium. If anyone has read Lance Armstrongs, It’s Not About the Bike, you’ll see he was alittle obsessive and he did okay.

ND,

Actually potassium citrate has been shown to produce a mild transient metabolic alkalosis(4). I do not know the exact mechanisms of actions as chemistry is not my field but I can tell you that it’s possible to alkalize your urine PH trough the ingestion of citrate forms of the aforementioned minerals. If it actually has some benefit is where the debate is…

But anyway, this is not related tyo the original topic but mild metabolic acidosis should actually be of some concern to all bodybuiders since high protein, high grain, low vegetable and fruit diets, coupled with lactic acid production resulting from training and in some cases high intakes of diet sodas rich in phosphorous lead easily to a elevated PH in tissues, not in the blood where it is very efficiently controled.

This usually mild metabolic acidosis will lead to increased cortisol levels (1), decreased protein synthesis (2) and decreased serum IGF-1 (3).

There has been some research showing inproved performance resultant from ingestion of bicarbonate (5,6,7).

What led me to start controling urine’s PH was the increased cortisol and descreasesd protein synthesis bits,in all honesty with all the changes in diet, supplementation and exercise protocol latelly I can’t reallly tell if it actually did anything other than turning that fish tank PHtest solution blue when I piss on it. Still, minerals are cheap and I figured why not trying it?

1-Am J Physiol Renal Physiol 2003 Jan;284(1):F32-F40

Neutralization of Western diet inhibits bone resorption independently of K intake and reduces cortisol secretion in humans.

Maurer M, Riesen W, Muser J, Hulter HN, Krapf R.

Medizinische Universitatsklinik und Zentrallabor, Kantonsspital Bruderholz, CH-4101 Bruderholz/Basel; Institut fur klinische Chemie und Hamatologie, Kantonsspital, CH-9007 St. Gallen, Switzerland; and Genentech, Incorporated, South San Francisco, California 94080-4990.

A Western-type diet is associated with osteoporosis and calcium nephrolithiasis. On the basis of observations that calcium retention and inhibition of bone resorption result from alkali administration, it is assumed that the acid load inherent in this diet is responsible for increased bone resorption and calcium loss from bone. However, it is not known whether the dietary acid load acts directly or indirectly (i.e., via endocrine changes) on bone metabolism. It is also unclear whether alkali administration affects bone resorption/calcium balance directly or whether alkali-induced calcium retention is dependent on the cation (i.e., potassium) supplied with administered base. The effects of neutralization of dietary acid load (equimolar amounts of NaHCO(3) and KHCO(3) substituted for NaCl and KCl) in nine healthy subjects (6 men, 3 women) under metabolic balance conditions on calcium balance, bone markers, and endocrine systems relevant to bone [glucocorticoid secretion, IGF-1, parathyroid hormone (PTH)/1,25(OH)(2) vitamin D and thyroid hormones] were studied. Neutralization for 7 days induced a significant cumulative calcium retention (10.7 +/- 0.4 mmol) and significantly reduced the urinary excretion of deoxypyridinoline, pyridinoline, and n-telopeptide. Mean daily plasma cortisol decreased from 264 +/- 45 to 232 +/- 43 nmol/l (P = 0.032), and urinary excretion of tetrahydrocortisol (THF) decreased from 2,410 +/- 210 to 2,098 +/- 190 &mgr;g/24 h (P = 0.027). No significant effect was found on free IGF-1, PTH/1,25(OH)(2) vitamin D, or thyroid hormones. An acidogenic Western diet results in mild metabolic acidosis in association with a state of cortisol excess, altered divalent ion metabolism, and increased bone resorptive indices. Acidosis-induced increases in cortisol secretion and plasma concentration may play a role in mild acidosis-induced alterations in bone metabolism and possibly in osteoporosis

2-Swiss Med Wkly 2001 Mar 10;131(9-10):127-32

Metabolic and endocrine effects of metabolic acidosis in humans.

Wiederkehr M, Krapf R.

