Posted In: Biomechanics & Physiology
Here is a very interesting article re: the interaction of K+ and Lactic Acid and force production. Granted, it is an in vitro study, but…
https://jp.physoc.org/cgi/content/full/536/1/161
Very interesting…
The findings in someway dovetail with Italian data that show an inverse relationship between post-race lactic acid levels and 100m times (e.g. higher LA levels, shorter/faster 100m running times).
lots of views.. no replies…. we are all padawans to JJ.
maybe super-ranter can break it down for us peons.
Things to consider regarding the study:
*It has long been known (though not to the general exercising public) that lactate can actually be an energy source and is not the devil it was once thought to be. It is interesting to see these results which indicate that it may not even be a source of acute fatigue.
*Isometric contractions were used to measure fatigue (via decreases in force output). This could potentially create difficulties in applying these results to events with cyclic concentric contractions because of any effect the muscle pump may have on electrolyte (K+) concentrations.
*Research on this topic seems to produce contrasting results and it would be interesting to see what the commonalities and differences are between the various studies.
Regarding all or other studies on this topic:
*Couldn’t the results be highly influenced by the fiber type of the muscle(s) tested? That is if 2 studies follow similar methodology but in study A the gastroc (mostly Type II) is tested and in study B the soleus (mostly Type I) is tested, one would expect the different glycolytic properties of each fiber type to effect the results of the test and potentially account for the conflicting results. I’m not familiar enough with the research literature to say if this really matters or not.
*Following up with my previous point, could it be possible that the results of the Italian study you mention could just be because the faster athletes are those with a greater proportion of Type II fibers and as a result they have higher power outputs, shorter contraction times, etc. but also enter anaerobic glycolysis sooner and as a result have greater lactate at the end of the race despite running for a shorter time…..just a thought.
ELITETRACK Founder
Great points Mike. Might I add the following thoughts?
Re: Italian Study:
That could be true, but I think the supposition that fiber types is the only determinant between the sprinters might be a bit of a jump. The study was performed on Italian National Team members, not just average folks. That would lead me to believe that the fiber type differences would be minimal.
Re: Differences in fiber types in the Nielsen study:
I think the point of the study was that a protective effect of the sarcolemma itself, or possibly effecting the inactivation of the Na+ K+ channels. I doubt that the differences in fiber type would make a difference. Why would capillary and mitochondiral density, oxidative vs. glycolytic capacity have an effect on the mechanism of acidosis on the inhibitory effects of K+? Not sure. Regardless of the muscle fiber type, intense exercise results in a increased concentration of K+. This increased concentration has shown to be inhibitory to muscle function (see the review: https://physrev.physiology.org/cgi/content/full/80/4/1411). Why does lactic acid (or acidosis caused by propionic acid or increased CO2 tension, as shown by Nielsen) exhibit a supporting effect to the muscle cell?
I just think that this study could challenge certain beliefs regarding microcycle design (i.e. placing intensive tempo session on day 6 of 7) as well as the contention held by some coaches (CF) that intensive tempo does not have a place in a high level sprint program.
I know that this will make me reconsider the balance required between neuromuscular development (‘battery building’) and glycolytic capacity (‘engine building’) for the 100 and 200, not just the 400m.
😉
I was told as a young swim coach that you must learn to do the following to improve speed endurance.
(1) Produce Lactate (requires a great gpp and spp)
(2) Reduce Lactate (during precomp)
(3) Use lactate (early comp)
Now my question is does the italian info shed light why the faster guys were higher LA wise? They took the same steps, same distance traveled, and the faster guys ran less time. 45 strides in 10.3 sconds. In theory speed endurance training should shift the lactate curve at least one full second (charlie francis) and I am under belief that this shift compresses the total amount into a shorter period, thus making the numbers higher.
I do thing lactate acts like a hormone instead of a byproduct to send messeges of fatigue or as fuel depending on the training preparations. Fatigue is a way to prevent physical harm to the connective tissues in my opinion. I think CNS fatigue helps keep high impact forces from damaging tendons and ligaments…..
This entire post goes back into mechanisms of fatigue of the 100m dash and if lactate is a problem to the equation. I think it is only if you have not prepared.
[i]Originally posted by Phoenix[/i]
In theory speed endurance training should shift the lactate curve at least one full second (charlie francis) and I am under belief that this shift compresses the total amount into a shorter period, thus making the numbers higher.
I do thing lactate acts like a hormone instead of a byproduct to send messeges of fatigue or as fuel depending on the training preparations…..
