Ketones, Inflammation, and Some Thoughts on Cholestrol

http://www.sciencedaily.com/releases/2015/02/150216131146.htm

The article linked above is kind of important.  One of the points I make repeatedly in my manifesto is that in regard to the ketogenic diet, we are still in uncharted territory as there are still a lot of questions that need to be answered and there is a lot of important science that still has not been done.  (Even worse, there is a lot of science that has been done that just hasn't hit the mainstream as well though, too.  Check this book out to see a collection of it.)

In a part of the manifesto I spoke briefly on reduced inflammation with the ketogenic diet, I think with regard specifically to more and healthier mitochondria, but I remember I also linked out to the /r/keto subreddit, stating that reduced inflammation is one of the most common side effects brought up by new dieters.  Browse /r/keto for a while and you will see it come up in so many different ways it is astounding.

The ketogenic diet is being studied as a new possibility for the treatment of many diseases, mostly inflammation based, all the way from acne to arthritis, bipolar disorder to Alzheimers, and diabetes to atherosclerosis.  The link above says that Yale University has discovered a direct link between Beta-Hydroxybuterate, one of the prevalent ketone bodies, and inhibition of one of the components of what they call the "inflammasome."  Please take time to read the article at the link above.

This would explain a lot.

We have known for decades that the ketogenic diet is often effective in treating epilepsy.  Heck, even back to biblical times we knew that just not eating could cure a person of "demons."  Nothing brings about high ketone levels like fasting.  Beta-Hydroxybuterate has also been tied to anti-aging, which makes sense when you consider the direct implications for fighting inflammation.

I am curious though, if this might also be at the heart of our scientific disagreements regarding cholesterol numbers and their relevance to heart disease.

My cholesterol went up to above 500 the first time I was tested after starting on the ketogenic diet.  I am not sure what it was before the diet, but I am pretty sure that was an increase as it is incredibly high.  An increase is often reported by people new to keto, but usually it calms down after a while. There are also a few other things I was doing that might have helped it go that high as well.  You see, there is a theory that excess ketones can enter the cholesterol synthesis pathway, which would be the reason that cholesterol goes up in new converts to paleo or keto and then often eventually goes down as our bodies become more efficient at absorbing them and using them for fuel.  This is evidenced by increased ketones in the urine.  Eventually, when fat-adapted for long enough, we don't create excess ketones and we have to use blood monitoring to detect ketones as they won't show in urine samples.

I was running pretty hard at the time.  Ketones tend to test higher after a run.   I apparently had not reached that point yet the first time I was tested.  Also, there is a chance I am just a hyper-responder to saturated fats, which might be genetic.

I had been warned once in a forum on reddit that drinking saturated fats is not a good idea, especially if you are having a sedentary day, as it causes those fats to be quickly processed by the liver.  Add MCT's like coconut oil, and you have a cocktail for high ketones, and possibly high LDL particle count as well.  If you are looking to raise your cholesterol, I have to recommend my routine of fasted running in the morning followed by coffee with butter, heavy cream and coconut oil.  Yikes!

Taking a look at Dr Attia's "Straight Dope on Cholesterol" or Ash Simmonds fantastic summary here, we see that the correlation of cholesterol levels to heart disease is all over the place, with the only significant strong correlation being with particle count when the dust finally settles...

but then here, we have a heart doctor who questions even that.  He claims that even with high particle count after switching to paleo, his heart disease showed a reversal according to scans.  The significance there is that he was looking at actual disease rather than risk factors.  He hypothesizes that maybe the reduced inflammation associated with paleo makes even particle count lose it's correlation with heart disease.

Then we have this interview with Loren Cordain.  In it he states that even the Inuit had signs of atherosclerosis, but that without the inflammation from eating carbohydrate they would most likely not have had heart attacks.  A heart attack requires inflammation to rupture any build-up that might be present.  Dr Kummerow at this link explains it very well, as he fought the system over it for decades.

Of course, it gets even more complicated.

