You know how I keep bringing this up and nobody seems to throw out an answer? I think I found the answer in an old deVries textbook, Physiology of Exercise.
On Page; “…the effect of training in delaying the end point of a workbout due to fatigue depends upon the rate of work done. In very heavy work, which can be maintained only ten to twenty minutes, the improvement is probably due to a combination of O2 transport and the improved cellular oxidative capacity which results in a slower build-up of lactic acid. …work…which can be supported for sixty to 180 minutes, improvement in the endurance time will depend largely upon the overshoot of cellular glycogen storage. …work…which can be maintained for longer than three hours may be limited in duration at least in some cases by hypoglycemia resulting from the depletion of both muscle and liver glycogen.”
To me, this explains why higher (than normal) hemoglobin levels benefit the more intense workload activities where Oxygen delivery and consumption is most important, and actual energy availability is the limiting factor in longer events, such as triathlons.
So, it depends upon your event as to what THE limiting factor is in being able to continue to have the muscle function. Road racers, depending upon the high-power fast twitch fibers to create speed to match surges may do better with higher (than normal) Hb levels, but slowtwitch endurance athletes aren’t helped by abnormally high Hb levels.
BTW, another interesting note is that Neural firing seems not to be fatigued at any physiologically possible workload…i.e., the local nerves aren’t “tired”…they still fire to tell the muscle to contract, the muscle just gradually loses it’s ability to follow the command.
I don’t know if a podium finisher at an Ironman has ever been on EPO, or the like.
I know that blood doping has produced spurious results among it’s users…some seem to benefit, others don’t. It could be as simple as the fact that for high energy activities that require more oxygen carrying capacity (such as road racers that must jump/sprint/climb at very high effort levels), those athletes benefit. But, for longer-term exercise, such as with endurance athletes that don’t have the sudden bursts of energy, the benefits disappear, because it is local muscle fatigue that is THE limiting factor.
I do know that nobody has offered any serious answers to the question. May I suggest you offer an answer?
I also know that it is modern knowledge to consider the recruitment of fast twitch fibers to be glycogen-expensive in the total energy available over longer term exercise compared to utilizing predominantly slow twitch fibers…one reason that the forward- positioned seat angles tend to give better results in longer distance events. Namely, that although there is a lower peak power produced when riding steeply, the average power is similar compared to slacker seat tube angles, so there are less glycogen-expensive fast twitch fibers utilized in the first instance.
This, once again, leads me to believe that THE limiting factor in exercise (at least longer events) is local muscular fatigue (due to depletion of glycogen stores, first in the local muscle, then in the liver), not Oxygen carrying capacity and cardiac output.
Again, instead of just taking shots, write about what is correct or incorrect about this idea.
K, im not an expert, but i have been studing muscles all year.
An answer i got from a prof, was that the first thing to fatigue is the neruological component.
The muscle will not run out of glucose before you run out of Ca2+ or other such NT’s that cause muscular contraction, or are part of the pathways.
Your logic is backwards. For anaerobic sprints, O2 delievery is useless (or nearly). The body switches into anaerobic pathways. Ie, a 100m runner, the last breath that matters is actually the one just before the race.
Aerobic training uses O2, where as anaerobic does not. By taking EPO/or altitute training, and increasing Hb levels in blood (either via more blood cells, or something else), you increase the ability for the blood to bind with more O2, which will allow for aerobic activity to take place longer in the body, and will prevent lactic acid buildup, which will increase endurance ability.
The fatigue that your legs feel in a long race is not from glucose deficency, but from lack of NT’s as well as a buildup of lactic acid. Therefore, increasing aerobic potential will make you less fatigued.
I dont know what book you are reading, but you may want to look at a new textbook.
Might want to at give full credit to authors, etc. next time so as to avoid potential copyright infringement suit against the site and yourself. Just a thought, but as the risk manager for a publishing firm I’ve seen suits for lesser offenses. The other way to do it is to paraphrase the content rather than quote it. In my experience the authors of this kind of material can be far touchier than those write popular fiction
Kevin, I’m not talking about all-out anaerobic sprints, I’m talking about exertions that last for 10 to 20 minutes in the “fast” group…not 100 meters. I’m referring to those efforts “just above your lactate threshold” for the fastest of the events. NOT maximum efforts. Big difference. The book remains correct in its premise.
As far as the nerves…the nerve fibers are almost indefatiguable. The thing that you are referring to is the neuromuscular synapse transmitters…yes, they do “get used up” and can be a big reason for decreased muscle function during exercise. I didn’t mean to suggest otherwise.
One correction I do need to make, though. I did have one PhD write back to me in my earlier post about THE limitation to exercise…he essentially state what this book stated. The only thing he added was that there is a possibility that heart function may actually decrease in very long exercise bouts (ironman? ultradistances?), to the point that cardiac output may then be a limiting factor to exercise…but, he said that was just a guess about that possibility.
