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In exercise physiology textbooks, three energy systems are described: aerobic (uses oxygen), anaerobic (glycolytic; “without oxygen”), and alactic anaerobic (CP-ATP or phosphogen system). This is correct but unfortunately does not address fuel substrate utilization as a function of energy demand which is what matters in defining training protocols. Hawley and Hopkins in their paper published in 1995 proposed that the aerobic energy system be decomposed to two pathways: aerobic lipolytic and aerobic glycolytic. This accommodates for the graded shift in fuel source from fat to carbohydrate as power demand increases from low to moderate levels of intensity under aerobic conditions. This illustration displays the real-time logic of energy production as the demand for ATP increases. The reason for the shift from lipids (fat) to carbohydrate is that the pathway for lipids to be converted for inputs (the beta-oxidation pathway) to the Kreb’s cycle in the sub-cellular structure called the mitochondrion is O2 dependent while the process for carbohydrates to be converted to the same convergent downstream pathway is not. But the real reason is the rate in which these pathways produce ATP: the aerobic glycolytic pathway can generate ATP at twice the rate compared to the aerobic lipolytic pathway. This is crucial to understand! In other words, if under “aerobic conditions” the demand for energy becomes too great, your body uses carbs instead of fats: biochemistry and biophysics dictates this without any wiggle room. Once the threshold of maximal fat utilization (called maximal lipid power and measured in grams/min) is exceeded, all further fuel used is carbohydrate BUT at intensities producing a blood lactate concentration of 4 mM/liter (approximately the anaerobic threshold for elite athletes), fat utilization drops to ZERO–100% carbohydrates are used. Alas, at around 85% of VO2 max (92% in elite endurance athletes), the body uses no fat at all! The reason for this is the differential rate of ATP production as a function of fuel source and metabolic pathway (illustrated on bottom left). It even gets worse: for non-elite endurance athletes (or elite non-endurance athletes) this phenomenon occurs at even lower relative intensities (see bottom right of illustration). 

In my book The Digital Mantrap: An Operating System for the Human Organism (2000), Chapter 6 goes into the theory and practice of these facts in depth. Knowledge of maximal lipid power and how to train to increase it is not new and has been used by serious long-distance (i.e. 4+ hour competitions at close to steady-state pace) endurance athletes for a long time (remember LSD training (long, slow distance)?). The science has gotten more refined and quantitative but the basic concept is not new. Stage race cyclists, Ironman triathletes, long distance runners (like 100 milers, etc.) have the training down to a science. For example, here is a paper from triathlon.org that goes into detail on training protocol for Ironman distance triathlons. Contrary to popular belief, the marathon is not a ultra-distance endurance event: the marathon is primarily a glycogen-fueled event and race-pace is around a 2.5 +/- 0.5 mM/liter lactate concentration in elite competitors. In 4+ hour to multi-day events, maximal lipid power is the performance-limiting factor. The additional benefit of improving maximal lipid power in any long-distance or ultra-distance endurance event is conservation of glycogen stores. This is obvious.

So, what happens as endurance capacity increases? The following diagram from my first book illustrates the training effects at the organism level. Assuming that you do the training properly, you are able to go longer at a fixed heart rate and at higher power levels before there is a heart rate inflection point (fatigue ensues as you deplete glycogen stores). In the diagram observe the pie charts on the right where the pie chart’s area represents total energy expended and the relative contributions from carbohydrate, adipose fats, and intramuscular triglyceride stores (yes, fats stored inside the muscle, called IMTGs, increase and their % contribution increases as well, to a point). Chapter 6 describes this in detail.

The training heart rate ranges, technically speaking, are determined by plasma lactate concentrations and are individualized for each athlete. But this is expensive and requires a lot of technical expertise! I provide a good rule of thumb for determining heart rate ranges for improving endurance capacity (which is the area under the curve in the above diagrams: power (watts) x time = energy expended (kjoules)). Of course, improving endurance capacity like this approximates the intensity range for impacting maximal lipid power. You cannot have one without the other: the entire biological reason for this adaptation is to increase your survival under conditions where food is lacking (thus a chronic semi-fasted state) and you must move at low power (evolutionarily speaking, doesn’t walking on uneven terrain sound like the lion’s share of daily energy expenditure for any primate’s lifespan?) for hours or days. This is the most basic adaptation to stress that exists for mammals and is entirely ignored by the entire human population–at their peril–except for a miniscule population of serious long-distance endurance athletes. I call it “woolly mammoth training” because it is the most ancient metabolic adaptive response there is.

