THE VIKING MANIFESTO: Piecing Together a New Approach to Nutrition and Training for Swimmers from Scientific and Anecdotal Evidence.
Part 5: Muscle Fiber Types, Recruitment and Specificity.
At this point, I hope my arguments are interesting enough that you want to read more, but I understand if you feel like this guy. It's a lot to take in.
In the last chapter we focused on energy metabolism within the muscle, paying particular attention to the idea that mitochondrial density, the utilization aspect of the supply vs. utilization argument, is supremely important, and that the ketogenic diet may enhance this metabolic adaptation in athletes. This would open the door for the LCHF diet making a difference in swimming no matter the race distance. Today, we are still on the topic of metabolism, but we will also be looking more at the supply side, as well as looking into how it applies to the concept of specificity, which should be at the heart of any athletic training, especially for a sport as training and technique intensive as swimming.
In the past, only ultra-endurance athletes paid much attention to the concept of fat-adaptation, almost as though it was something that really only mattered if you planned to hold steady state for several hours. Interestingly, a good marathon runner will tell you, you don't have to be "in ketosis" to be fat adapted. You can actually become somewhat fat-adapted as a carb eater if you work out often enough with long enough workouts to deplete glycogen stores often and force the adaptation, but it will not bring the same level of adaptation. Obviously LCHF isn’t the only way to go, but I defy you to find a better way to make that adaptation in a person training for a 1-2 minute race. While swimming has had generations of continuous success with high-carb and long workouts, I am guessing that soon there will be more people training and eating smarter who can have the same or higher levels of success and have more chance at a life outside of the pool.
I am hoping to be one of the pioneers who proves it. I don’t have time to train even a tenth of what I did twenty years ago, but I am certain I can go faster than I did at what would be considered my “prime” in spite of the twenty year taper I am trying to manage. I am certain we will start seeing some world class athletes improving and loving the sport for longer careers, and you will see young athletes develop in a new way by training for the most appropriate adaptations, and getting rid of all metabolic interference that they didn’t even realize was standing in their way. New science is emerging all the time regarding the benefits of carbohydrate restriction. Just check out this finding by Yale University that was released this week. It implies confirmation for me of a lot of the anecdotal evidence I have seen all over web forums regarding things like acne and arthritis improving, as well as with many of the claims made in the low-carb community about heart disease and more.
I found a fantastic write up from the Gatorade Sports Science Institute called Muscle Adaptations to Aerobic Training that I will refer to as a textbook of sorts since they cite the sources that have made these concepts accepted standards. Even without considering diet, I love this as a resource because, while it agrees with a lot of what I have spoken about already regarding mitochondria, muscle capillarity and blood flow capacity, they do a great job of interjecting research findings into their descriptions that enhance our knowledge of the complex interactions between these contributing factors and create a good picture of what a smart training program will look like when we are specific about the adaptations we are striving toward. I just want to point out and paraphrase a few things from this resource:
- MITOCHONDRIA: They make the same points I did earlier about mitochondria increasing aerobic capacity, but they add that it was previously thought that “increased enzymatic capacity was not utilized because mitochondrial content was considered in excess of maximal needs even in untrained muscle, but now there is evidence to indicate that an increase in mitochondrial content is necessary to realize the increased potential for aerobic ATP provision induced in muscle training.” So basically, once they thought that we naturally had plenty of mitochondria so we should just focus on increasing blood supply to muscles, but now they have backtracked and think mitochondrial enhancement is pretty important because it gets muscle to burn more fatty acids and less glycogen to improve muscle performance. This is pretty much the point I made in part 4 of the manifesto.
- BLOOD FLOW CAPACITY: Here they say that blood flow to skeletal muscle is so exceptionally high that cardiac output can’t sufficiently perfuse all of the blood vessels in our muscle mass even if they were to maximally dilate. Thus, even during intense exercise requiring max oxygen consumption, this limitation means that only a fraction of an individual’s entire muscle mass can be active, and then it only functions at a fraction of its blood flow capacity. Nevertheless there is evidence that the peak capacity of muscle is increased by endurance training, BUT the value of this adaptation that further increases the ‘unused’ blood-flow reserve in muscles is unclear. It is likely that the important features of vascular adaptations to training involve the optimal utilization of the flow delivered to the muscle and the exchange of nutrients between capillaries and fibers. Once again they point toward utilization being the more important factor.