Medizinische Universitatsklinik Bruderholz, Bruderholz/Basel, Switzerland.

Metabolic acidosis is an important acid-base disturbance in humans. It is characterised by a primary decrease in body bicarbonate stores and is known to induce multiple endocrine and metabolic alterations. Metabolic acidosis induces nitrogen wasting and, in humans, depresses protein metabolism. The acidosis-induced alterations in various endocrine systems include decreases in IGF-1 levels due to peripheral growth hormone insensitivity, a mild form of primary hypothyroidism and hyperglucocorticoidism. Metabolic acidosis induces a negative calcium balance (resorption from bone) with hypercalciuria and a propensity to develop kidney stones. Metabolic acidosis also results in hypophosphataemia due to renal phosphate wasting. Negative calcium balance and phosphate depletion combine to induce a metabolic bone disease that exhibits features of both osteoporosis and osteomalacia. In humans at least, 1,25-(OH)2 vitamin D levels increase, probably through phosphate depletion-induced stimulation of 1-alpha hydroxylase. The production rate of 1,25-(OH)2 vitamin D is thus stimulated, and parathyroid hormone decreases secondarily. There is experimental evidence to support the notion that even mild degrees of acidosis, such as that occurring by ingestion of a high animal protein diet, induces some of these metabolic and endocrine effects. The possible role of diet-induced acid loads in nephrolithiasis, age-related loss of lean body mass and osteoporosis is discussed.

3-Kidney Int 1997 Jan;51(1):216-21

Effect of chronic metabolic acidosis on the growth hormone/IGF-1 endocrine axis: new cause of growth hormone insensitivity in humans.

Brungger M, Hulter HN, Krapf R.

Klinik B fur Innere Medizin, Kantonsspital, St. Gallen, Switzerland.

The effects of metabolic acidosis on growth hormone and IGF-1 are poorly understood. We investigated the effects of chronic metabolic acidosis (induced by administration on NH4Cl, 4.2 mmol/kg body wt/day) on the growth hormone/IGF-1 endocrine axis in 6 normal male volunteers during metabolic balance conditions. NH4Cl administration resulted in hyperchloremic metabolic acidosis with plasma bicarbonate decreasing from 25 +/- 0.4 to 15.5 +/- 0.9 mmol/liter (P < 0.001). Metabolic acidosis significantly decreased serum IGF-1 concentration from 45 +/- 6 to 33 +/- 6 nmol/liter (P = 0.002), while serum IGF binding protein 3 concentration was not affected significantly. The growth hormone response to growth hormone releasing factor administration (1 microgram per kg body wt, intravenous bolus) was enhanced significantly during acidosis. The IGF-1 response to growth hormone administration (0.1 U kg body wt subcutaneously, every 12 hr for 48 hr) was blunted significantly during acidosis. Apparent endogenous serum half-life and metabolic clearance rates of growth hormone were not altered significantly by acidosis. Metabolic acidosis in humans results in a significant decrease in serum IGF-1 concentration without a demonstrable effect on IGF binding protein 3, and is related to a resistance to the hepatocellular action of growth hormone. The primary defect in the growth hormone/IGF-1 axis occurs via an impaired IGF-1 response to circulating growth hormone with consequent diminution of normal negative feedback inhibition of IGF-1 on growth hormone, as evidenced by the exaggerated growth hormone response to growth hormone releasing factor administration.

4-[Therapeutic use of potassium citrate]

[Article in Polish]

Zmonarski SC, Klinger M, Puziewicz-Zmonarska A, Krajewska M, Mazanowska O, Dembinska E.