Carl,
can you elaborate/explain/go into more depth on the above two statements… they seem like interesting teasers.
This article is old news but the information will be eye-opening to some people and may revive this thread…
By GINA KOLATA
Published: May 16, 2006
Everyone who has even thought about exercising has heard the warnings about
lactic acid. It builds up in your muscles. It is what makes your muscles
burn. Its buildup is what makes your muscles tire and give out.
Coaches and personal trainers tell athletes and exercisers that they have to
learn to work out at just below their "lactic threshold," that point of
diminishing returns when lactic acid starts to accumulate. Some athletes
even have blood tests to find their personal lactic thresholds.
But that, it turns out, is all wrong. Lactic acid is actually a fuel, not a
caustic waste product. Muscles make it deliberately, producing it from
glucose, and they burn it to obtain energy. The reason trained athletes can
perform so hard and so long is because their intense training causes their
muscles to adapt so they more readily and efficiently absorb lactic acid.
The notion that lactic acid was bad took hold more than a century ago, said
George A. Brooks, a professor in the department of integrative biology at
the University of California, Berkeley. It stuck because it seemed to make
so much sense.
"It's one of the classic mistakes in the history of science," Dr. Brooks
said.
Its origins lie in a study by a Nobel laureate, Otto Meyerhof, who in the
early years of the 20th century cut a frog in half and put its bottom half
in a jar. The frog's muscles had no circulation – no source of oxygen or
energy.
Dr. Myerhoff gave the frog's leg electric shocks to make the muscles
contract, but after a few twitches, the muscles stopped moving. Then, when
Dr. Myerhoff examined the muscles, he discovered that they were bathed in
lactic acid.
A theory was born. Lack of oxygen to muscles leads to lactic acid, leads to
fatigue.
Athletes were told that they should spend most of their effort exercising
aerobically, using glucose as a fuel. If they tried to spend too much time
exercising harder, in the anaerobic zone, they were told, they would pay a
price, that lactic acid would accumulate in the muscles, forcing them to
stop.
Few scientists questioned this view, Dr. Brooks said. But, he said, he
became interested in it in the 1960's, when he was running track at Queens
College and his coach told him that his performance was limited by a buildup
of lactic acid.
When he graduated and began working on a Ph.D. in exercise physiology, he
decided to study the lactic acid hypothesis for his dissertation.
"I gave rats radioactive lactic acid, and I found that they burned it faster
than anything else I could give them," Dr. Brooks said.
It looked as if lactic acid was there for a reason. It was a source of
energy.
Dr. Brooks said he published the finding in the late 70's. Other researchers
challenged him at meetings and in print.
"I had huge fights, I had terrible trouble getting my grants funded, I had
my papers rejected," Dr. Brooks recalled. But he soldiered on, conducting
more elaborate studies with rats and, years later, moving on to humans.
Every time, with every study, his results were consistent with his radical
idea.
Eventually, other researchers confirmed the work. And gradually, the
thinking among exercise physiologists began to change.
"The evidence has continued to mount," said L. Bruce Gladden, a professor of
health and human performance at Auburn University. "It became clear that it
is not so simple as to say, Lactic acid is a bad thing and it causes
fatigue."
As for the idea that lactic acid causes muscle soreness, Dr. Gladden said,
that never made sense.
"Lactic acid will be gone from your muscles within an hour of exercise," he
said. "You get sore one to three days later. The time frame is not
consistent, and the mechanisms have not been found."
The understanding now is that muscle cells convert glucose or glycogen to
lactic acid. The lactic acid is taken up and used as a fuel by mitochondria,
the energy factories in muscle cells.
Mitochondria even have a special transporter protein to move the substance
into them, Dr. Brooks found. Intense training makes a difference, he said,
because it can make double the mitochondrial mass.
It is clear that the old lactic acid theory cannot explain what is happening
to muscles, Dr. Brooks and others said.
Yet, Dr. Brooks said, even though coaches often believed in the myth of the
lactic acid threshold, they ended up training athletes in the best way
possible to increase their mitochondria. "Coaches have understood things the
scientists didn't," he said.
Through trial and error, coaches learned that athletic performance improved
when athletes worked on endurance, running longer and longer distances, for
example.
That, it turns out, increased the mass of their muscle mitochondria, letting
them burn more lactic acid and allowing the muscles to work harder and
longer.
Just before a race, coaches often tell athletes to train very hard in brief
spurts.
That extra stress increases the mitochondria mass even more, Dr. Brooks
said, and is the reason for improved performance.
And the scientists?
