Creatine with "Lactic Acid buffers" - useful for 400m?

I have noticed that a few manufacturers have been bringing out creatine products with added ingredients to help buffer lactic acid to “enhance the ability to squeeze extra reps at the end of each set”!

My question is, if a 400m runner is doing lactic tollerence training to increase thier ability to deal with lactic will such a product be detramental to thier training?

If it reduces the lactic the body has to deal with on it’s own and when the athlete comes off of creatine before racing will they get a nasty surprise?

Sorry if I missed this in the archieves.


I would be VERY worried about a rebound effect with lactic acid nullifying some of your training. I would weigh the benefits of stopping creating before racing with the potential drawbacks of stopping the LA buffer. Personally I wouldn’t stop (if I were even taking the LA buffer in the first place :smiley: ). If you don’t want to keep using the creatine, I would test the effect before an important race, because how would you ever really know until you do it (even then it might be different every time)?

Wouldn’t be cheaper to use the baking soda trick instead for that kind of work? Then have cheap creatine after the workout?

Bicarb would be cheaper but it isn’t the most pleasent of substances to consume, especially on a regular basis! I would have thought a palatable alternative would be welcomed by 400m runners. It would seem logical that if you can reduce lactic build up from day one of training it will allow you to tollerate higher intensity speed work earlier in the year with obvious benefits. Input from anyone with experience in this area would be appreciated.



I think that most manufacturers of this products adds buffer agents to elevate the pH of the stomach, because the absorbtion of creatine is better if the pH is higher than 2, as it is usually.
The main buffer system is CO2/HCO3, than follows the phosphate system.
The phosphates are very useful, also bicarbonates, but you must take them not in to high doses, you may higher the pH of your body to much, what means a high drop in performance and the state of alcalosis.
A simple example, try to breath faster and deeper, so you breath out a lot of CO2, your ph will increase and you will feel very tired, your muscles will be wiped out, like after running 400m.

Lactic acid and running: myths, legends and reality - the ABC

Most runners still believe that lactic acid is released during hard or unaccustomed exercise and that this is what limits running performance, as well as being the cause of stiffness. Neither is correct. But not even is the terminology of “lactic acid”.

Lactic acid does not exist as an acid in the body: it exists in another form called “lactate”, and it is this that is actually measured in the blood when “lactic acid” concentration is determined, as is done from time to time. This distinction is important not only for the sake of correctness, but more importantly, because lactate and lactic acid would have different physiological effects.

The greatest myth is that lactic acid is the cause of the stiffness felt after an event such as a marathon. Stiffness is due mostly to damage to the muscle, and not an accumulation of lactic acid or lactic acid crystals in the muscle.

Another misconception is that lactate is responsible for acidifying the blood, thereby causing fatigue. To the contrary, lactate is actually an important fuel that is used by the muscles during prolonged exercise. Lactate released from the muscle is converted in the liver to glucose, which is then used as an energy source. So rather than cause fatigue, it actually helps to delay a possible lowering of blood glucose concentration, a condition called hypoglycemia, and which will cause a runner to feel weak and fatigued if it occurs.

A more recent addition to the muddled thinking is that of the anaerobic threshold. Pictures are seen of athletes having a blood sample taken with an accompanying caption indicating that the workout is being monitored by measuring “lactic acid”. The supposed rationale is that as running speed is increased, a point is reached at which there is insufficient oxygen available to the muscle and energy sources that do not require oxygen contribute to the energy that is needed. This results in a disproportionate increase in the blood lactate concentration, a point identified as the anaerobic threshold. This is also known as the lactate threshold or lactate ‘turnpoint’. There are two problems with this. Firstly, the muscle never becomes anaerobic: there are other reasons for the supposed disproportionate increase that is measured in blood lactate concentration. Secondly, the so-called disproportionate increase causing a ‘turnpoint’ is not correct, in that the increase is actually smooth and incremental. This led to another way of using blood lactate concentration to monitor running performance.

