Is there such a thing as Too Anaerobic?

[mchase]

Mike,

We have different backgrounds and our differences lead us down different paths in trying to accomplish the same goals. You have the wherewithal to publish the Wolverine Plan based on your cumulative knowledge gained in training lots of athletes and as an exercise physiologist.

Me, well I fell into this coaching gig out of love of the sport. I wasn't raised in a rowing environment surrounded by a coaching staff with huge experience passing down knowledge of what works and what does not. I coached novices for my first 10 years and frankly found it, after about 5 years, to be relatively easy to make them fast compared to most other novice teams. I didn't have to worry about HR, lactate, or anything else except get in the meters/improve their strokes. When my novice mens boat took first at Head of the Ohio with maybe 35 eights in the race, my thoughts were that this coaching thing is easy-- just put in the meters and work on the stroke. After my novice eight beat our varsity eight, I took over as varsity coach (~5 yrs ago). Successes in the varsity heavy and light 8s don't come as easily. You're up against coaches with lots of experience.

Successes in the past, perhaps due to an abundance of talent, now have to be eked out of a team with good coaching. You're fortunate enough to have this "good coaching" thing figured out; I am not. I draw lactates and see several patterns. You don't bother because you know the patterns don't matter. I haven't figured that out yet. It will take me months more, I believe, to see the results of altering the workouts of those I deem "too anaerobic".

[Mike Caviston]

Me, well I fell into this coaching gig out of love of the sport.

Huh. I was lured in because of the convenient hours, comfortable working conditions, and huge salary.

Successes in the past, perhaps due to an abundance of talent, now have to be eked out of a team with good coaching. You're fortunate enough to have this "good coaching" thing figured out; I am not. I draw lactates and see several patterns. You don't bother because you know the patterns don't matter. I haven't figured that out yet. It will take me months more, I believe, to see the results of altering the workouts of those I deem "too anaerobic".

You’ve made hundreds of posts on another forum asking for opinions and advice about various aspects of coaching. You’ve started an account on this forum to ask similar questions of a different audience. I’m not sure why you seek advice if your goal is to figure things out for yourself. But carry on, and best wishes.

[mchase]

Mike,
I asked for advice and received lots of it, including that I should institute lactate testing. That advice came from coaches with enviable track records from my research (but you know, success has a thousand fathers and so to whom the success belongs is arguable). I undertook lactate testing. I know your views. My choices are to either mimic other coaches, coaches who often don't provide lots of information, or to figure it out on my own. I could simply institute the WP and post the workout daily, as an example. But there is a part of me that wants to figure it out so that I have a deeper inventory of answers. "That is the way it is in the Wolverine Plan" would get old as a stock answer. Mimicking another coach, on the one hand, and understanding the processes of coming to those conclusions,on the other hand, are entirely different. I am not attacking your views or discounting them. I simply don't have the depth of knowledge that you do.

Your link was also broken to the "concerned with lactate dynamics, lactate and training, and lactate/anaerobic thresholds". I have read many papers by billat. She is a prolific researcher.

You don't believe that one can be too anaerobic. That's fine. You're in great company. I'm just having difficulty in coming to the same conclusion. I'm in a distinct minority.

[Mike Caviston]

Just for clarity, I have always strongly encouraged those interested in the Wolverine Plan to learn the principles and physiology behind the workouts, and not just copy them blindly. “Teach a man to fish”, and all that.

I didn’t perceive you as attacking or discounting anyone’s views, but you do seem to ask for advice but then spend a lot of time justifying why you are going to keep on doing what you’ve been doing. Just an observation, not a criticism.

As for being “too anaerobic”, I’m still not sure what that’s supposed to mean. If you mean that some athletes spend too much time training at high intensity, or exceed the desired threshold for longer endurance workouts, then I agree completely. If you mean there is some sort of penalty for an athlete being able to produce lots of ATP via rapid glycolysis, then I don’t agree at all.

Anyway, good luck to you and your athletes and if you find any definitive answers please pass them on.

[mchase]

Too anaerobic- The over-production of lactate as compared to similarly trained endurance athletes (undergoing similar training 5-6 days per week for at least 1 yr) using measures such as peak lactate after 1min all-out response, steady state rowing at a comfortable Borg factor, rowing at a fixed HR band, or rowing for a specified time period at a percentage of VO2 max. That is, think of a test and the lactate over-producers (called the "anaerobic group") will always have a higher lactate than the lower lactate group ("aerobic group").

