J Appl Physiol. 2004 Jun;96(6):2050-6. Epub 2004 Feb 06. Related Articles, Links 

 
Metabolic effects of induced alkalosis during progressive forearm exercise to fatigue.

Raymer GH, Marsh GD, Kowalchuk JM, Thompson RT.

Department of Medical Biophysics, The University of Western Ontario, London, Ontario, Canada. graymer@lri.sjhc.london.on.ca

Metabolic alkalosis induced by sodium bicarbonate (NaHCO(3)) ingestion has been shown to enhance performance during brief high-intensity exercise. The mechanisms associated with this increase in performance may include increased muscle phosphocreatine (PCr) breakdown, muscle glycogen utilization, and plasma lactate (Lac(-)(pl)) accumulation. Together, these changes would imply a shift toward a greater contribution of anaerobic energy production, but this statement has been subject to debate. In the present study, subjects (n = 6) performed a progressive wrist flexion exercise to volitional fatigue (0.5 Hz, 14-21 min) in a control condition (Con) and after an oral dose of NaHCO(3) (Alk: 0.3 g/kg; 1.5 h before testing) to evaluate muscle metabolism over a complete range of exercise intensities. Phosphorus-31 magnetic resonance spectroscopy was used to continuously monitor intracellular pH, [PCr], [P(i)], and [ATP] (brackets denote concentration). Blood samples drawn from a deep arm vein were analyzed with a blood gas-electrolyte analyzer to measure plasma pH, Pco(2), and [Lac(-)](pl), and plasma [HCO(3)(-)] was calculated from pH and Pco(2). NaHCO(3) ingestion resulted in an increased (P < 0.05) plasma pH and [HCO(3)(-)] throughout rest and exercise. Time to fatigue and peak power output were increased (P < 0.05) by approximately 12% in Alk. During exercise, a delayed (P < 0.05) onset of intracellular acidosis (1.17 +/- 0.26 vs. 1.28 +/- 0.22 W, Con vs. Alk) and a delayed (P < 0.05) onset of rapid increases in the [P(i)]-to-[PCr] ratio (1.21 +/- 0.30 vs. 1.30 +/- 0.30 W) were observed in Alk. No differences in total [H(+)], [P(i)], or [Lac(-)](pl) accumulation were detected. In conclusion, NaHCO(3) ingestion was shown to increase plasma pH at rest, which resulted in a delayed onset of intracellular acidification during incremental exercise. Conversely, NaHCO(3) was not associated with increased [Lac(-)](pl) accumulation or PCr breakdown.

PMID: 14766777 [PubMed - in process]

I do wonder about this study a bit though because they did not compare another mineral. Given sodiums involvement in motor-ion channels it might have been the sodium and not the alkanosis that increase muscular performance.

I definitely notice enhanced strength when taking larger doses of Calcium Carbonate about an hour before workout.

hmmm...do you think calcium carbonate might illicit a similair response due to its major contribution to muscle contraction?

Studies that have compared doses indicate that the optimal dose for performance is in the .4-.6 g/kg range. One study found that .6 g/kg of sodium citrate lead to the optimal changes in blood pH, while another found improved one minute spring performance in the .3-.5 g/kg range, with the greatest effect at .5 g/kg [1]. Another study reports that .5 g/kg sodium citrate is the ideal amount for changing blood pH [2]. For sodium bicarbonate, the lowest reported effective dose was .2 g/kg in one trial [1]. However, other literature indicates that .3 g/kg is not as effective as higher doses [3], and most studies utilize .3-.5 g/kg. It would appear that from a performance standpoint, .5 g/kg of either substance is optimal, while .3 g/kg, and possibly .2 g/kg, can still be of benefit. Doses lower than this are unlikely to change pH enough to significantly improve performance.

Research has also been done on the optimal timing of ingestion, which falls in the range of 1-3 hours before exercise [7]. In one study, ingestion of .5 g/kg sodium citrate lead to an optimal alkalotic state 100-120 minutes after ingestion [2] – but one must keep in mind that having this period coincide with the later period of exercise would be ideal, so for a 45 minute training session, for example, one would want to consume the buffering agent 80-90 minutes before exercise.

The performance standpoint is not the only one that should be taken into consideration. Reports indicate that gastrointestinal discomfort is quite common, although it generally occurs in the first hour after ingestion, and therefore shouldn't coincide with the exercise period [2]. The best way to reduce this side effect is by lowering the dose. Reports of gastrointestinal discomfort and stomach cramps are much more common after .6 g/kg sodium citrate than .4 g/kg (five of eight subjects complaining versus two of eight) [1]. This effect may also be worse with sodium bicarbonate [2]. In three trials with .5 g/kg sodium citrate, one reports GI discomfort in 3 of 8 subjects while the other two report no problems [2]. It would appear that .4 g/kg sodium citrate is a relatively comfortable dose, with .5 g/kg still being tolerable to many. Since individual reactions can vary, experimentation is necessary to determine the highest tolerable dose.

A final issue is whether or not chronic ingestion is superior to acute ingestion. To answer this question, a study was conducted comparing .5 g/kg sodium bicarbonate acutely or over a period of six days on 90 second maximal cycling performance. Both groups had improved performance, but performance was still increased two days after chronic supplementation was discontinued [8]. This indicates that chronic ingestion of buffering agents may yield a greater and longer lasting effect. It is also possible that the required dosage needed for a benefit is lower with chronic ingestion.