Next we have to look at things like the phenomena of endurance runners having heart attacks due to undetected calcification of arteries when they otherwise seem ultra-healthy.  Mark Sisson at Mark's Daily Apple warns against chronic cardio often.  He insists this is why we should exercise intermittently, keeping our cardio low-intensity and mixing in some form of short burst sprinting. Chronic cardio might be providing even some of us fat-adapted athletes with too much repetitive inflammation. There are so many variables it is hard to keep track.  Would marathon runners not have this issue if they ate a ketogenic diet?  Who knows? Ugh... it is such a puzzle.

So the question still remains that needs to be answered with more science:  "are low carb dieters somehow immune to heart disease in spite of the possibility of higher cholesterol and increased saturated fat intake?"

It seems like a silly question, but it is one that has been asked repeatedly.  With the new finding at Yale, I would think that we need to get NUSI on the job as it might be a much more relevant possibility.  In the paper cited above where it is implied that excess ketones can enter the cholesterol synthesis pathway, he insists that it would be stupid for low-carb dieters to just not worry about their high cholesterol and assume they are somehow specially exempt.  He even suggests adding some carbs back into the diet just to help this level off.  So then we are left wondering: is the high cholesterol more of a risk factor than the inflammation we would get by adding the carbs and reducing the ketones?

I lean toward inflammation being worse than particle count, but I would rather let scientists duke it out as opposed to just going with my gut feeling. I plan to stay low carb and keep eating my saturated fats, but without the bulletproof coffee, without chronic cardio (keeping the running at around three miles if I run at all,) and hanging on to my sprinting with USRPT and short workouts as the majority of my exercise.

and oh yeah... I am going to make a gamble that dark chocolate and red wine will help too, because if eating those every night is wrong, I don't want to be right.

THE VIKING MANIFESTO Part 6: USRPT. Duh...

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

Part 6: USRPT.  Duh.

Okay guys, it's time to add one more thing to the list of topics to avoid when you are drunk:  the list is now religion, politics, nutrition, your friend's mom, and USRPT.  That’s right SwimSwam commenters, I know which of you loudmouth regulars is playing that game where you take a shot every time Braden mentions Michael Andrew’s name in an article.  If the SwimSwam comments section was a bar, I know which of you guys I would want to party with.

Yup, in case you haven't already pieced it together, the Viking does Ultra-Short Race Pace Training.  What other type of training could I fit in with only 20-30 minutes, two or three times a week to swim?  

Crush your enemies, see them driven before you, and don’t waste a lot of time training old-school when you could be doing USRPT.

I decided after reading through Dr Rushall’s work that the science made sense and some of his claims seemed to fill in the gaps for me. There was something missing in the translation from training to racing with the way I was running my program.  I was frustrated with the inconsistency and guess work involved in managing the various aspects of coaching so many athletes and I figured that since none of my athletes are world-class there really wasn’t that much risk in making the switch to USRPT to see how it goes. I essentially threw the old EN-SP chart out the window.

“Let go, Viking. It’s outdated science.”

I also decided though, that if I am going to do it, I cannot make an informed decision without these two things:

1. Making sure I do it by the book so I am not still left with questions later.
2. Getting in the water to try it myself.  Hey, why not?  I had been jogging and had lost some weight, and I had to know what it felt like to truly make an educated analysis.

At the end of last summer I gave a presentation on USRPT to a group of high school coaches to talk about how it worked in our first seasons of training.  I had to admit to all of these coaches that while it was great for my team, it seemed to work better for me over the summer than it did for my athletes even though I trained significantly less than any of them. I usually did one USRPT set for 200 breast one or two nights a week in the LCM pool and one USRPT set for 100 breast pace one or two mornings per week in the SCY pool.  My training was very inconsistent, usually less than 90 minutes per week, and at times throughout the season I was stuck with up to ten days straight with no exercise at all due to my work and family responsibilities. When the dust settled I was confused that I had done so well and showed continuous improvement throughout the whole season, even after being sick for the last two weeks before sectionals. Some people think that USRPT isn’t for younger athletes and might assume that my age somehow made it more ideal for me.  I almost bought into this, even though there really isn’t any logical reason why this might be.  Now that I have spent some time investigating, I am certain I know why:  I started my LCHF journey several months before starting my USRPT journey.  It was not my age that helped me adapt better-- it was my diet.  It is clear as day now.