Klinika Nefrologii Akademii Medycznej we Wroclawiu Kierownik Kliniki. klinef@priv2.onet.pl

Therapeutic indications of potassium citrate include: 1. Oxaluric renal stone disease and some cases of uric acid stone disease. Prevention of stone formation in patients with renal polycystic disease. Prevention of stone relapse after ESWL or lithotomy; 2. Distal renal tubular acidosis complicated by hypercalciuria, mainly in children. 3. Renal hypercalciuria and hyperoxaluria. 4. Prevention of renal complications at the time of glaucoma treatment with acetazolamide. 5. Potassium supplementation during treatment of hypertension. Potassium citrate is usually contraindicated in the case of: 1. Urinary tract infection. 2. Struvite renal stone disease. 3. Hyperpotassemia and advanced chronic renal failure. 4. Peptic ulcer or gastritis. 5. Gastrointestinal bleeding. 6. Disorders of coagulation, crural varices. 7. Metabolic alkalosis. Potassium citrate, when used at therapeutic doses, is to be considered as quite safe. The average daily dose even if admitted as a single dose day engages 60-75% of free renal capacity for potassium excretion. Physiologic and therapeutic citrate concentration in urine exceeds much those available for other inhibitors. The therapeutic dose does not induce any significant changes in any biochemical or endocrine parameter of blood except mild transient metabolic alkalosis. The decrease of urine calcium and increase in oxalate calcium phosphate excretion is observed. In hypo-cytriaturic patients the response to therapeutic dose of citrate is smaller. One-year remission of stone disease is observed in 70-75% cases.

5-Effects of Bicarbonate Ingestion on Leg Strength and Power During Isokinetic Knee Flexion and Extension
Jeff Coombes and Lars R. McNaughton

Human Performance Laboratory, Centre for Physical Education, University of Tasmania at Launceston, Newnham, Tasmania, Australia 7250.

ABSTRACT

The aim of this experiment was to determine whether sodium bicarbonate ingestion of a 300 mg ? kg1 body mass dose improved either total work or peak torque values during isokinetic leg ext/flex exercise in 9 healthy male subjects using a Cybex 340 isokinetic dynamometer under control, alkalotic, and placebo conditions. Basal and pre- and postexercise arterialized venous blood samples were collected and analyzed for lactate, pH, partial pressure of O2 and CO2, base excess, and blood bicarbonate. Preexercise, the bicarbonate increased the blood pH levels, indicating a state of induced metabolic alkalosis. Postexercise in all conditions, blood pH was significantly lower than preexercise values, indicating that metabolic acidosis had occurred. The amount of work and peak torque completed in the control and placebo trials was not significantly different. During the experimental trial, however, more work was completed than in either the control or placebo conditions, and peak torque also increased. This suggests that bicarbonate could be used as an ergogenic aid during isokinetic work and enables the athlete to become more powerful.

6-Exercise Physiology Laboratory, University of Louisville, Louisville, Kentucky 40292

ROBERT J. ROBERTSON

Center for Exercise and Health-Fitness Research, University of Pittsburgh, Pittsburgh, Pennsylvania 15261

ABSTRACT

In this investigation we studied the effect of manipulating the acid-base balance through sodium bicarbonate (NaHCO3) ingestion on ratings of perceived exertion for the overall body (RPE-O) and on differentiated ratings for the leg and chest (RPE-L, RPE-C) during exercise recovery. Six women of college age underwent 3 experimental conditions in which NaHCO3 was ingested in either a single (bolus) or periodic (distributed throughout the exercise) dosage, with calcium carbonate serving as a placebo control. Each subject pedaled a cycle ergometer at 90% O2peak for three 5-minute exercise sessions, each separated by 10 minutes of recovery. Repeated-measures analysis of variance with Tukey post hoc analysis was performed for acid-base and perceptual variables. Results indicate that a gradient of acid-base balance was established such that pH and bicarbonate concentration were significantly greater (p < 0.05) for the single condition in comparison with periodic and placebo conditions, and the periodic condition was significantly greater (p < 0.05) than placebo. The average percentage of recovery for RPE-L and RPE-C was 8% greater (p < 0.05) for the single condition than for the periodic and placebo conditions, at the first and second minutes of recovery. During the first minute of recovery, the average percentage of recovery for RPE-O was 10% greater (p < 0.05) for the single condition than for the placebo condition. During the second minute of recovery, the percentage of recovery for RPE-O for the single condition was significantly greater than those for both the periodic and placebo conditions by an average of 9%. These results strengthen the relationship between the acid-base balance and the subjective perception of exertion. In addition, this study provides preliminary data in support of RPE as an adjunct measure to quantify the extent of recovery from exercise.

