Thanks for your response. I only have one further point to make and I won't keep stirring the matter up. If mprevost has his own materials or has written materials that an amateur like myself can read I will look at them when I have the time.
He did come into someone else's domain and say that what they teach is wrong. That is what got me fired up. He didn't say that he has seen some research or evidence that gives him reason to believe otherwise, he said that what Pavel teaches is all wrong.
If you come into someone else's house and say they are all wrong you should expect trouble. If you come into a community discussion where the people adhere to that teaching and tell the people there they are all wrong you should expect to be challenged not coddled.
Ok, I will let the matter drop and I will keep my focus on the anti-glycolitic approach that Pavel teaches for my daily training.
Thank you and thanks for your response. The articles and the discussion board on the Strongfirst page are a great source of information and motivation.
Hi Robert
I apologize for the tone of my post. It was not intended to be sarcastic or critical at all, but sometimes, in a written venue like this (as opposed to face to face communication), the tone or intent is a bit lost. I should have also established who I was and my background, and intent.
I am Mike Prevost, born in 1967, from Louisiana, and graduate of Louisiana State University, with a PhD in exercise physiology. Back in graduate school (in the late 90s) my specialty was muscle physiology and metabolism. I was really interested in biochemistry and took many biochemistry courses and I managed the department's biochemistry lab. My advisor and I were keenly interested in the control of gene expression in skeletal muscle. What we observed was that any experimental treatment that challenged the energy charge of the cell (expended energy and reduced stored energy in the cell), turned on a whole host of genes that caused a shift to a more energy efficient muscle cell, and a shift towards slow twitch properties. I was looking mainly at the type of myosin protein expressed, but also looked at some other muscle enzymes involved in metabolism. Other labs were measuring mitochondrial density and aerobic enzyme concentration/activity. It was more groundbreaking at the time, but is old news now. What we (collectively, the scientific community) discovered was any time a muscle is recruited and active, it turns on gene expression aimed at increasing aerobic capacity of that muscle. this included high intensity exercise. What has been demonstrated in numerous studies is that you can shift the fiber type of muscle cells from IIx (fast) to IIa (intermediate) with an increase in activity, regardless of if that activity is high intensity, or continuous, low intensity. What integrates all of this is a decrease in the energy charge of the cell. While capillary density does not typically increase with resistance training, and increases only a little with high intensity aerobic exercise, capillary biogenesis does occur. For example, if a muscle gets bigger and capillary density is preserved, some capillaries must have been added. The prevailing view was, and is, that high intensity training adds aerobic capacity to the recruited skeletal muscles, plus it increased stroke volume (amount of blood pumped per beat) in the heart.
The second point was from watching the American College of Sports Medicine's position stand on quantity and quality of exercise for preventing disease and death. I have been watching the changes in this position stand for over 20 years. The trend is that they have been emphasizing higher intensity exercise more and more over the years. This is a significant shift from 20 years ago, when the emphasis was on low intensity cardio exercise. However, the research evidence has begun to demonstrate that shorter, higher intensity exercise seems to be protective from heart disease, stroke, diabetes, and probably cancer (and more). They are now talking about a dose/response relationship where more is better (up until a point). So, the new position stand discusses either doing more volume of low intensity work, or a lighter volume of high intensity work. The recommendation is to accumulate 500-1000 MET minutes per week. A MET is a metabolic equivalent, or the equivalent of resting metabolic rate. So a work rate of 10 METs is 10X resting metabolic rate, and if you do this for 10 minutes, you have accumulated 100 MET minutes. I can hold 10 METs for a long, long time. I do 90 minutes of rucking and 90 minutes of running per week at about 10 METS, so between those two workouts I get 1800 Met minutes (10 METS X 180 minutes). I also do about 9 minutes at about 17 METs (6 X 1/4 mile hard intervals). This short workout alone gives me 153 MET minutes. I am exceeding the ACSM recommendation, but the evidence shows a benefit from exceeding the recommended dose, as long as you recover adequately.
Finally, VO2 max is strongly correlated with less risk of "all cause mortality" and less cardiac damage and better survival rates in the event of a heart attack. It is not known if this is due to the higher VO2 max itself, or if it is due to the training that improves VO2 max. I am not waiting 20 more years for scientists to figure this out. I am actively trying to improve my VO2 max. As Izumi Tabata showed many years ago, and others as well, high intensity work provides big "bang for the buck" in improving VO2 max. Plus, as an older athlete (49 years old) I can see my top end fitness (VO2 max) declining, and keeping some high intensity work is key to slowing that decline.
I meant no disrespect to Pavel. I have purchased several of Pavel's books and have recommended Pavel's work to others countless times. I don't think we are at the opposite ends of this discussion either. I fully understand and agree with avoiding excessive high intensity anaerobic work. Too much is definitely a problem. But I do feel like some anaerobic or high intensity work is necessary, especially for aging athletes. It is also a powerful stimulus for improving/maintaining VO2 max, which seems to be important.
One, final, final point. By posting a short reply earlier, with no background, and not identifying myself clearly, I was (unintentionally) making an unethical post. Unethical in that I had no "skin in the game." By clearly identifying who I am below, and putting my credibility and reputation at risk, by stating my position in public, I have put "skin in the game" and have cleared up the ethical issue, in my mind anyway. My intent is to share what I have been given.
Mike Prevost
US, Navy Retired
Visiting Assistant Professor, Loyola Marymount University
Department of Health and Human Science
P.S. feel free to PM me if you want more explanation, or copies of research reports.