One of my favorite classes as a PE major was called Perceptual Motor Development.  It had a lot to do with neurology, the brain, and how we learn movements through different developmental stages.  The class was designed so that we coaches can have a better understanding about how to teach students of different ages physical skills in a progression.  When it got really interesting though was when we would talk about neurology and training because several researchers out there, (including Dr Tim Noakes, remember him?) have shown us that the brain is so specific in regard to motor learning that, as those of us who have bought into USRPT like to point out:  “the brain doesn’t even treat slow swimming and fast swimming as the same activity.”  This means that much of the traditional training I did in my first swim career served little more purpose than to increase capillarity to slow twitch muscle fibers.  In my opinion, when we train that way, only the most talented continue to improve and a lot of kids are left to fade away. In Bob Bowman's cup analogy, I guess I just don't buy that we need the Big Gulp. I believe we can throw a better party with shot glasses as long as we fill them with the right stuff. I guess my idea of "capacity vs utilization" is a little different than his.

Now, for most people who have skimmed Dr Rushall’s work, the concept of specificity usually stands out enough to have a little bit of a conversation.  As a matter of fact, John Leonard somehow scrounged together $23k of our USA-S membership dollars to try to prove to us that Dr Rushall hardly knows what specificity is.

It is time to tell John Leonard  what he can do with that $23 grand.

While I do believe that most of us understand that with the way the brain works, specificity is king in athletics, I feel that many of us neglect it in traditional training.  Dr Rushall claims that technique specificity and mental training are vital throughout his works and are just as important as the actual sets they do.  It’s just that when I hear anyone talk about specificity, it focuses on the neurological, and it almost sounds as though many coaches think we can just not worry about it after we have taught our swimmers proper stroke technique as long as we mix in some sprinting once in a while.  Worse, I hardly ever hear coaches talk about specificity regarding muscle fiber recruitment and adaptation, even among those who use USRPT.  In my opinion, this is just as vital.  This is why LCHF can optimize USRPT, why USRPT can optimize LCHF, and this is also why so many people don’t quite understand why USRPT is truly a brilliant and unique way to train. Lots of people love to talk about Ultra-Short Race Pace Training, but it is very apparent that not many of those people have actually read Dr Rushall's work.  I can't even count how many times I have heard coaches on deck rail against it with gems such as:

"we have been doing that for years.  It's just race pace."

"it's the same as the Sprint Salo book. Why is everybody acting like this is some new thing?"

or the best one--

"It's just lactate tolerance work all the time.  What's the big deal?  Developing kids need aerobic training."

Read it or keep your mouths shut guys.  USRPT is far from any of those things that people assume.  I would recommend USRPT to anyone at any age or any level of competition, especially in conjunction with the LCHF diet.  The following passages from Dr Rushall's work should help tie the two together:

"Some think that USRPT neglects the aerobic system. On the contrary, USRPT exerts nonstop, maximal stress on every oxygen-using source of energy. Its format of short repeats and rests creates a training stimulus that 1) energizes aerobic, slow-twitch muscle fibers beyond the capability of standard aerobic sets; 2) converts a substantial fraction of anaerobic, fast-twitch fibers to the use of oxygen; and 3) binds oxygen to hemoglobin and myoglobin. The overall training effect is to maximize not only base aerobic capacity but also the subsuming “oxidative capacity.” The result is greater speed endurance ― the ability to bring home a race before acid build-up takes its toll...

