In past articles, I have written about mitochondria. One way to think about mitochondria is that they perform the final committed step to actually make ATP. That final step involves two linked components: the reaction that converts oxygen (O2) to water (H2O) and the reaction that actually makes ATP. The first of these two reactions is the one that so many people associate with the term “oxygen uptake.” But it is the second one that actually matters in a setting of exercise. So, the question at hand is: “what kinds of things can actually adapt as a result of exercise training?” What follows is part 1 of a series that will start at the most central components of the endurance adaptation and gradually move out to eventually touch the mitochondria themselves.

As I wrote in a previous article:

In 1971, Drs. Jere Mitchell and Gunnar Blomqvist, both cardiologists at UT Southwestern Medical School in Dallas, published a paper in the New England Journal of Medicine entitled “Maximal oxygen uptake.” What Drs. Mitchell and Blomqvist demonstrated was both simple and fundamental: oxygen uptake is linearly proportional to cardiac output and peak cardiac output is linearly proportional to cardiac size. What does this mean? If you want to increase your maximal oxygen uptake, increase the size of your heart (meaning mostly the size of the left ventricle). How do you do this? The same way you increase the size of any muscle – physical exercise.

So, what does this actually mean? How do you “exercise” the heart? You do it the same way you exercise any other muscle – you make it work hard. So, what does that mean? You make it beat more often (the functional equivalent of any exercise with more reps) and contract more strongly (the functional equivalent of any exercise with a higher resistance).

Let’s start with heart rate. Anything you do that results in an increase in heart rate will be the functional equivalent of any exercise with more reps. From the perspective of your heart, it does not matter what the rest of your body is doing. All your heart does is respond to whatever metabolic load there is with an increase in heart rate. Whether it is the result of running, cycling, swimming, rowing, burpees, a crossfit WOD, or anything else, if you do something that causes your heart rate to increase, you generate this component of the central adaptation.

But increasing heart rate is simple. Increasing the “resistance” is much more complicated. So, let’s take this one step at a time. First, from the perspective of your left ventricle, what is “resistance?” It is a combination of three things: (1) starting the contraction with a larger end-diastolic volume, (2) pushing blood out more rapidly, and (3) pushing blood out against an increased pressure head. So, in order:

  • How do you start the contraction with a larger end-diastolic volume? Anything you do that uses large muscles in a dynamic manner (movements that alternate contractions with relaxations and that involve movements through a large range of motion) pushes blood back up the venous system to the heart. The more blood that is pushed back to the heart, the more the left ventricle will fill. The more the left ventricle fills, the more blood is pushed out per heart beat (this is described by the term “stroke volume”). The larger each heart beat, the harder the left ventricle must work. The harder it must work, the bigger and stronger it gets. In practice, stroke volume continues to increase until the work rate is roughly 50% to 60% of the way from heart rate during to heart rate during maximum exercise. Anything more than that causes no further increase in stroke volume;
  • How do you push blood out more rapidly? The higher your heart rate, the less time your left ventricle has to push out all its blood. So, as your heart rate increases, the left ventricle must contract more rapidly. The more rapidly your left ventricle contracts, the harder it must work. The harder it must work, the bigger and stronger it gets. In practice, this is very simple – the higher the heart rate, the faster and harder the left ventricle must contract;
  • How do you push blood against an increased pressure head? Via a complicated set of interrelated circulatory adjustments, exercise results in an increase in blood pressure. In particular, the heart must overcome the greatest amount of blood pressure during exercise that involves some combination of upper body muscles and very high amount of force application. So, upper body resistance exercise causes the largest increase in blood pressure. As above, the harder the left ventricle must work, the bigger and stronger it gets.

So, from a practical perspective, what does this all mean to the athlete or coach? From the perspective of the heart, any exercise paradigm that is greater than about 50% of the maximum possible will maximize the size-stress on the heart. Any further strength increases come from exercise paradigms that push the heart rate up towards peak heart rate or that involve very heavy (particularly upper body) efforts. How much can the heart adapt? From completely untrained to maximally endurance trained, the heart can become roughly 25% larger and, thus, push roughly 25% more blood per minute. Once this adaptation has occurred, all the subsequent adaptations are peripheral. More on that in the future.

If any of you have any specific questions, including any greater details about this, please do not hesitate to ask me directly. I am available on Facebook  @PangeaBiomedical


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.