PDA

View Full Version : PM 43: Greg E. Interview


steve solano
08-01-2008, 06:48 PM
As usual, great PM. The interview with Greg is top notch and hit the nail re: the officer training. Most officers do not train while in full uniform. Out of uniform I could get my 43 year old body over a fence no problem. Add 35-40 lbs. of gear (some useless) and restricted clothing and it a different fence.

I have been following the CA WOD for over a year, but skipping out on the met/con workout (pure laziness). Several weeks ago I had to sprint and jump a chainlink fence four times. Finally caught the guy but I was spent. The strength and power assisted but I was still winded and embarrassed.

Anyway after that episode I went total crossfit and felt the degree of suckness. This article brought me back to thinking strength, power, and met/con.

Nice work.

Derek Weaver
08-01-2008, 11:18 PM
This was indeed a very good interview. Really came along at a good time with some of the different approaches that are emerging around here in regards to GPP vs. SPP, hybrid etc.

I personally thought that the point about laying the foundation and all the layers accordingly was the best point made in that interview.

Good stuff as usual.

Pat McElhone
08-03-2008, 04:57 AM
I believe some form of very high intensity is necessary to get the body used to operating in an oxygen debt. Oxygen debt is defined as oxygen demands exceed oxygen supply. I believe very high intensity exercise where the body enters oxygen debt stesses the body and forces the body to adapt to this environment just like strength training forces the body to adapt to lifting heavier loads.

Why is this important, the wars right now tell us, if you are in combat enough times, you will get hit. Period. When you are hit, you will go into an oxygen debt. Conditioning helps the body deal with this situation, probably buffers some acids, prevents cell break down and will be the difference between one dying or living.

Liam Dougherty Springer
08-03-2008, 07:28 AM
Why is this important, the wars right now tell us, if you are in combat enough times, you will get hit. Period. When you are hit, you will go into an oxygen debt. Conditioning helps the body deal with this situation, probably buffers some acids, prevents cell break down and will be the difference between one dying or living.


Powerfull!

Steven Low
08-03-2008, 09:05 AM
I believe some form of very high intensity is necessary to get the body used to operating in an oxygen debt. Oxygen debt is defined as oxygen demands exceed oxygen supply. I believe very high intensity exercise where the body enters oxygen debt stesses the body and forces the body to adapt to this environment just like strength training forces the body to adapt to lifting heavier loads.

Why is this important, the wars right now tell us, if you are in combat enough times, you will get hit. Period. When you are hit, you will go into an oxygen debt. Conditioning helps the body deal with this situation, probably buffers some acids, prevents cell break down and will be the difference between one dying or living.
I disagree here.

Well, main reason being why we breathe is moreso because we need to exhale CO2 rather than breathe in oxygen (at least regularly). So in the event of a case of severe blood loss, yes, we will be able to operate under duress a bit longer (but definitely less than a minute depending on the bleed), if the CO2 can't get out you're going to get acidification of the blood anyway and die. Well, that if the bleed is severe enough your brain is gonna starve from lack of oxygen quickly as well.

If, however, we're talking about say having the ability to save a buddy by carrying him. Hell, yeah, that's a big one. I would venture to say that it's better moreso in the case of being able to operate under the extreme stress of a situation building pain tolerance (as my friend calls the long metcons) and perseverance as well to finish the job. This, along with being able to carry your buddy, are going to make far more of a difference than the effect of it on your own life (depending on the type of wound of course).

Pat McElhone
08-05-2008, 03:35 PM
[QUOTE=Steven Low;36121]I disagree here.

Well, main reason being why we breathe is moreso because we need to exhale CO2 rather than breathe in oxygen (at least regularly). So in the event of a case of severe blood loss, yes, we will be able to operate under duress a bit longer (but definitely less than a minute depending on the bleed), if the CO2 can't get out you're going to get acidification of the blood anyway and die. Well, that if the bleed is severe enough your brain is gonna starve from lack of oxygen quickly as well.

