THE VIKING MANIFESTO Part 2: Energy Systems and Swim Training 101

THE VIKING MANIFESTO: Piecing Together a New Approach to Nutrition and Training for Swimmers from Scientific and Anecdotal Evidence.

Part 2:  Energy Systems and Swim Training 101

Butter up that bacon and listen good… Viking is here to teach ya a little about fuel.

This post covers the three energy systems that contribute to the different intensities of athletic movement and how those relate to swim training.  I feel that while most coaches probably have a pretty good grasp on this topic, not all readers are coaches, and it never hurts to have a refresher.  Hopefully this helps us all to follow some of the ideas I am trying to get across throughout this multi-part series. Please understand that this is a simplified rundown on the complex science behind energy systems and training zones.  If you want more detail on the info I am summarizing here, there is more in-depth information available at the links throughout the article below. Much of the info here is cut, pasted and paraphrased from the links throughout the article.

All three energy systems basically boil down to different methods of making ATP available for muscle contraction, and it is a game of percentages, with each system contributing something all the time.  We never exclusively use one system as it is much more like a sliding scale based on intensity and substrate availability.  

• First is the phosphagen system which gives you about 10 seconds of explosive power from the ATP and CP (creatine phosphate) stored within the muscles. We can’t store much, so even Vlad Morozov with a really good relay exchange couldn’t blast through a 50 free solely on the explosive energy this provides.  
• Next in line is glycolysis.  It can contribute about 30 seconds to 2 minutes of all-out power based on available blood glucose and/or stored muscle glycogen.  This is the second fastest way to generate ATP, but for every glucose molecule broken down to pyruvate, only two molecules of useable ATP are produced.  The trade off is that when not enough oxygen is available, some of the pyruvate converts to lactate for energy. This is a fantastic source of power, but causes acidity which starts a cascade of events that interfere with muscle contraction.  It is anaerobic glycolysis that builds lactic acid.  When we reach the point that we are no longer able to clear lactic acid as quickly as we are producing it, we have passed our “anaerobic threshold” and will start seeing a diminished performance.
• The aerobic system is more complex as it can use glucose, glycogen, and fats for oxidation.  The aerobic system can produce 36 molecules of ATP from glucose which is 18 times the contribution from glycolysis, but the hang up is that it is a much more slowly moving system.  The aerobic system can also produce a significantly higher amount from oxidation of fatty acids, with some fats shown to create up to 129 molecules of ATP per molecule of some specific types of fat.  This is why the aerobic system can keep you going through those long practices and events.  That is a lot of energy.  It’s too bad we can’t make fat metabolism work faster.  That could be a game changer, right?

Standard swimming training aims at increasing a few specific parameters, so most of our sets traditionally focus on these variables, in order from least intense to most intense: technique to develop hydrodynamic efficiency and propulsion, increasing anaerobic threshold, increasing VO2 max, increasing “lactate tolerance” and developing explosive power.  

...and ‘beefcakiness’.  Admit it.  This is why you swim.

Here is the standard chart most USA Swimming coaches tend to follow that guides set design based on these levels.  Please note that there is some cross-over between these levels and their intended adaptations. Sprinting and race-pace training are typically considered “lactate sets” in swimming, and these are the sets normally designed to improve lactate tolerance, which includes mainly SP 1-2 but depending on the design of the set this can also be part of the equation in the higher EN 2 and 3 categories as well. The higher intensity work like speed play, ultra-short sprints, dynamic start/turn work and using the power-rack would be included in the SP3 category, designed to train the creatine-phosphate contribution to racing.

Long, low intensity endurance training has been the meat and potatoes of swim training for decades due to it’s effect on improving oxygen delivery and uptake to muscles.  This is primarily based on adaptive increases in blood flow capacity and mitochondrial density, thus increasing oxygen delivery to muscle and oxygen metabolism within the muscle, thus enhancing our ability race well, while relying less on anaerobic glycoysis. This defines aerobic training in swimming and is directly tied to improving anaerobic threshold and VO2 max in some way at all of the REC, EN1 and EN2-3 intensity levels.  VO2 max measurement has been accepted as defining the limits of the cardiorespiratory system, and obviously increasing your ability to generate power from oxygen would boost swimming performance.  

There is of course a lot more detail behind these processes but we aren’t really pursuing a chemistry or biology degree here.  I just hope that if you find any of the points I plan to make in following points confuse you, that you will come back here to have a reference to help make sense of it when it starts getting detailed.  My next post is about potential modern advances in aerobic training.  I hope you stay tuned and that I can make this easy enough to follow along.