I take 1 or 2 600mg tablets.

A few months ago, I was wondering why my strength was always greater in the mornings than afternoons. I just put it down to having more energy. I had no idea the 2g CaCO3 I was taking before hand(at breakfast) could enhance strength.

take it before bed, you'll absorb more! And due to the nature of the role of Ca+2 in muscle contraction I would imagine it would be an additive effect, much like creatine, not instantaneous. I would guess increases levels of Ca+2 in the body would equal more Ca+2 in the sarcoplasmic reticulum which would accumulate over time. Nothing to prove this, just speculation.

SPook, I'll check out the calcium thread. I haven't been reading here long. I did find the acetic acid / citric acid thread interesting, although a little anti-climactic

the guys over at Animals board like potassium citrate, any thougts?

No, not .5 g/kg per week, .5 g/kg daily for six days. Sorry, realized that is worded really badly. I'm sure this is correct.

the guys over at Animals board like potassium citrate, any thougts?

That is 50 g daily for 100 kg person.

Are you SURE about this? 50 g?????

http://www.whas.com.au/shop/products/cal_c...aa0a7def62a4052

would this work as a calcium citrate source? it's dirt cheap, none of the other ingredients would interfer?

yeh can't seem to find somewhere in backward australia that sells just calcium citrate powder.

Well the best I can think of is

1 teaspoon Now Magnesium Citrate (450 mg magnesium)
1 tablespoon Now Calcium Citrate (2100 mg calcium)
1 teapoon sodium bicarbonate (1200 mg sodium)

I think this is ~19 g of powder. If you are 200 lbs. this would be .2 g/kg.

"For those that have experimented with sodium bicarbonate, at what dosage did you cross the threshold of uncomfortable "bathroom problems". I'd like to try this out since I take cal and mag citrate anyhow but don't want to be running back to the locker room between every set. "

For the last ~10 years or so, I have used ~8-11 grams of sodium bicarbonate ~2 hours pre-work with great results.

I would say I had diarrhea/stomach upset around 10% of the time using this protocol...

The use of sodium bicarbonate w/o other buffers makes the likelihood of stomach upset/nausea etc. more likely in my experience...

For those that have experimented with sodium bicarbonate, at what dosage did you cross the threshold of uncomfortable "bathroom problems". I'd like to try this out since I take cal and mag citrate anyhow but don't want to be running back to the locker room between every set.

I do wonder about this study a bit though because they did not compare another mineral. Given sodiums involvement in motor-ion channels it might have been the sodium and not the alkanosis that increase muscular performance.

You are right the sodium could have been altering the resting membrane potential.

I think bicarbonate as a supplement is very dubious but under some circumstances could have short term benefits. If your kidney doesn't excrete it (dictated by its bicarbonate threshold) your lungs will begin retaining CO2 (an acid) in order to keep plasma ph in the narrow range it likes.

I've used Potasium citrate before also which actually alkalizes your urine and releases bicarbonate from your body.

I've used Potasium citrate before also which actually alkalizes your urine and releases bicarbonate from your body.

How about something like Greens+? I would think this stuff would have an akalyzing effect, being veggie/fruit based.

I like Greens+ But I need to find a version without all the herbs in it. I don't need no stinking gingko biloba every damn time I need greens, not to mention the thirty bazillion other herbs they add so that people will get a zing from it and think it's because of the greens. I just want the greens thank you very much.

Pretty sure the one we have headed to NP is what you are looking for.

Let me get an update on delivery.

1: J Am Soc Nephrol. 2007 May;18(5):1426-36. Epub 2007 Apr 11. Links
Acidosis-sensing glutamine pump SNAT2 determines amino acid levels and mammalian target of rapamycin signalling to protein synthesis in L6 muscle cells.Evans K, Nasim Z, Brown J, Butler H, Kauser S, Varoqui H, Erickson JD, Herbert TP, Bevington A.
Department of Infection, Immunity and Inflammation, University of Leicester, John Walls Renal Unit, Leicester General Hospital, Leicester, United Kingdom.

Wasting of lean tissue as a consequence of metabolic acidosis is a serious problem in patients with chronic renal failure. A possible contributor is inhibition by low pH of the System A (SNAT2) transporter, which carries the amino acid L-glutamine (L-Gln) into muscle cells. The aim of this study was to determine the effect of selective SNAT2 inhibition on intracellular amino acid profiles and amino acid-dependent signaling through mammalian target of rapamycin in L6 skeletal muscle cells. Inhibition of SNAT2 with the selective competitive substrate methylaminoisobutyrate, metabolic acidosis (pH 7.1), or silencing SNAT2 expression with small interfering RNA all depleted intracellular L-Gln. SNAT2 inhibition also indirectly depleted other amino acids whose intracellular concentrations are maintained by the L-Gln gradient across the plasma membrane, notably the anabolic amino acid L-leucine. Consequently, SNAT2 inhibition strongly impaired signaling through mammalian target of rapamycin to ribosomal protein S6 kinase, ribosomal protein S6, and 4E-BP1, leading to impairment of protein synthesis comparable with that induced by rapamycin. It is concluded that even though SNAT2 is only one of several L-Gln transporters in muscle, it may determine intracellular anabolic amino acid levels, regulating the amino acid signaling that affects protein mass, nucleotide/nucleic acid metabolism, and cell growth.

PMID: 17429052 [PubMed - indexed for MEDLINE]

Bumping old posts I find interesting/research worthy....