This is actually wrong. Under normal situations, yes, CO2 does trigger our respiratory drive, however hypoxia is a potent stimulant of respiration. In fact, in most people who are in shock, their CO2 is low because their are hyperventilating because cellular oxygen demands are far exceeding supply. Also, the acidosis caused in shock is metabolic, not respiratory, that is it is due to acid built up from excessive metabolism of substrate, not CO2. A typical blood gas of a victim of hypovolemic shock is ph 7.1, PCO2 30, PO2 80, HCO- 10! It is this acidosis that is deadly and the body can survive a lot longer then a minute. It is this same acidosis that occurs, at least on a smaller scale during any intense exercise. At the cellular level intense exercise conditions the body to deal with this acidosis and when you get hit, that conditioning is the difference.

I did 2 tours as a Nurse Anesthetist on a Forward Surgical Team (FST) with SOF over there. I saw this first hand. I can go on and on about it. But for the record, I saw some very fit SOF personnel survive some severe hits. In the end, I do not this it is because of what I (or my surgical team did), but rather their personal physical fitness that saved their life.

Steven Low
08-05-2008, 06:37 PM
Hmm, interesting. I do agree most of the acidosis is due to metabolic from the muscles (ATP hydrolysis, glycolysis, Krebs, etc.). However, isn't some of the blood pH drop because of CO2 + H2O <-> H+ + HCO2- ? Do you know of any articles that discuss this if this is not the case or at least discusses how much of a pH drop there is because of this. I do see what you mean when someone is shot and starts hyperventilating thus lower pCO2 though so I can see how this applies in this situation.

Cool stories though.. mind detailing any? :D

Alex Europa
08-06-2008, 07:20 AM
It is this acidosis that is deadly and the body can survive a lot longer then a minute. It is this same acidosis that occurs, at least on a smaller scale during any intense exercise. At the cellular level intense exercise conditions the body to deal with this acidosis and when you get hit, that conditioning is the difference.


Wow, that's an amazing tidbit. I've always known (to quote Rippetoe) that "strong people are harder to kill..." but this explains it. Or at least part of it, I don't think the effects of mental hardening can be quantified.

- Alex

Pat McElhone
08-07-2008, 07:02 PM
Hmm, interesting. I do agree most of the acidosis is due to metabolic from the muscles (ATP hydrolysis, glycolysis, Krebs, etc.). However, isn't some of the blood pH drop because of CO2 + H2O <-> H+ + HCO2- ? Do you know of any articles that discuss this if this is not the case or at least discusses how much of a pH drop there is because of this. I do see what you mean when someone is shot and starts hyperventilating thus lower pCO2 though so I can see how this applies in this situation.

Cool stories though.. mind detailing any? :D

This is a very, very long post. These ideals have been in my head for awhile, this is the first time, I have actually collected my thoughts and wrote them down.

Here is the over view of development of Lactic Acidosis, taken from Mason: Murray & Nadel's Textbook of Respiratory Medicine, 4th ed.

Pathophysilogy of Lactic Acidosis:
Production of excessive quantities of lactic acid is frequently related in some way to tissue hypoxia. As indicated in Figure 7.5 , glucose is normally metabolized to pyruvate, which is in equilibrium with lactate. Metabolism of lactate can only occur if it is converted back to pyruvate. Pyruvate can be transported into the mitochondria in either of two ways. CO2 can be added to pyruvate by the enzyme pyruvate carboxylase to form oxaloacetate, which can then be metabolized by the Krebs cycle and the electron transport chain. Alternatively, the pyruvate can be oxidized to acetyl coenzyme A (CoA) by pyruvate dehydrogenase. The acetyl CoA then combines with oxaloacetate and is metabolized in the presence of oxygen to form both ATP and nicotinamide adenine dinucleotide (NAD+). In the absence of oxygen, the reduced form (NADH) cannot be oxidized to NAD+, and ATP production by the cytochrome system is blocked. Because the carboxylase reaction requires ATP and the dehydrogenase reaction requires NAD+, pyruvate can no longer enter the mitochondria, and the concentrations of both pyruvate and lactate in the cytoplasm increase. Increases in NADH within the cytoplasm result in a disproportionate increase in lactate (in accordance with the equation in Fig. 7.5 ). In addition, the accumulation of ADP, AMP, and phosphates within the cytoplasm accelerates the activities of phosphofructokinase and pyruvate kinase. This in turn increases metabolism of glycogen and glucose, which are effectively converted to lactate, a sequence of events referred to as the Pasteur effect. In effect, hypoxia promotes lactic acidosis both by increasing lactate production and by reducing its metabolism (see Fig. 7.5 ).