Ultra-short training produces maximal aerobic adaptation because the aerobic system (Type I fibers) is stimulated continually and maximally and the production of oxidative fast-twitch fibers adds further aerobic function. That contrasts with "aerobic training" or lower-intensity training that, at best, only stimulates maximal aerobic energy production in the Type I fibers. Higher intensity work (race-pace in swimming) is needed to develop maximal aerobic capability (Type I plus Type IIb fiber adaptations). Ultra-short training stimulates maximal energy source production for race- pace techniques. It trains the body to use its alactacid and lactacid energy resources for race-specific tasks better than does traditional (irrelevant) "lactate training".

Traditional training gives us capillarity through distance, and mitochondrial density through intensity, and there is no doubt it can work. This is how Bob Bowman's "capacity/utilization" concept applies to developing athletes.  I am not trying to tell anyone that traditional training won’t work. We see it every day.  I just believe it is inefficient and not optimal, especially with the standard high carb diet.  Now just imagine that you are eating a diet that is shown to make changes within muscle fibers that enhance the ability to work at high intensity without spilling over into anaerobic glycolysis, essentially maximizing your ability to tap fat and oxygen as fuel at high intensities. Then add to it a method of training that converts more fast twitch muscle to be oxidative, meaning a higher percentage of your muscle fibers are programmed to burn oxygen and fat at high intensity rather than relying on the glucose and lactic acid system. Then we basically have an abundance of the right fuel, the right method of fuel injection to make the most of it, and the right engine attached to the car to crank out all that power with less fear of locking up.

Remember these points I made earlier in the manifesto?:

1. The formula for success in swimming should be technical efficiency and speed at the intensity as close as you can possibly hold to your VO2 max, for the specific distance of your intended race without the negative impact of lactate clearance not keeping up with production.  
2. 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.  

Essentially, USRPT, when done properly and consistently, is designed to maximize the conversion of fast-twitch muscle fibers to be oxidative, rather than glycolytic. KABLAM!  The ultimate bio-hack.  Fast twitch power optimized to use oxygen and fat as fuel.  LCHF plus USRPT is a lot of capital letters, I know, but I truly believe that this is the optimal way to train swimmers at any age.  Better oxygen utilization, better oxygen supply, and all of this applied specifically to fast twitch muscle fibers, while also warding off the fatigue associated with depending too much on fast twitch glycolytic muscle fibers and anaerobic glycolysis. What better combination could there be to help an athlete go out fast and finish strong in a race?. I believe that this could truly revolutionize our sport.  Add to this all of the general health benefits that we get from leaving the standard high-carb diet behind, and we have a winner.  

LCHF plus USRPT.  This is the Viking Method.

Think about this.  I don't care who you are-- once you start creating more lactate than you can clear in a race your performance is going to suffer.  No amount of "lactate tolerance" training or mental toughness is going to change that to the degree that it should be the focus of high-intensity swim training.  Also, training slow-twitch muscle fibers to optimize a race that lasts less than two minutes doesn’t seem that smart either.  These are flaws in the most basic concepts of swimming training.  We have been shooting arrows at either side of the target, with very few of us lucky ducks ever actually hitting the metabolic bullseye.

and then there’s Vlad Salnikov…  apparently he could train however he wanted, smoke a couple cigarettes behind the blocks and then get up and sprint a world-class mile. That guy had it all.

Again, most aerobic work done in a traditional swim practice serves to maximize the aerobic potential of slow twitch fibers, and any speed work with enough rest between repeats to recover beyond the optimal time will train fast twitch muscle fibers to be more dependent on anaerobic glycolysis.  USRPT brings about a better training response to fast swimming due to the short repeat distances short rests between repeats allowing for maximal oxidative adaptations and allowing more actual swimming time to be devoted to accurate race-specific swimming.   In USRPT the amount of rest between repeats is probably the biggest factor that sets the reality apart from what people assume about USRPT.  When you also consider that USRPT is self-regulating to avoid neural fatigue as well as the cumulative fatigue that can lead to over-training, it is like the cherry on top of a really huge sciency sundae.  Not that I would eat the cherry… or the sundae.  Just making a point.  This is the best of both worlds in specificity, as it covers the neurological side as well as the metabolic side with pointed specificity regarding muscle fiber recruitment and adaptation.