You were right about 100m sprinters but wrong about endurance performance. YaquiCarbo had it right. Long term aerobic exercise endurance is not limited by oxygen consumption. If it were, you would have high lactate levels at your end point. Yaquicarbo’s statements are in line with the currently accepted theories on fatige for long duration endurance events. You are right to say that metabolism during these events is aerobic, but endurance is not limited by oxygen consumption rates as it is for shorter duration work where lactic acid builds up and reduces performance.
Think of it this way: A Ferrari can go very fast (lots of power) but doesn’t get far on a tank of gas. A Geo is not very fast but can go a long way on a tank of gas. In comparison, a very good miler can cover that distance very fast (high aerobic power or high VO2 max) but an ultramarathoner is more efficient and has better endurance (and would probably win a 35 mile running race). The miler’s performance in the 1 mile event is limited by his aerobic power (VO2 max). The ultra endurance athlete’s performance is related to his endurance. The prevailing theory is that this endurance is related to energy substrate availability to the contracting muscles and perhaps some neural factors (CNS fatigue).
You’re kidding, right? He was clearly quoting from a book and had no intention of crediting himself or this site with the ideas therein. He’s simply asking questions based on material he’s read. This is no different than raising a hand in a classroom and asking a question about material you’ve read for the class, and beginning the question by reading from the passage. The logic doesn’t add up.
Ahh, the litigious society strikes again. I know that the internet is the bane of original authors of all types, but lets use a bit of reasonable man theory here.
Thanks. Maybe I should have said Herbert A. deVries instead of just deVries? I thought his last name and the name of the book would suffice.
BTW, I just received the following e-mail from Pat Courtney, a fellow perfusionist:
"Author C. Guyton, MD, age 83, the world’ foremost pioneer in physiology,
died in an automobile accident, Thursday, April 3, 2003, in central
Mississippi.
Dr Guyton’s past discovery that blood flow is regulated by the body’s
capillary system, and not by the heart, was a great hallmark in medical
understanding."
It has been said that Dr. Guyton’s Physiology book has been published more than any other single book other than the Bible…this sounds like something someone just might have said off the cuff, and I doubt it is true…but, he did write a book that is very widely known.
To not a PCer: as for finding the idea in the original post in a 25 year old textbook…just like Dr. Guyton’s discovery of this capillary/heart relationship many years ago, neither ideas are false just because it’s old news.
I totally agree with you, but I’ve seen the irrational in this area and it ain’t pretty. It’s not so much the what we believe to be reasonable, it’s what the author(s) believe to be unreasonable. And it is usually driven by the academic ego. So sometimes it’s better to give full credit than to line a defense attorney’s pocket to get the thing thrown out at a later date.
Remember, in this land that we love you can sue or be sued for almost anything.
I just spoke with one of our intellectual property attorneys (why does that sound like an oxymoron?) because I thought that perhaps 25 year old material might have been past its statute and part of the public domain. Unfortunately he tells me that the statute on copyrighted material runs for 70 years after the death of the author, and 95 years after the death of the author for works for hire.
Anyway, it is sad that we even have to think about such things, but trust me when I say that I have seen some of the most petty lawsuits in this area. We do publish in the medical area, and doctors are some of the worst.
Not really sure as we do not deal in music. It is my understanding that there are different statute dates for different types of property ie. books, music, films. They also vary from country to country by law. I can’t imagine there was a copyright remaining on that stuff though. What would surprise me even less would be if it were reversed and the soap company had to pay a royalty based on the copyright while a consumer group complained that “all” music should be public domain. Thet is the direction it is going with content, especially content available online, despite whether or not it was originally published in a hardcopy version.
Well I studied some of this crap in college and have come to this conclusion: KISS thats right KISS. Find out what your limits are figure out what works best (Training, nutrition) for you to decrease these limits. Thanks to Mother Nature all you have to do is force your body to adjust, over time it will. Even the foremost authorities can’t pinpointexactly what makes you better or faster. They certainly try and have made huge gains but none can uquestionably say that such and such was the determining factor. To many variables. The human body has the capability to adapt, no need to figure out exactly what the body does example - need more speed train at a faster pace etc., which brings me to my next thought.
Our litigious society is equivalent to the old fist fight but now its tag team. Which in my opinion kind of screws up Mother Natures survival of the fittest thing, which is some cases the mind nor body is not forced to adapt.
I also know that it is modern knowledge to consider the recruitment of fast twitch fibers to be glycogen-expensive in the total energy available over longer term exercise compared to utilizing predominantly slow twitch fibers…one reason that the forward- positioned seat angles tend to give better results in longer distance events. Namely, that although there is a lower peak power produced when riding steeply, the average power is similar compared to slacker seat tube angles, so there are less glycogen-expensive fast twitch fibers utilized in the first instance.
I’m not familiar with the basis of this statement, could you give references or a source please?
I don’t know the name of the study right off the top of my head, and I thought Mr. Empfield might. I have read the study though, and it makes sense.
