In my last article, I wrote about the adaptations that occur, as a result of training, within the myocardium. This is the whole-body central adaptation that responds to almost any kind of activity that increases the workload of the myocardium. For anyone interested in doing exercise training to increase the capacity of the myocardium, it is clear what you must do. So, OK, your myocardium is maximally adapted. Now what? In what follows, I will trace the adaptations spatially out from the myocardium and ending at the mitochondria within muscle cells. In so doing, I will address two sub-questions: (1) what do you do now to increase your capacity to do endurance-type activities? and (2) where do those adaptations occur?

With a well-trained myocardium, you can pump more blood per minute than prior to training. So, what would be a good thing to do with all this capacity? Make sure it actually goes to working muscle. To do this, it would be very useful to increase the number of capillaries you have in and around your working muscles. With more capillaries, you get two major benefits: (1) a greater capacity to actually direct blood away from other parts of the body and to your working muscles and (2) as the blood is going through your working muscles, the oxygen in your blood now has to traverse a shorter distance to actually get to a mitochondrion so that it can contribute to the synthesis of ATP. OK, so what triggers the growth of new capillaries? At the simplest level, any kind of energy supply-demand mismatch will eventually cause this to occur. So, what does this kind of training look like? It is the traditional “endurance” training we all know – sustained (more than 20 minutes at a time) exercise at a work rate that is at least moderately intense. This would be a work rate that would result in having a sustained heart rate that is more than 65% of the way from the heart rate you have during rest to the maximum heart rate. Do this and you will stimulate the growth of new capillaries around your trained muscles.

All these new capillaries now increase your ability to get oxygen to the mitochondria. But, in order to make ATP, you also need carbon-based fuel. There are two types of molecules that you use for fuel – fats and carbohydrates. Although you have both types of fuels inside your cells, those supplies are relatively limited and anyone performing an extended bout of exercise (2-3 hours of sustained training and/or competition) can become internal-fuel limited. The good news is that the supply of these fuels outside your muscle cells is relatively limitless. To get at these fuels, you need to create more transporters that can move these fuels from the blood to the inside of your muscle cells. The two transporters that are most important for this are the transporters that move fatty acids and those that move lactate. OK, so what triggers the growth of new transporters? As above, at the simplest level, any kind of fuel supply-demand mismatch will eventually cause this to occur. The problem is that the training required to stimulate the growth of these two different types of transporters are also different.

Fatty acid transporters – in order to trigger the growth of new fatty acid transporters, the exercise training activity must be one that results in a large increase in free fatty acids in the blood. At a very simple level, this will occur as a result of any exercise training activity that is sustained for a long enough period of time to trigger (mostly via hormone activity) lipolysis from adipose tissue. In essence, the longer the training time, the more this will occur. Thus, athletes like distance runners, cyclists, swimmers, etc… will trigger this to occur as a natural outcome of their training. After this has occurred, these athletes will be able to use (oxidize) the fat stored in adipose tissue. The result of this will be to increase the capacity to perform long-duration sustained exercise.

Lactate transporters – in order to trigger the growth of new lactate transporters, the exercise training activity must be one that results in a large increase in lactate in the blood. At a very simple level, this will occur as a result of any exercise training activity that is intense enough to trigger an excess production of lactate. In essence, the more intense the training, the more this will occur. This kind of training is not very much fun. It works best in some sort of “interval” training where an intense bout of exercise, with a duration between 30s and 2 minutes, generates excessive lactate production. After a short period of rest (a work-rest ratio of 1:1 or something like that), the exercise bout is repeated, with another big burst of lactate production. After this adaptation has occurred, these athletes will be able to transport the lactate produced in one (hard-working) muscle cell into an adjacent one (not so hard-working) and use (oxidize) the lactate instead of depleting any more of its own internal glycogen stores. The result of this will be to increase the capacity to perform medium-duration intense exercise.

So, from a practical perspective, what does this all mean to the athlete or coach? The training required to trigger these peripheral adaptations are more intense than what you would need if the only interest were to increase the capacity of the myocardium. It should not surprise anyone reading this that this kind of training intensity is not only difficult to perform, it often results in post-exercise soreness. To accommodate this, the athlete should be following a proper training program developed by professionals in this area as well as be following a proper program of diet and, when necessary, nutritional supplements. I designed Pangea Origins to address the specific needs of endurance athletes by increasing mitochondrial volume, this allowing your own cells to generate more ATP .

If any of you have any specific questions, including any greater details about this, please do not hesitate to ask me directly.


Dr. Loren Bertocci
Following his undergraduate career at Stanford University, Dr. Loren Bertocci earned his PhD in Biochemistry/Biophysics with a specialization in skeletal muscle mitochondria and has dedicated his career to studying the role of mitochondria in secondary metabolism (skeletal muscle).
The outcome of his 20+ years of research at UT Southwestern Medical School is the creation of a product that triggers mitochondrial biogenesis to reduce the effects of the aging process.
Dr. Bertocci’s publication record is world-class, including 26 papers in peer-reviewed journals. He has been awarded (as Principal Investigator, Co-Principal Investigator, or Collaborating Investigator) more than $3 million in grants from the American Heart Association, the Department of Defense, the Department of Veterans Affairs, the Muscular Dystrophy Association, NASA, and the National Institutes of Health.
With athletic backgrounds swimming, water polo, triathlon and track, Dr. Bertocci is also an accomplished Crossfit athlete and recently earned a Bronze Medal in Olympic Weightlifting at the 2015 Pan Am Masters Championships. He is currently training to qualify for the World Weightlifting Championships in the 65+ category.
Dr. Bertocci is Director of Science at Pangea Biomedical, which produces supplements designed for the specific needs of athletes over 40.

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