Doesn't it make sense to focus on recruiting more fast twitch fibers to fire aerobically with fatty acids and/or ketones rather than through glycolysis?  Before reading my manifesto, many people might say no, because glycogen is the “preferred” fuel and fat is the "slow-burning fuel," but, oh yeah, the textbooks were wrong about that. Aren’t the high adaptations shown in the UCONN study enough to convince you that the longer we adapt to the LCHF diet, the more we can take advantage of this metabolic software hack by increasing our ability to oxidize fat as a fuel at increasingly higher intensities? Since it is possible to train our muscles to burn fat and ketones more efficiently through the LCHF lifestyle, it seems to me that there could be a compounding effect when combining it with USRPT.  How fast do I have to swim in my forties to give y’all proof?  I fantasize that a swimsuit company will sponsor me and help me afford to drop one of my stipends and free up a couple of hours to train like the young pups again.  My 15 hour work days just don’t leave much time for training… but I don’t think I need it.  I am gonna keep getting faster just doing what I am doing.  Watch and see.

Too old to swim lifetime bests at 40?

The only negatives I have found with USRPT so far are that it can be hard to expect kids to have the mental will to make the most of it day in and day out (hence Dr Rushall’s insistence that mental training is just as important as physical;) organizing a crowded practice can be tough (although my team has gotten pretty damn good at it;) and that one of my swimmers who had been accustomed to high yardage gained about 15 pounds after the switch (which would have never happened with LCHF.  He has dropped some carbs and already lost most of it in a few weeks.)  Anyone who has never tried USRPT probably would not guess how damn hard it can be when an athlete wants to improve.  Last night my workout was a total of 300 warm up and 15x50 breast on 50, holding 32 high’s in the yard pool.  Holy crap it hurt.  By my third fail I was nearly hyper-ventilating.

The best parts of it:  the kids on my team get into it and it gives them more accountability.  I love doing it and feel I am wasting so much less time. My role as a coach has changed for the better.  My swimmers can expect to race well all season, yet we have had very few disappointments when they suit up at the big meet at the end of the season.  So far, it has been a win, win, win, win, win for us.  I am happy to give coaches advice for implementing this with their teams, but that is a post for another day.  I made a few mistakes in the transition to becoming a USRPT team, but right now it is a pretty well-oiled machine. My greatest recommendation if you are thinking about giving USRPT a try?: Read every damn word of those Swimming Science Bulletins.

The next chapter in my manifesto is a pretty important one…  “How in the heck do I even get started on a Low-Carb High-Fat Diet?” Yes, I realize I have talked a lot about LCHF without really talking about what I actually eat.  More to come!

THE VIKING MANIFESTO Part 5: Muscle Fiber Types, Recruitment and Specificity

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:

1. 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.  
2. 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.  
3. 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.  

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.

THE VIKING MANIFESTO Part 4: LCHF and Energy Metabolism Within the Muscle

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

Part 4:  LCHF and Energy Metabolism Within the Muscle

In part 3 I explained that while VO2 max may be important, focusing training on raising anaerobic threshold to maintain longer durations at high intensities that are close to VO2 max would probably yield more applicable results. I then presented research that implies that a low carbohydrate, high fat diet can help improve this aspect of aerobic conditioning, even in already extremely fit athletes, by making fat a more available and faster burning fuel.  Now I intend to show that the implications for adaptation to the LCHF diet go beyond long-distance swimming at low intensity levels.  

To do this, I must start with some of the perceived limitations to the LCHF diet and why they might not be limitations at all.  