- MUSCLE CAPILLARITY: This is where the two points above come together. Basically, they say that exercise training increases the number of capillaries surrounding individual muscle fibers, so when a fiber is recruited it becomes more effectively “bathed” in the flow of blood delivered to the muscle. This development of increased capillarity can occur in all fiber types but is most easily observed when improved in low-oxidative fiber and can contribute to total max oxygen consumption.
Low-oxidative muscle fibers? Now we are getting somewhere. This brings us to another one of those extremely important concepts in exercise science that many coaches have not been versed in: muscle fiber types 1, 2a and 2b (which the fantastic description I cut and pasted below from athletics.wikia.com calls type 2x.) Many coaches talk of fast-twitch and slow-twitch, but may not quite have their head grasped around the fact that we are considered to have two types of fast-twitch muscle fibers and the difference between the two might just be one of the most important physiological aspects related to training in the sport of swimming. Here is the run-down on fiber types so we know you are up to speed:
Type I
Type I muscle fiber is also known as "slow twitch oxidative" fibers. Muscle fiber types can be broken down into two main types: slow twitch (Type I) muscle fibers and fast twitch (Type II) muscle fibers Type I fibers are used in lower-intensity exercises such as very light resistance work aimed at muscular endurance and long-duration aerobic activities such as 5K and 10K runs. Type I fibers are identified by slow contraction times and a high resistance to fatigue. Structurally, they have a small motor neuron and fiber diameter, a high mitochondrial and capillary density, and a high myoglobin content. ST fibers also have a low supply of creatine phosphate, low glycogen content, and a high store of triglycerides (the stored form of fat). ST fibers contain few of the enzymes involved in glycolysis, but contain many of the enzymes involved in the oxidative pathways (Krebs cycle, electron transport chain). ST fibers are predominantly used for aerobic activities requiring low-level force production, such as walking and maintaining posture, but are also the primary fiber type found in endurance athletes. Most activities of daily living use ST fibers.
Type II
Type II muscle fiber is also known as fast twitch muscle fibers. These fast twitch fibers can be further categorized into Type IIa and Type IIx fibers, which are also known as "fast twitch oxidative" and "fast twitch glycolytic," respectively. Type I fibers are characterized by low force/power/speed production and high endurance, Type IIx fibers are characterized by high force/power/speed production and low endurance, while Type IIA fall in between the two. It is possible that a fiber might be transformed from Type IIx to Type IIA with exercise training.
Type IIA
Type IIA fibers (Fast Twitch 1), or fast oxidative fibers, are used more during sustained power activities such as sprinting 400 meters or doing repeated lifts with a weight below maximum (but not with very light weights). They contain very large amounts of myoglobin, very many mitochondria and very many blood capillaries. Type IIA fibers are red, unlike Type IIx fibers, which are white. Type IIA fibers have a very high capacity for generating ATP by oxidative metabolic processes, and split ATP at a very rapid rate. They have a fast contraction velocity and are resistant to fatigue. Such fibres are infrequently found in humans.
Type IIx Fibers
Type IIx fast-twitch fibers (Fast twitch 2), or fast glycolytic fibres, are recruited for very short-duration high-intensity bursts of power such as maximal and near-maximal lifts and short sprints. Type IIx fibres contain a low content of myoglobin, relatively few mitochondria, relatively few blood capillaries and large amounts glycogen. Type IIx fibres are white, while Type I (slow twitch) fibers are red. Type IIx fibers are geared to generate ATP by anaerobic metabolic processes, however, they are not able to supply skeletal muscle fibres continuously with sufficient ATP, and fatigue easily. Type IIx fibers split ATP at a fast rate and have a fast contraction velocity. Such fibres are found in large numbers in the muscles of the arms.