7-Sodium bicarbonate can be used as an ergogenic aid in high-intensity, competitive cycle ergometry of 1 h duration.

McNaughton L, Dalton B, Palmer G.

Sports Science, Kingston University, Kingston upon Thames, Surrey, UK.

The aim of this study was to determine whether a dose of 300-mg x kg(-1) body mass of sodium bicarbonate would effect a high-intensity, 1-h maximal cycle ergometer effort. Ten male, well-trained [maximum oxygen consumption 67.3 (3.3) ml x kg(-1) x min(-1), mean (SD)] volunteer cyclists acted as subjects. Each undertook either a control (C), placebo (P), or experimental (E) ride in a random, double-blind fashion on a modified, air-braked cycle ergometer, attached to a personal computer to which the work and power data was downloaded at 10 Hz. Fingertip blood was sampled at 10-min intervals throughout the exercise. Blood was also sampled at 1, 3, 5, and 10 min post-exercise. Blood was analysed for lactate, partial pressure of Carbon dioxide and oxygen, pH and plasma bicarbonate (HCO-) concentration. Randomly chosen pairs of subjects were asked to complete as much work as possible during the 60-min exercise periods in an openly competitive situation. The sodium bicarbonate had the desired effect of increasing blood HCO3- prior to the start of the test. The subjects in E completed 950.9 (81.1) kJ of work, which was significantly more (F(2,27) = 5.28, P < 0.01) than during either the C [835.5 (100.2) kJ] or P [839.0 (88.6) kJ] trials. No differences were seen in peak power or in the power:mass ratio between these three groups. The results of this study suggest that sodium bicarbonate may be used to offset the fatigue process during high-intensity, aerobic cycling lasting 60 min.

The following was something I had saved and was taken from Dr. T Albers in Germany who is interested in the effects of metabolic acidosis in athletes. Here are a couple of abstracts followed by a reply from him.

The first suggests that a western diet may induce a state of chronic metabolic acidosis which could lead to a host of deleterious effects on muscle and bone. The second implicates a lowered IGF-1 response to GH, as well as increased glucocorticoid production, as primary culprits.

Athletes are of course even more prone to acute acidosis. Coupled with a low grade chronic acidosis this could compound the problem.

Dr. Albers believes that the administration of acid buffers should be a key element in an athlete’s nutritional strategy.

The degree of induced acidosis is probably responsible for the differing effects on the various hormones in each study.

Am J Physiol Renal Physiol 2003 Jan;284(1):F32-F40

Neutralization of Western diet inhibits bone resorption independently of K intake and reduces cortisol secretion in humans.

Maurer M, Riesen W, Muser J, Hulter HN, Krapf R.

Medizinische Universitatsklinik und Zentrallabor, Kantonsspital Bruderholz, CH-4101 Bruderholz/Basel; Institut fur klinische Chemie und Hamatologie, Kantonsspital, CH-9007 St. Gallen, Switzerland; and Genentech, Incorporated, South San Francisco, California 94080-4990.