Causes of Lactic Acidosis:
Type A: Tissue Hypoxia
Poor tissue perfusion: shock due to hypovolemia, sepsis, cardiogenic, idiopathic
Severe hypoxemia: pulmonary disorders (e.g., asthma, after inhaled β2-adrenergic agents), acute respiratory distress syndrome, carbon monoxide poisoning
Exercise above anaerobic threshold, seizures, shivering
Severe anemia, carbon monoxide

NOTE: This first and third causes: poor tissue perfusion and exercise above the anaerobic threshold.

Here is my $0.02 based on my first hand observation of very, very fit guys who believed "the more you sweat in training the less you bleed in battle":

The human body adapts to stressors to the point it is able to overcome most stressors if, there is a gradual introduction of the stressor to the body. The body will face the stressor, adapt to it and next time it can handle more of the stressor. On and on it goes. The stressor may be squatting 2.5x BW, running a marathon or a virus that one has been immunized against.

How is lactic acidosis any different? In the above overview we see the steps of how someone develops lactic acidosis, if one trains at high intensity where most of the energy production is from an anaerobic source, they will face an acidosis, over time, they will be able to handle more and more of an acidosis and they will be more efficient at operating in the acidosis, or buffering the acidosis. These pathways are laid in high intensity training. Now if some one is hit, now has a cellular hypoxia developed by decreased tissue delivery of oxygen (hemorrhagic shock), these pathways can still function and buy this indivdual some time.

Finally, Viet Nam gave traumatology the concept of the "golden hour". This is the ideal that if you get to someone fast enough, they will live. Now, we see the triad of death in trauma as acidosis, hypothermia and coagulopathies. Once these develop, shock becomes harder and harder to treat, so that first hour is really just a period to prevent this triad from developing.

The case for high intensity exercise is that through measured periods operating at a supra-aerobic level the body will face an acidosis and develop some way to deal with it for a little longer and over time a little longer still. For some, that might mean a faster "Fran", for a small subset of the population that might turn their "golden hour" into a "golden three or four hours", which is the difference between life and death.

Steven Low
08-07-2008, 07:54 PM
Oh, well, I already knew the physiology behind acidosis, and that book is actually probably out of date. Basically, increased H+ concentration is because of ATP->ADP+P hydrolysis & glycolysis & krebs reactions themselves. Not because of pyruvate<->lac.

See the posts in this thread for a bit more explanation on that.. if you feel like it:
http://www.performancemenu.com/forum/showthread.php?t=2704

I could see how one would be able to operate under those conditions a bit longer. I was actually kinda hoping you were going to detail why CO2 doesn't have a significant impact on blood pH as I already knew muscles did...

Pat McElhone
08-08-2008, 06:45 AM
Do "they" really know why acidosis develops in a hypoperfusion state? I do agree that the term "lactic acidosis" is probably out dated by the physiologists, but it is still used and recognized in patient care. The book qouted is one of the main text books in Pulmonary Medicine, 2005 edition.

Are you asking about CO2 effect on acidosis in a hypoperfusion state? I do not know the biochem off the top of my head (my last biochem exam was 10 years ago), but I can say from experience, that in a hypoperfusion acidosis, CO2 is not a factor.

Steven Low
08-08-2008, 11:46 AM
Do "they" really know why acidosis develops in a hypoperfusion state? I do agree that the term "lactic acidosis" is probably out dated by the physiologists, but it is still used and recognized in patient care. The book qouted is one of the main text books in Pulmonary Medicine, 2005 edition.

Are you asking about CO2 effect on acidosis in a hypoperfusion state? I do not know the biochem off the top of my head (my last biochem exam was 10 years ago), but I can say from experience, that in a hypoperfusion acidosis, CO2 is not a factor.
Well, I agree with saying "lactic acidosis" in the sense that the acidosis accompanies the rise is lactate, but it's definitely not the cause (according to the stoichiometry & analysis) and such references have already been refuted in peer reviewed journals. Just saying.. :p

Okay, with the CO2 I guess. Hmm, I guess I'll go look it up later.