Now back to the page from the Gatorade Sports Science Institute:
Please allow me to cut, paste and paraphrase a few things from their section on Training Stimulus: it is clear that the muscles (or fibers within a muscle) not involved in the exercise task do not adapt. Thus, the critical stimulus for adaptation is something very specific to the active fibers and not likely to be some generalized factor circulating in the blood that influences all muscles. Further, for a given exercise program, training must be performed for a sufficient duration of days or weeks to allow the muscle-specific biochemical adaptations to reach steady-state. For example, mitochondrial content appears to reach a steady-state after approximately 4-5 weeks of training.
The magnitude of the training-induced increase in mitochondrial content is also influenced by the duration of the daily exercise bout. Longer exercise bouts generally produce greater increases in mitochondrial content. However, the influence of exercise bout duration is not linear, as training sessions become increasingly prolonged, the additional training time appears to be relatively less important as a signal inducing an increase in mitochondrial content. Further, exercise intensity interacts with the duration of the exercise bout to make the initial minutes of exercise even more effective in establishing a stimulus for adaptation. Note in figure 2 that the peak adaptation in mitochondrial content seems to occur with shorter durations of exercise as the intensity of each training bout is increased. The benefit of very prolonged training sessions in enhancing performance may be related to adaptations in cardiovascular function, fluid balance substrate availability, or other factors not directly related to muscle-specific adaptations. At least part of the beneficial effect of increasing exercise intensity on training induced adaptations in muscles can be attributed to the effect of intensity on muscle fiber recruitment.
Let that sink in for a second. All of the above basically makes the case that the high-volume traditional swim training that we all grew up with is old-school, and that if we want a better adaptation we can shorten up the workouts and just make them more intense. They also make the point that seeking a “general” fitness adaptation is a waste of time because muscle fiber recruitment is specific and muscle fibers not specifically recruited for an activity don’t adapt. The longer exercise bouts inherently involve lower intensities, and thus would be effectively adapting slow-twitch fibers to be more efficient at metabolizing oxygen. Remember, slow-twitch fibers cannot become fast-twitch and fast-twitch cannot become slow-twitch. The only change of muscle fiber type we can make is from fast-twitch oxidative to fast-twitch glycolytic and vice-versa-- so, essentially, high-intensity trumps long-distance training in regard to utilization and supply, since mitochondria increase with intensity AND as stated above in the section on muscle capillarity: development of increased capillarity can occur in all fiber types but is most easily observed when improved in low-oxidative fiber and can contribute to total max oxygen consumption.
Therefore, I contend that if we want to improve supply and utilization both, we should focus on high-intensity swimming done in a way that is designed to cause type 2b muscle fibers to convert to type 2a, and the LCHF diet is the key to unlocking a higher level of potential if we can train for this specific adaptation along with it. Maximum power drawn aerobically, with the most efficient glycogen sparing possible to save anaerobic glycolysis for only the highest intensities at the end of the race.
Therefore, I contend that if we want to improve supply and utilization both, we should focus on high-intensity swimming done in a way that is designed to cause type 2b muscle fibers to convert to type 2a, and the LCHF diet is the key to unlocking a higher level of potential if we can train for this specific adaptation along with it. Maximum power drawn aerobically, with the most efficient glycogen sparing possible to save anaerobic glycolysis for only the highest intensities at the end of the race.
Whoa. Damn… apparently, I wasted a lot of time training the speed right out of me back in the day. I never did get any good at that 1200 IM I was training for either. Hmmm…. Ever get the feeling you’ve taken some kids and done that to them? I know I have felt that way with a few of my most talented. I have a couple of former athletes I wanna talk back into the water when they bring their 4 year olds to sign up for our swim lessons program, and a few more I want to apologize to for just for wasting so much of their time. Yup, coaches… I said it. I admit that I wasted their time by just swallowing what I was taught and not researching it for myself.
The next chapter will be about the way we should train for the absolute best adaptations to translate to effective racing within the rules of the Viking Method. I am sure that many of you SwimSwam commenters can guess where I am heading with this. Time to break out the flame-throwers, y’all. There’s gonna be a lot of acronyms coming your way.
Please, don’t hold back on the comments.
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