Again, how about citing your own references that disagree with Dr. deVries, Dr. Prevost, and others instead of just taking shots at me? Certainly you must have some that have a view that disputes what I wrote above, and therefore would do me a world of good to read. I’m always interested in learning…I’m not interested in participating in a back and forth about nothing…because nothing new is learned.
I think that the depletion of muscle fuel is a limiter but I don’t think you can seperate them. I think that recruitment of both fast and slowtwitch muscles takes place simultaneously therefore you are depleting both oxygen and glycogen at the same time, and building lactate. Maybe more efficient atheletes recuit more slowtwitch than Fast but maybe they just have better glycogen stores, a system that clears out lactate faster and provides more oxygen??
You posed a great question I still think you should KISS.
Sorry bout that. When he said sprint, i assumed very fast exertions, nothing over 1 minute at most. What is the point at which exercise stops becoming anaerobic, and becomes aerobic though?
There is a book on lactate training that i have read, and it delves into this. Ie, you run a 1/2 marathon at 99% of your lactate threshold, whereas a 100m sprint is 210%.
Basically then, at any point at which your exceed your Lactate threshold, you have become anaerobic, and thus O2 becomes the limiting factor? Am i right in saying that?
Therefore, if run properly, a marathon/ironman should keep you anaerobic,(according to this book) and thus o2 is not the limiting factor…? if thats right, it makes sense now. I think i misunderstood the original statement.
(That said, some keyan marathoners run 27 minute 10k’s aerobically…!)
Everyone is getting parts of this question right. The reality is that the answer is very complicated.
Being in shape is a very complicated combination of oxygen carrying capacity which relys solely on the hebaglobin content of your blood, pulmonary function (how well you can oxygenate your blood) cardiac output, metabolic capacity of your cells, capillary perfusion of your muscles, efficiebcy of your movements, etc.
A drug like EPO will increase your hemaglobin and hematocrit which will increase the amount of oxygen in your blood. This will help you in every situation except for purely anaerobic exercise such as a 100M sprint. This is becuase it would raise the effort at which you can stay aerobic because of the greater amount of oxygen getting to your cells.
CO (cardiac output) is rarely a limiting factor with endurance athletes. There is some hypertrophy (stengthening of the heart) with sustained exercise. Unless you have a heart abnormality you are going to be much more limited by the oxygen carryign capacity than way before you run into problems with CO. High HR are a result of low oxygen carryign capacity not the other way around… if that makes sense…
In regards to Neuron fatigue, it only happens in very very very extreme situations. I read a paper where an animal model with some insect or it might have been an animal was able to “fry” their neurons after a huge exertion… this would be much more akin to explosive activities such as power lifting… I don’t remember the specifics though.
Again I think the answer to your question is that a drug like EPO will help you in all exercise but flat out sprints. However as you point out if the o2 carrying capacity is not what is holding you back it wont really do much. The problem with ultra endurance athletes is that EPO will “thicken” your blood which is not a very good thing in a sport where hydration is difficult. So I would especially warn against a ironman athlete from using said drug.
I hope that this helps you out… if you have a more specific question please reply and I will try to get a better answer to you…
Better ask Mr. Empfield for the references on your question…I got the idea straight from something Mr. Empfield wrote here on Slowtwitch.
Thanks…it’s sort of an inside joke. Most athletes get it…other people ask me if I’m lactose intolerant or if I’m lactating.
I think Taku nailed right on, in that there are many angles to the question of aerobic exercise limitations. While some studies define improvement as increased time to fatigue at a set performance/work-load, other studies call it increased work accomplished during a time period. In the case of triathlons, I’m inclined to believe that having a greater aerobic engine (meaning you can sustain a higher oxygen intake without fatigue) with higher power output leads to increased performance. Some people just build their engines with “chemical” means, while others rely on that “training” thing.
As to the exercise physiology community about the limitations of exercise…just look up Dr. Noakes in Medline…like:
Noakes TD. 1996 J.B. Wolffe Memorial Lecture. Challenging beliefs: ex Africa semper aliquid novi. Med Sci Sports Exerc 1997 May;29(5):571-90.
That’ll get you started in one way…just make sure you read the rebuttal to that (as well as the rebuttal to the rebuttal)…haven’t seen Mr. Slowman post his info yet…however, I’m guessing it’ll be anecdotal. Just tell me it wasn’t measured on Spinscan…
Stewart, I agree that training doesn’t have to be as complicated as all of this theory. I also agree that it isn’t like a switch where suddenly you use fast twitch then suddenly you use slow twitch fibers, and that blood flow/delivery is a big important piece of the pie in determining the lactate threshold in an endurance session. Especially at lactate threshold…you are bound to be teetering back and forth across an imaginary line that may have elements of several theories as relative truths. I’m just interested in learning about these different theories for the sake of curiosity, and I appreciate any helpful ideas that people may present. Thanks!