If blood lactate concentration is measured at different, increasing running speeds, it is possible to eventually draw a curve depicting the continued increase in concentration as the running speed gets faster. The position of this curve changes as fitness level changes. Particularly, the fitter a runner gets, the more the curve shifts to the right, meaning that at any given lactate concentration the running speed is higher than before. Often, the running speed at a lactate concentration of 4 mmol/l is used as a standard for comparison. This can also be used as a guide for training speed i.e. a runner could do some runs each week at the speed corresponding to the 4 mmol/l lactate concentration, some runs above this speed, and recovery runs at a slower speed. Of course, as fitness changes and the curve shifts, these speeds will change, and so a new curve will have to be determined. This is all very well, but the problem is to know how much running should be done below, at, and above the 4 mmol/l concentration. Remember, 4 mmol/l is a fairly arbitrarily chosen amount. Thus the real value in determining a “lactate curve” is to monitor how it shifts with training. The desirable shift is one in which a faster running speed is achieved at a given lactate concentration than before. This regular testing can be done in the laboratory with the athlete running on a treadmill or on a track in which running speed can be carefully controlled, such as by means of pace lights. Both types of testing are done at the Sports Science Institute, usually for research purposes.

While useful information can be gained from regular testing to determine a runners’ lactate curve, it is important to keep in mind what is fact and what is fiction.

What’s the relevance of the above post to the original question?
Sorry, I don’t get it…

lactic tollerence training to increase thier ability to deal with lactic

Because the theory lactic tollerence training and the whole idea of “lactic acid” is misguided.

Daniel where are you getting your info from? Just pick up an ordinary physiology book!

Lactic acid does exist in the body (in cells) but quickly dissociates into lactate and H+ (hydrogen ions, which are the acid part). It is the H+ that contribute to fatigue and probably the burning sensation. Lacate does provide energy to oxidative fibres and is converted to glycogen in the liver. Both lactate and H+ enter the blood.

tc0710 some manufacturers do add buffers to creatine so that it isnt converted to creatinine (waste product) in the stomach acid.

Re lactic acid (rather H+) buffering: when using a buffering substance the total lactic acid released will be greater than usual since the buffering substance will be removing the H+ and alowing you to run further and faster. There should be plenty of H+ left for your own system to cope with in order to develop as it needs to.

Daniel where are you getting your info from? Just pick up an ordinary physiology book!

Lactic acid does exist in the body

Regardless, what is the purpose of “lactate tollerance training”??

We dont train specifically for lactate tolerance, we train for H+ tolerance. Lactate is used as a measure of approx how much energy is coming from anaerobic glycolysis. Lactate is produced along with H+ and once lactate starts to accumulate in the blood we know enough energy is being produced from anaerobic glycolysis for fatigue to start ie. if lactate is high then H+ will be also. We also know how fit (aerobically and lactic (H+) tolerant) an individual is by measuring the lactate threshold (above of which lactate rises rapidly) compared with their VO2 max. The lactate threshold (LT) is higher for trained athletes than untrained; high LT showing that an athlete is buffering H+ well and is metabolising lactate well ie. lactate contributing beneficially to the fuel pathways.

Can anyone elaborate on this or explain it more clearly?

What exaclty is Vo2 max, I have an article thats scepticle about that:

The Great VO2 max Myth by Doctor Andrew Bosch

I often receive telephone calls from runners wanting to know if it would be possible to measure their VO2 max. My standard answer is something along the lines that it is, indeed, possible. However, I then go on to ask why they want to have their VO2 max measured? There is usually one of two replies. Firstly, I am told, by knowing his or her VO2 max the runner will know that esoteric time that he or she is ultimately capable of running for some particular race distance, and therefore their ultimate potential as a runner. Secondly, once their VO2 max is known it will be possible to prescribe the ultimate personalised training schedule. My response to both is that knowing the VO2 max of a runner does not answer either question.

It is widely believed that the VO2 max is genetically determined and unchanging and that an individual is born with either a high or low “max”. Someone with a high value has muscles that are capable of utilising large amounts of oxygen and a cardiovascular system capable of delivering this volume of oxygen. The athlete is able to run at a maximum aerobic speed that this oxygen supply can sustain. In this paradigm it does not appear to matter whether the runner is unfit or superbly fit, the outcome of a VO2 max test remains the same. However, it is intuitively obvious that when fit the athlete can run much faster on the treadmill than when unfit. Thus, since VO2 max is genetically determined and does not change (in this model), VO2 max would be reached at a relatively slow running speed when a runner is unfit compared to when very fit, when a much higher speed can be reached on the treadmill. This means that in a totally unfit world-class runner we would measure a high VO2 max (say 75 ml/kg/min or higher) at a speed of maybe 17 km/hr on the treadmill. When very fit the same athlete will reach the same VO2 max at a speed of about 24 km/hr. The problem is that such a high VO2 max is never measured at a speed of just 17 km/hr. This would be almost impossibly inefficient. The theory of a genetically set and unchanging VO2 max therefore begins to appear a little shaky.