A Western-type diet is associated with osteoporosis and calcium nephrolithiasis. On the basis of observations that calcium retention and inhibition of bone resorption result from alkali administration, it is assumed that the acid load inherent in this diet is responsible for increased bone resorption and calcium loss from bone. However, it is not known whether the dietary acid load acts directly or indirectly (i.e., via endocrine changes) on bone metabolism. It is also unclear whether alkali administration affects bone resorption/calcium balance directly or whether alkali-induced calcium retention is dependent on the cation (i.e., potassium) supplied with administered base. The effects of neutralization of dietary acid load (equimolar amounts of NaHCO(3) and KHCO(3) substituted for NaCl and KCl) in nine healthy subjects (6 men, 3 women) under metabolic balance conditions on calcium balance, bone markers, and endocrine systems relevant to bone [glucocorticoid secretion, IGF-1, parathyroid hormone (PTH)/1,25(OH)(2) vitamin D and thyroid hormones] were studied. Neutralization for 7 days induced a significant cumulative calcium retention (10.7 +/- 0.4 mmol) and significantly reduced the urinary excretion of deoxypyridinoline, pyridinoline, and n-telopeptide. Mean daily plasma cortisol decreased from 264 +/- 45 to 232 +/- 43 nmol/l (P = 0.032), and urinary excretion of tetrahydrocortisol (THF) decreased from 2,410 +/- 210 to 2,098 +/- 190 &mgr;g/24 h (P = 0.027). No significant effect was found on free IGF-1, PTH/1,25(OH)(2) vitamin D, or thyroid hormones. An acidogenic Western diet results in mild metabolic acidosis in association with a state of cortisol excess, altered divalent ion metabolism, and increased bone resorptive indices. Acidosis-induced increases in cortisol secretion and plasma concentration may play a role in mild acidosis-induced alterations in bone metabolism and possibly in osteoporosis

Swiss Med Wkly 2001 Mar 10;131(9-10):127-32

Metabolic and endocrine effects of metabolic acidosis in humans.

Wiederkehr M, Krapf R.

Medizinische Universitatsklinik Bruderholz, Bruderholz/Basel, Switzerland.

Metabolic acidosis is an important acid-base disturbance in humans. It is characterised by a primary decrease in body bicarbonate stores and is known to induce multiple endocrine and metabolic alterations. Metabolic acidosis induces nitrogen wasting and, in humans, depresses protein metabolism. The acidosis-induced alterations in various endocrine systems include decreases in IGF-1 levels due to peripheral growth hormone insensitivity, a mild form of primary hypothyroidism and hyperglucocorticoidism. Metabolic acidosis induces a negative calcium balance (resorption from bone) with hypercalciuria and a propensity to develop kidney stones. Metabolic acidosis also results in hypophosphataemia due to renal phosphate wasting. Negative calcium balance and phosphate depletion combine to induce a metabolic bone disease that exhibits features of both osteoporosis and osteomalacia. In humans at least, 1,25-(OH)2 vitamin D levels increase, probably through phosphate depletion-induced stimulation of 1-alpha hydroxylase. The production rate of 1,25-(OH)2 vitamin D is thus stimulated, and parathyroid hormone decreases secondarily. There is experimental evidence to support the notion that even mild degrees of acidosis, such as that occurring by ingestion of a high animal protein diet, induces some of these metabolic and endocrine effects. The possible role of diet-induced acid loads in nephrolithiasis, age-related loss of lean body mass and osteoporosis is discussed.

Kidney Int 1997 Jan;51(1):216-21

Effect of chronic metabolic acidosis on the growth hormone/IGF-1 endocrine axis: new cause of growth hormone insensitivity in humans.

Brungger M, Hulter HN, Krapf R.

Klinik B fur Innere Medizin, Kantonsspital, St. Gallen, Switzerland.

The effects of metabolic acidosis on growth hormone and IGF-1 are poorly understood. We investigated the effects of chronic metabolic acidosis (induced by administration on NH4Cl, 4.2 mmol/kg body wt/day) on the growth hormone/IGF-1 endocrine axis in 6 normal male volunteers during metabolic balance conditions. NH4Cl administration resulted in hyperchloremic metabolic acidosis with plasma bicarbonate decreasing from 25 +/- 0.4 to 15.5 +/- 0.9 mmol/liter (P < 0.001). Metabolic acidosis significantly decreased serum IGF-1 concentration from 45 +/- 6 to 33 +/- 6 nmol/liter (P = 0.002), while serum IGF binding protein 3 concentration was not affected significantly. The growth hormone response to growth hormone releasing factor administration (1 microgram per kg body wt, intravenous bolus) was enhanced significantly during acidosis. The IGF-1 response to growth hormone administration (0.1 U kg body wt subcutaneously, every 12 hr for 48 hr) was blunted significantly during acidosis. Apparent endogenous serum half-life and metabolic clearance rates of growth hormone were not altered significantly by acidosis. Metabolic acidosis in humans results in a significant decrease in serum IGF-1 concentration without a demonstrable effect on IGF binding protein 3, and is related to a resistance to the hepatocellular action of growth hormone. The primary defect in the growth hormone/IGF-1 axis occurs via an impaired IGF-1 response to circulating growth hormone with consequent diminution of normal negative feedback inhibition of IGF-1 on growth hormone, as evidenced by the exaggerated growth hormone response to growth hormone releasing factor administration.