They took much longer to figure it out.
"They said, 'You're anaerobic, you need more oxygen,' " Dr. Brooks said.
"The scientists were stuck in 1920."
ELITETRACK Founder
That's very interesting to think about. Now, I'm not stating my philosophy, but I think it's only fair to touch on the questions that this article raises. I'd like to see some more in depth evidence about lactate being used as fuel, but from what I took after reading this, it seems like this is saying that having sprinters do classic endurance training is beneficial to their sprint performance. I know this flies in the face of CF theorists, and some people on here are probably going to blow an O ring over it, but let's hear some thoughts…
After reading this, do you think that classic endurance training COULD have some benefit to a sprinter??
PS. Mike, would you mind posting the entire reference for this article, or where it could be found? You definitely piqued my interest.
I don't think it is really CF theorists… I don't know of many programs that are successful that do this anymore–on the collegiate or pro level–in the 100m, except for Tyson Gay.
i didnt know that any sprinter now days perfrom the old school endurance.
The fact that lactate is used as a fuel has actually been a well known fact for about 10-15 years. The real revelation (at least to the general public) that this research raises is the fact that lactate is NOT what causes fatigue.
Also, note that classic endurance training (i.e. long runs / milage) is not the only way to produce lactate. General strength circuits, body building, and med ball work can all be used to produce lactate.
ELITETRACK Founder
I am new to the forum so I may be repeating some ideas covered before. The article seems to imply that lactic acid and lactate production are synonymous. The Robergs et al article (https://ajpregu.physiology.org/cgi/content/short/287/3/R502) does a good job of arguing the point that lactic acid is not actually produced and therefore is not an acidifying product. The drop in pH counteracting the K+ effects are not caused by lactate production. So the real ???news??? to the lay public is not so much that lactate can be used a fuel but it is not (may not) be involved in metabolic acidosis at all.
I am new to the forum so I may be repeating some ideas covered before. The article seems to imply that lactic acid and lactate production are synonymous. The Robergs et al article (https://ajpregu.physiology.org/cgi/content/short/287/3/R502) does a good job of arguing the point that lactic acid is not actually produced and therefore is not an acidifying product. The drop in pH counteracting the K+ effects are not caused by lactate production. So the real ???news??? to the lay public is not so much that lactate can be used a fuel but it is not (may not) be involved in metabolic acidosis at all.
Where does the lactic acid come from then? There are countless studies indicating high levels of exercise-induced lactic acid. Also, if you click on the link to "articles citing this article" in the right menu you'll find quite a few articles that by the title alone refute this article by Robergs and colleagues. The most forthright is titled Lactic Acid Still Remains the Real Cause of Exercise-Induced Metabolic Acidosis.
ELITETRACK Founder
Robergs is theorizing that there is no lactic acid production, biochemically speaking, and the drop in pH comes from the splitting of ATP. The citation you mention is a letter to the editor in responce to the Robergs article. It is a some what hotly debated idea that metabolic acidosis is not caused by lactic acid. SOme consider it a semantics issue, but if it bears out then the Ex Phys text books will have to be changed in the future. What impact does it have on coaching and training techniques – not much at first blush. But getting the biochem right is an important step in a full understanding.
What is lactate and what is it's role as a biomarker?
Cfranko-
Thanks for the reply and the interesting discussion. My physiology is a hair rusty so please tell me where the lactic acid comes from if it isn't produced as Roberg and colleagues says. Lactic acid has been detected in numerous in vivo studies. I'm certainly not closing my mind to the possibility of what Roberg and colleagues suggests but I'm having a hard time reconciling his stance with what I know of aerobic and anarobic glycolysis.
ELITETRACK Founder
His point is what has traditionally been called lactic acid is a misnomer. The metabolic acidosis, drop in pH (increase in H+) is not from "lactic acid" but is primarily from ATP splitting. The historical context is covered in the article but I have to admit that there is not total agreement on the issue …yet. Just because there is a increase in lactate (la-) as anaerobic energy increases there has thought to be a causal relationship. But alternative explanations would include more anaerobic ATP and acidosis from that as a source.
To answer Carl's question lactate is a marker (a way to measure) anaerobic metabolism, but not as a causal factor but as a product that occurs at the same time.
What impact does this have on training? Not much from a coaching standpoint, except for possibly lactate threshold testing and interp. The fact that lactic acid is identified as present in metabolism and as a cause of metabolic acidosis is wrong – if Robergs explanation is accepted. He is not the first to come up with this line of thinking Brooks was on this line years ago.
