Are we over thinking antiglycolic training?

North Coast Miller

More than 2500 posts
Dr. Prevost,
Thank you for summarizing the current state of the scientific literature in this area.

I have two questions:

Is there evidence to support the notion that glycolytic training damages mitochondria in any cells or in muscle cells specifically, or in cardiac muscle cells very specifically?

Is there evidence to support the notion that glycolytic training and the creation of metabolic byproducts like "lactic acid" results in anything other than a temporary downward change in blood pH? In other words, does glycolytic training make you "acidic"?
I'd like to hear the current state of research on this as well.

Based on my own digging it appears to cause harm to some mitochondrial enzymes and is presumed to cause mitochondrial harm proper at some point of overtraining. I haven't been able to find any studies that qualified the effect with any detail.

I'm also curious how this reconciles with blood flow restriction/Kaatsu training.
 

mprevost

More than 500 posts
Dr. Prevost,
Thank you for summarizing the current state of the scientific literature in this area.

I have two questions:

Is there evidence to support the notion that glycolytic training damages mitochondria in any cells or in muscle cells specifically, or in cardiac muscle cells very specifically?

Is there evidence to support the notion that glycolytic training and the creation of metabolic byproducts like "lactic acid" results in anything other than a temporary downward change in blood pH? In other words, does glycolytic training make you "acidic"?
I typed up a really long, complex answer but honestly it was getting way too complex to be helpful. I have some theories about all of this but to really get a good handle on the state of the science I would need to spend 2-3 weeks full time with about 250 or so research reports and I have not done that yet.

However, I don't think that is entirely necessary (though it would be beneficial). How you should train depends on the results you seek. If it is health/longevity then the American College of Sports Medicine Position Statement ( http://www.aliceveneto.com/1/upload/quantity_and_quality_of_exercise_for_developing.26_1_.pdf) covers that well. You don't need much. If it is performance, then it is simple enough to find a path already established by athletes, without having to get into the detailed biochemical adaptations.

I have a theory about the biochemical adaptations that centers on maintaining NAD/NADH REDOX potential, which may result in different adaptations in fast twitch and slow twitch muscle and may also result in different long term and short term adaptations to the same protocol. But it would take the aforementioned research review to really start to confirm the theory.

If you want to see more discussion about this topic by a coach/scientist, Google Jan Olbrecht. He definitely believes that anaerobic and aerobic interfere with each other, but he has developed training protocols to achieve a peak performance in both for key races.
 

Bill Been

More than 500 posts
Thanks for the point out toward Jan Olbrecht. Reminds me of some of the stuff Dave Costill used to use with swimmers. He was also fighting for higher intensity and more specificity with respect to conditioning.


And forgive me but, without expecting you to have done some sort of comprehensive literature review, using your understanding of the the biochem of energy production, is there a plausible mechanism for either one of these maladaptions: glycolytic byproducts causing mitochondrial damage with particular concern for cardiac muscle mitochondria; and for anything other than a very short-lived dip in blood pH due to all-out bouts of HIIT?
 

mprevost

More than 500 posts
Cardiac muscles are different because they cannot produce lactate. They are purely aerobic. I am not aware of any mechanism whereby high intensity work would reduce mitochondrial function in cardiac muscle. In skeletal muscle, upgrading Krebs cycle enzymes (which are in the mitochondria) can exacerbate the NAD shortage since the Krebs cycle uses NAD to produce NADH. NAD is needed for glycolysis. So upgrading mitochondrial content might reduce anaerobic capacity (by competing for NAD that are needed by glycolysis). However the electron transport chain uses NADH and produces NAD (also in the mitochondria), so one part of the mitochondria reduces NAD concentration and the other increases it. But, more flux through the electron transport chain produces more free radicals and the potential for free radical damage. So, perhaps the muscle cell adapts to certain high intensity protocols by increasing anaerobic capacity at the expense of aerobic capacity in order to preserve and improve the capacity to do high intensity work anaerobically.
 

Bill Been

More than 500 posts
Thanks you very much for taking the time, Mike. That's the kind of "sciency stuff" I like to read, particularly from those who've been elbow-deep in this stuff. Bio-energetics is blindingly complex and it seems that we occasionally have to re-order our thinking about it.
 

North Coast Miller

More than 2500 posts
If you want to see more discussion about this topic by a coach/scientist, Google Jan Olbrecht. He definitely believes that anaerobic and aerobic interfere with each other, but he has developed training protocols to achieve a peak performance in both for key races.
Thanks for the tip, just reading the 1st chapter of his book has me wanting to buy it. His ability to express key concepts and how they are applied is incredibly straightforward considering the complexity of the topic.
 
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