It is easy to say that they are just not aerobic enough (and deduce that they must do more aerobic training). So they already train 5-6d per week. Have them come in for extra long and slow to get more aerobic? Or have them tone down their workouts in the anaerobic zone? Or write them off as having bad genotypes?

Is there anything in the cellular metabolism literature that could possibly support a "too anaerobic" hypothesis? That is, a factor that could enhance the anaerobic system while limiting the aerobic? A factor that is active in making one "more anerobic and less aerobic" based on the workout intensity (versus a more passive, you just aren't aerobic enough answer)? If there is such a factor, has it been studied for its dynamics in an endurance trained athlete? What augments its effect in the cell? What limits it? What is its half-life? If there is such a factor, how complicated are its downstream effects and how easily are they measured? Does it follow an arithmetic dose-response curve, or exponential?

You're an exercise physiologist. Certainly the thought of this must intrigue you.

[auerli]

Has anyone here tried polarizing their training like most of the studies recommend? It seems like most training plans focus on a lot of threshold work (pete plan, interactive, wolverine), while the articles talking about elite athletes focus on the 80/20 split, with most work at low intensity and then some at a much higher intensity.

Obviously it's different with elite athletes, who have been training for many years and for tons of hours a week, just wondering if anyone had experience with that strategy.

I am no elite rower but a competitive long-distance rower and for this reason strongly focussed on the work on the aerobic capacity.
I do none of the sprinty stuff but about 90% of my training in the boat and on the machine consists of long, rather intense steady state workouts (mostly at 80 to 85% max HR; my AT was tested at about 90% max HR). If I do interval work this is never at very high intensities (concerning HR and application of power) but some kind of endurance intervals (active rest). Although I am not particularly interested in 2k and I have never done any specific training for it ("sharpening"), this kind of foundational aerobic training allowed me to to row sub 6:20 in my late 30ies.
I strongly believe in the benefits of training mainly consisting of long workouts and concentrating on technique. I don´t think the fitness will be significantly increased by high intensity-short duration interval workouts (this is what was recently told on a course in Ratzeburg, too). Of course the body needs to get used to anaerobic exercise. However, I cannot see a reason to do this kind of short interval sessions more often than once or twice a week to perform a good 2k.

Just my personal opinion and experience,

Matthias

[NavigationHazard]

Too anaerobic- The over-production of lactate as compared to similarly trained endurance athletes (undergoing similar training 5-6 days per week for at least 1 yr) using measures such as peak lactate after 1min all-out response, steady state rowing at a comfortable Borg factor, rowing at a fixed HR band, or rowing for a specified time period at a percentage of VO2 max. That is, think of a test and the lactate over-producers (called the "anaerobic group") will always have a higher lactate than the lower lactate group ("aerobic group").

It is easy to say that they are just not aerobic enough (and deduce that they must do more aerobic training). So they already train 5-6d per week. Have them come in for extra long and slow to get more aerobic? Or have them tone down their workouts in the anaerobic zone? Or write them off as having bad genotypes?

Is there anything in the cellular metabolism literature that could possibly support a "too anaerobic" hypothesis? That is, a factor that could enhance the anaerobic system while limiting the aerobic? A factor that is active in making one "more anerobic and less aerobic" based on the workout intensity (versus a more passive, you just aren't aerobic enough answer)? If there is such a factor, has it been studied for its dynamics in an endurance trained athlete? What augments its effect in the cell? What limits it? What is its half-life? If there is such a factor, how complicated are its downstream effects and how easily are they measured? Does it follow an arithmetic dose-response curve, or exponential?

You're an exercise physiologist. Certainly the thought of this must intrigue you.

This isn't meant to be critical, but rather constructive....

1) Why do you assume that what you're measuring (notionally excessive blood lactate during exercise) is necessarily a function of something going on in the working skeletal muscles? Why rule out underutilization? I'm not a doctor but in browsing the literature on hyperlactatemia I can come up with of all sorts of reasons adversely affecting the body's ability to process lactate once it's in the bloodstream. Presumably your "overproducing" athletes aren't taking retrovirals for AIDS, or suffering from liver or kidney impairment, hypovolemic shock, hemhorrage, circulatory disorders, malignancy, sepsis and/or pulmonary disease, etc. etc. Still. Could there be something more subtle going on, like ribobflavin (B2) or thiamine deficiency, or something hormonal affecting liver or kidney (or even heart) mitochondrial ability to process blood lactate? Alternatively, do your "overproducing" athletes drink? I gather binge drinking has an association with elevated blood-lactate levels. Etc. etc. etc. Or to put all this another way: blood lactate levels are going to reflect the relationship between production and utilization. Might not the latter (or both) be involved in what you're observing?