The above equations are expressed in the Karvonen heart rate reserve format. HR(target) is the starting heart rate for a training session and you don’t stop the training session until HR(termination) is reached. If you are out of shape this may only take a few minutes or less (I have seen that happen many times). If that is true, then you need to begin a walking program until you can do this or else reduce the heart rate percentages in the equations from 60 and 70% to 45 and 55%, respectively. When you improve to the “Early Adaptation Stage” in the diagram, you will be able to stabilize the heart rate at HR(target) for a longer time. Eventually you will be able to stay at HR(target) for 60 to 90 minutes. What progresses are the two variables: load and time. As you improve, at a given load your observed heart rate decreases so you increase the load until you are back at HR(target). Tremendous progress can be achieved with two training sessions per week in six months. Additionally, this is the best weight management approach that exists if coordinated properly with macronutritional management.

Now here is the most common error: instead of going longer you increase HR(target) to shorten the workout. You cannot substitute intensity for duration! This is the tragic error that I have seen and it seems to be going viral for two reasons: (1) ignorance of the complex physiology and biochemistry of maximal lipid power and endurance capacity and the stress requirements for optimal adaptive response; and (2) people think they can prepare for an Ironman or equivalent through interval training. No one has ever won an Ironman or equivalent metabolic event doing this and never will. The error is as follows: if you shift your training to higher intensity (meaning going from an ideal intensity at or just beyond maximal lipid power and move closer to the next metabolic switching point of the anaerobic threshold) the adaptive response shifts to improve the glycolytic pathway at the expense of the lipolytic pathway. You need to understand that the lipolytic pathway is progressively abandoned as intensity moves between the two switching points and is totally abandoned at the anaerobic threshold. It is a nonlinear relationship as the anaerobic threshold is reached meaning fat metabolism falls off a cliff.

Now if you are beginner and are sedentary you can go do hill repeat sprints and improve the lipolytic pathway. But that is not what I am talking about: I am talking about as you become more adapted to improving O2 and fuel transport and utilization, the margin for error in defining your training protocol substantially decreases. In fact, a point is reached in advanced endurance athletes even doing the correct training will fail to improve because the damage caused by training will exceed their ability to recover. It reaches the extreme right end of the human performance envelope and yields negative marginal returns (think “pushing the envelope”) as your genetic limits are approached (your theoretical phenotypic ceiling) and survival capacity approaches zero. I call people that operate at this level Red Zone Operators. This is because Homo sapiens are not designed to do the Tour de France, Ironman, climb K2 solo without oxygen, or the 135 mile Badwater run!  At this point, micronutrition, macronutrition, recovery modalities, sleep, functional strength training and stress management must be optimized or else you are doomed to the fate of Sisyphus. For more information on my theory of human performance envelopes (a facet of my Unified Theory of Fitness) and Red Zone Operators see this.

If you want to learn how to execute training for long-distance endurance events professionally and affordably, contact Mark Allen at http://markallenonline.com. He is the greatest endurance athlete of all time and nobody has more experience than him on this kind of training. (Mark Allen's bio). I have known him since 1991. He walks his talk.

Note: Red Zone Operator David Goggins, a BIONX SUPERMODEL 2 client, is preparing to do the 2013 135-mile Badwater run on July 15-17, 2013. He finished 3rd in 2007 with a time of 25:49:40 and 5th in 2006 with a time of 30:18:54. He broke the Guinness 24-hour pull-up world record with 4030 repetitions on his third assault of the record on January 20, 2013.

Note: in my example training session and video I was around 136 bpm for slightly over 90 minutes at a load of 200 watts before heart rate inflection. I stopped at 120 minutes at a heart rate of 144.

–James Autio

www.jimautio.com

For more information: 

BIONX SUPERMODEL (pdf)

www.bionxpro.com

www.bionx.com