Pat McElhone
08-08-2008, 01:53 PM
The point of my orginal post was a place for high intensity training (above "anaerobic threshold") for people whose lives really do depend on their physical fitness. It was not to discuss the roles of CO2, lactate or any other basic science. This is one point I believe very much it, but I do not want to see the forest get lost in the trees.

Liam Dougherty Springer
08-08-2008, 05:23 PM
Is it possible that improved neuro-endocrine response do to the high intensity anarobic training involved could prolong someones ability to maintain critical body functions in a state of stress and shock. I feel like I have read about similar hormonal and bio chemical reactions in both. I am probrably way off to the side here but the thread is interesting to me and it seems to be a highly relevent topic to functional training and longevity being that it may keep you alive under trauma.

That may also be exactly what Pat was getting at and it dosn't deal with CO2 saturation but... (shrug)

It seems like the end result is the same either way if the training allows you to be resistant to death when seriously injured.

Pat McElhone
08-08-2008, 06:35 PM
Steven,

There is no increase in CO2 in hypovolemic shock because there is no increase in metabolism. The acidosis is due to an imbalance between O2 supply and demand because of a decreased supply, not increased demand. In exercise or any other hyper-metabolic state (malignant hyperthermia, infections, seizures, etc) there is an increase in CO2 and the acidosis is a mixed respiratory and metabolic. Also, minute ventilation will increase due to pain from injury, cellular hypoxia, and an attempt to compensate for the metabolic acidosis and PaCO2 levels will actually be lower then normal.

Again, this is not the point of the post, but I have been thinking about your question.

Jerry Hill
08-12-2008, 09:28 AM
The point of my orginal post was a place for high intensity training (above "anaerobic threshold") for people whose lives really do depend on their physical fitness. It was not to discuss the roles of CO2, lactate or any other basic science. This is one point I believe very much it, but I do not want to see the forest get lost in the trees.

Pat,
This is some quality information!
There are many folks who would benefit by hearing more from you about your experience.

The idea behind doing the interview with Greg and other experts was to increase awareness for those whose lives could depend on what type of shape their in.

Do you have any desire to put the heart of your thread together in an article?
I know at the least, it would help my cause here in Alexandria and I would distribute your info to the best of my abilities. I also think it has the value and potential to be a subject in the PM or CF Journal.

Thank you for what you’ve shared already and most importantly for your service.

In Strength,
Jerry

Pat McElhone
08-12-2008, 03:49 PM
Is it possible that improved neuro-endocrine response do to the high intensity anarobic training involved could prolong someones ability to maintain critical body functions in a state of stress and shock. I feel like I have read about similar hormonal and bio chemical reactions in both. I am probrably way off to the side here but the thread is interesting to me and it seems to be a highly relevent topic to functional training and longevity being that it may keep you alive under trauma.

That may also be exactly what Pat was getting at and it dosn't deal with CO2 saturation but... (shrug)

It seems like the end result is the same either way if the training allows you to be resistant to death when seriously injured.

I do not think the compensatory mechinisms for neuro-hormonal, that is based on actions of either the nervous or endocrine systems. The cause of cell death is ultimated failure of the pumps that regulate chemicals going into and out of cells, cells swell and ultimately burst. I would bet that the mechanisms are intra-cellular and involve some type of adaption that allows cellular function to continue.

Also, a simular thing may happen locally in rhabdo. Rhabdo has many causes, but one is failure of the ion pumps to function, muscle cells swell, then burst releasing myoglobin into the blood stream. This could help explain the lower, incidence of rhabdo in fit people. I do not know this, just thinking about it.

Yeah, these thoughts have been in my head for awhile. I thought about submitting it to CFJ or PM. I am interested in getting this message out to the actual guys kicking down doors, not debating with a bunch of intellectuals about whether or not this is possible.

Thanks to the those who do show interest in this subject

Pat McElhone
08-20-2008, 06:38 AM
I feel the need to say the following: My posts are based on my personal opinions seen taking care of combat casualties, they are not medical advice. I also believe any high intensity training should be introduced very gradually, in measured increments, by a responisble individual. While, I do argue how high intensity training maybe useful, I also believe it can cause harm and even death.