Dr. Albers says,

"I think the metabolic acidosis of bodybuilders is very much underestimated. My athletes report better stamina and recovery from their workouts. As well there is better lactate tolerance. For myself I noted this as I forgot to take my buffering powder before training last week. I had the feeling all the time that ?this was really not my day?, my power wasn?t so good, every exercise a rep less than usual. Then I recognized what I had forgotten?
First: All enzymes in the body work best only at a pH-optimum (this is a measurement of the grade of acidosis, pH 7 is neutral, under seven acidic, above seven alkaline). Any time when you ingest food, the minerals will be absorbed and phosphorus, chlorine and sulphur are known as acidic (producing H±ions), magnesium, potassium and sodium are known as alkaline minerals. Fruit and vegetables are typical alkaline foods while meat and fish as well as white flour products (white bread etc.) are acid producing. To eliminate the excess acids the body has to bind the H±ions to NH3 which it gets from catabolizing tissue (mostly muscle). Most bodybuilders produce lot of lactic acid while training, this is the first factor for the common acidosis, second is the protein-rich diet (remember that protein by itself isn?t acidic, because NH3 from the amino acids can act as a H±buffer, it?s the sulphur and phosphate content of the typical amino acids e.g. in meat, whey is better against acidosis because of a lesser content of these amino acids). Third factor is the common drinking of cola sodas (light or not), lots of phosphorus?Forth factor is late eating that gives the fermentation processes in the gut over night with late night food. So what to do?
My athletes have to check their urine pHs early in the morning. This should be about 7. All the bodies I have coached had less than 5,5 in the morning urine (keep in mind from pH 7 to pH 6 means 10 times more acidic!). So they have to take a moderate dose of buffering agents before sleeping to help the body getting rid of the acids over night without catabolizing muscle tissue. And the second time to take quite a lot of buffering powder is 30 minutes before training. The rest of the day they eat quite a lot of potatoes (3-5 lbs), because these are THE buffering food (lots of potassium in it) and veggies (1-2 lbs) together with meat or protein shakes. This normally eliminates the acidic excess from the animal foods.
So what to take. In Germany we have a product called Nemabas, which contains sodium bicarbonate, potassium bicarbonate, magnesium carbonate and calcium bicarbonate. For my athletes sort of ?I will never take salt in my food? with sky high aldosterone levels I recommend calcium citrate, potassium citrate and magnesium citrate (no sodium in it). Recently I read citrates are three times more effective in buffering than bicarbonate,can?t explain the mechanism why, have to dig further for that.
So what to do in the US? I would stay away from combinations with minerals in phosphate or chlorine form (less effective).
I have found one website in the US (http://www.shelbyhealth.com/othersup.htm) which sells caps with potassium, magnesium and calcium citrate (not mentioning the buffering capacities). Dosage? Probably about 10-20 caps before training (I take 10 g of mixed powder of these three forms and it works great. Some more reading about bicarbonate and buffering: Bicarbonate's Importance to Human Health
The common misconception that cheese is good for the bones is probably immortal, fruit and veggies rules for the bones!! Have to look for the cortisol mechanism, you?re right!

Hope this helps

Torsten

BTW an alkaline urine leads to less elimination of ephedrine products, so EC + buffering would be a great retard formula for stimulation?