This concept of VO2 max evolved from misinterpretation of the data of early experimental work. It was believed that as an athlete ran faster and faster during a treadmill test, the muscles needed an increasing volume of oxygen, a process, which continued until the supply of oxygen, became limiting or the ability of the muscle to utilise oxygen was exceeded. At this point there would be no further increase in oxygen uptake. This plateau in oxygen utilisation was regarded as the VO2 max of the runner. If high, then the athlete had great genetic potential. However, in addition to the problem described in the previous paragraph, half of all runners tested in exercise laboratories never have a plateau in their oxygen uptake. Instead, the oxygen uptake is still increasing when the athlete cannot continue the test. The conventional view of VO2 max now appears to be even more suspect.

Consider a different scenario. A runner on a treadmill requires a certain amount of oxygen to run at a given speed. When the speed is increased, there is a corresponding increase in the volume of oxygen needed to run at the higher speed. The runner runs faster and faster, with corresponding increases in the oxygen required, until something other than oxygen supply to the muscle prevents any further increase in running speed. The volume of oxygen being used by the muscle when this occurs is at a maximum value, which is then termed the VO2 max. With this theory, oxygen requirement merely follows the increase in running speed, until a peak running speed and therefore peak oxygen requirement (VO2 max) is reached. It is easy to see why the VO2 max value will change as a runner gets fitter and can run faster. Within this framework, the genetically determined limit of VO2 max is determined by the highest running speed that can be reached, or in some instances a true limit in the supply and utilisation of oxygen by the muscle.

The inability to use the VO2 max test as a predictor of future performance in someone who can still improve his or her running by using a scientifically designed training programme becomes obvious. A great training-induced increase in running speed will result in a substantial change in VO2 max.

Knowing a VO2 max value is not going to assist in the construction of a training programme any more than will knowing current race times. There are, however, some potential uses of a VO2 max test. When constructing a training programme for someone who has not run any races and who therefore has no race times, a VO2 max test will help give an indication of the current ability of the athlete on which to base training schedules. Secondly, if done regularly, the test can provide information about the efficacy of a training programme. Finally, its fun to compare ones’ own VO2 max value with that of elite runners, who have VO2 max values higher than 70 ml/kg/min. What is yours in comparison ?

What is your theory on Vo2 max? Im still learning.

VO2max is maximum oxygen uptake and this corresponds to the maximum amount of oxygen that can be used during aerobic excerise. VO2 max does not change greatly, approx 80% is genetic

It can be useful to show:
-the approx aerobic potential of an individual
-to see the progress of a particular training programme or where abouts an individual is on their aerobic fitness scale compared to previous periods.
-the intesnity to train at ie. a particluar % of VO2 max may be desirable eg. to judge lactate threshold

The lactate threshold (relates to the ability to metabolise lactate which coincides with H+ buffering also) maybe a better parameter for the affectiveness of a training programme or relative fitness of an individual since it more highly trainable than VO2max.

VO2peak is the oxygen uptake you observe after such a test, not necessarily the maximum one though. Moreover, it is the amount of O2 you see at that point, where “anaerobic” contribution also exists -you could say perhaps that the maximum amount of O2 consumed under “exclusively aerobic” conditions is that up to the lactate threshold point, Maximal Lactate Steady State; beyond this point the balance between accumulation and clearance isn’t there, hence the “anaerobic” contribution -lactate, of course, is always there and doesn’t not mean/indicate anaerobic metabolism (see lactate paradox).

Bear in mind that what you see from such a test may not apply to high level athletes (e.g., same VO2max, but at a faster pace/higher workload) and therefore, VO2max as such is not comparable to previous values, or has much less significance anyway.

I would avoid prescribing training intensity based on %VO2max, as the same percentage might correspond to completely different exercise stress to the body between two individuals.

Also, training at a “%VO2max” will also positively affect your lactate threshold; these don’t work independently, but they are rather inter-related.

Upto the lactate threshold there is still anaerobic metabolism occuring and so ‘exclusively aerobic’ conditions do not happen.

You are right when you state that we cant use VO2max alone to strictly compare 2 individuals or the same individual from phase to phase. Other training parameters eg. speed would also have to be considered.

If there is “anaerobic” metabolism, how is O2 there? :slight_smile:
Just joking, I know what you mean; however, the balance in lactate kinetics is there up to the LT point and hence my attempt for focusing on the “aerobic” part below it…