2) Do you know this study? http://www.thelancet.com/journals/lance ... 3/abstract

It's a rather early magnetic-resonance study I dug up that apparently supports well your observation of cellular overproduction during exercise. Unfortunately my university subscribes to Lancet but for some reason has a gap in the on-line holdings for 1984. Thus I can't read more than the abstract from off campus without paying $30 or bothering a librarian. Neither can I easily look at the references to follow any trail that might exist.....

[mchase]

NavigationHazard,

A couple of thoughts nudge me more toward an intracellular factor induced by training intensity rather than a pathological process. First, it's almost predictable by watching the workout habits of the kids who will be more anaerobic. Lactate testing is the objective measure and shows that those kids who push themselves daily harder than others are indeed more anaerobic. These are the kids at a 22-24 spm rating who are pushing HRs >= 185. I could not have predicted the same by looking for a pathological process.

Secondly, the biggest sink for lactate in the exercising rower is muscle. Lactate is a big energy source and is effectively used in the Krebs (citric acid) cycle. This substitute for pyruvate is better studied in brain cells (ostensibly because stroke leads to hypoxic conditions in the brain with cell death and stroke is a huge health concern that gets more attention).

Thirdly, from my experience in the practice of emergency medicine, you don't come upon a walking/talking/very physically fit/normal-on-exam patient with a diagnosis of lacticacidemia. Finding a bunch of kids with acidosis in one setting from a pathological process would have one thinking about toxin ingestion (ie, a party with punch in which someone dumped some cheap wood alcohol (methanol) but that acidosis is from the metabolite formic acid, not lactate).

[mchase]

I found something interesting. In researching if there might be any models of HIF-1 over-expression in the real world, an article popped up: Regulation of human metabolism by hypoxia-inducible factor by Federico Formentia et al. in The Proceedings of the National Academy of Sciences of the United States of America (PNAS July 13, 2010 vol. 107 no. 28 12722-12727 ). Hyperlink: http://www.pnas.org/content/early/2010/ ... l.pdf+html

Here's the Reader's Digest version: In the central European part of Russia, there is an endemic autosomal recessive disorder called Chuvash Polycythemia (CP). In this disease, there is a moderate over-expression of HIF-1 due to the genetic disorder whereby the VHF regulating gene (that prevents over activity of HIF-1) does not function properly.

The idea of the researchers was to put some of these subjects through an exercise step test to learn the effects of HIF-1 over-activity (something that had not been documented in humans). They found these subjects to be "more anaerobic", and as they stated, "Venous blood lactate concentration increased early in the CP patients, becoming significantly higher than in the control group at ∼4 min into the exercise test at a work rate of 80 W. CP patients stopped exercising at lower work rates than controls. "

In reviewing the article, the lactate curve of the Chuvash patients showed the leftward movement, the opposite that we wish to see in endurance athletes. That is, a higher lactate at a lower wattage or an anaerobic shift (my term) than the controls.

They also used the 31P MRS method of analyzing aerobic/anaerobic contribution of the energy systems and these subjects were "more anaerobic".

The articles suggests to me that there can be a "too anaerobic" state in humans that is not due to simply being "not aerobic enough". It would be quite a leap to say that prolonged repeated exercise at a high enough intensity can lead to this state, but in looking for an explanation why some of these kids are "too anaerobic", this certainly provides some food for thought.

[mchase]

Another article:
Enhanced leukocyte HIF-1α and HIF-1 DNA binding in humans after rapid ascent to 4300 m By Tissot van Patot, et al in Free Radical Biology & Medicine 46(2009) 151-1557

The Readers Digest summary is the authors wanted to actually test the assumption that global hypoxia will induce hypoxia inducible factor (HIF-1) in vivo in humans. To test this, they exposed 14 subjects to a relative hypoxia (12% 02) by placing them in a hypobaric 02 chamber for 18 hrs at a simulated altitude of 4300m. The researchers drew blood samples just before hypoxic exposure and at the tail end of the 8 hr exposure. Those samples were tested for dozens of metabolites, including glutathione, lactate, and succinate (and 39 others!). The results: There was a significant rise in lactate suggesting anaerobic glycolysis; a rise in succinate suggesting inhibition of the oxyidative (aerobic) pathway (specifically a switch from succinate dehydrogenase to fumarate reductase consistent with hypoxia; a decreased glutathione (used in Krebs cycle). ELISA and Western blot analysis for HIF-1 (and its DNA-binding activity) was assessed. Both increased.
____________

Hopefully I can find an article that might shed light on the downstream "half-life" of the HIF-1 effect.