First, I have to make you aware that many people who train with the low carb high fat diet believe that with keto there is a loss in VO2 max and peak power, as though keto-adaptation only serves to improve lower intensity activities and can hinder fast twitch or high-power activities.  This has been backed up in some studies, but it is questionable whether those studies allowed proper conditions to truly know whether this is the case or not.  There are world class triathletes out there who have a train-low/race-high philosophy regarding carbohydrate, simply because they want the adaptations associated with LCHF but want to avoid the limitations associated with glycogen stores not being refueled on race day.  That makes sense, I guess, except that an insulin spike and full liver glycogen stores can stand in the way of ketosis, which I think would be a disadvantage on race day.  Dr Attia actually endorses a product called Generation UCANN, which is what they call a “super-starch”: an extremely low glycemic carbohydrate gel that can feed an athlete carbs without the insulin spike.  It is also known that eating small amounts of non-fructose carbs after exercising hard (creating a glucose deficit) will immediately go toward refueling muscle glycogen first, rather than toward fat storage or replenishing liver glycogen, meaning that you can use your workload to calculate how many carbs you can eat without interfering with ketosis at all.  I don't bother with all that, but there is also some speculation that the little bit of carbs I do eat, in conjunction with the protein amounts I eat which are higher than the typical ketogenic dieter, might be refueling muscle glycogen to some degree anyway since my training load is so low. Ketogenic dieters often try to keep protein intake low so that gluconeogenesis, (creating glucose from proteins,) does not stand in the way of their weight loss.  There is evidence that while a high protein meal might reduce ketosis temporarily, it doesn’t necessarily stand in the way of the adaptations I am looking for, as it is most likely the calories taken in that cause lower ketone measurements after meals, and the protein has other benefits in regard to training that are a good trade-off for athletes.

I am not sure I buy into the whole idea that we need carbs for peak performance and I certainly feel that more science needs to be done.  I don't have specific measurements so my experience is completely anecdotal, but I have never felt better at high intensities than I do now that I eat extremely low carb. Of course, I have been adapted for over a year and a half, and so far no study has even approached this-- especially one with swimmers. I tend to lean toward an almost completely carnivorous diet and I think my results are better when I cut out nearly everything but animal products.

My wife hates ordering at the drive-thru with me in the car.

There is evidence that with proper adaptation we might not lose that peak power that everyone is so worried about.  Remember those two adaptations that we are training for: increased blood-flow and oxygen supply through capillarity and increased mitochondrial density within muscle cells?  Well, mitochondrial density just might be the main reason the LCHF diet can give us such a boost and it ties directly into being able to churn out high intensity exercise.

Enter Dr Bill Lagakos.  He is a guy who likes to tweet, and occasionally his tweets are links to recent research regarding health, along with write ups to help the layman understand their findings and implications. Dr Lagakos did a write up about two studies recently that showed increased mitochondria in mice with a switch to LCHF, and these adaptations came about within a few weeks. The best part-- these adaptations came about with no additional exercise.  They did not torture these mice on a treadmill.  This means that the diet prompted increased mitochondria on its own.  Could it be that high fat prompted this response, or could it be that carbohydrate was previously holding this natural potential back?  Take a look at it yourself. According to Dr Lagakos, it “increased mitochondrial everything.”  

Most mice are herbivores.  Get them away from the vegetarian thing and look what happens.

This is a very interesting finding.  In that post, Dr Lagakos makes the analogy that if glucose were gas and mitochondria were hoses, then ATP would be the rate at which you can fill your tank.  He then compares fat to this by likening it to trying to draw syrup from a tree with a spout. Remember how much ATP fat can generate compared to glucose from earlier in my manifesto?:  129 molecules from some fats vs only 2 molecules from glucose...  Keep that in mind when reading as he theorizes: “So how would you get your bucket filled with syrup faster?  Try “more spouts.”  And reduce the viscosity of your maple syrup by diluting with some ketones.  More than 3 weeks on a ketogenic diet and you have more better mitochondria and can generate ATP just as fast as high carb.”

Here Dr Lagakos points at a few more studies.  One is from the 1980’s and shows the same improvement in aerobic capacity along with lower RQ that Dr Attia found in his self-experimentation, but this study also includes some athletes whose VO2 max scores improved as well. (Remember how I pointed out that we should focus on improving anaerobic threshold since it is so difficult to improve VO2 max in well trained athletes?  Hmmm…  this indicates that for some we might see an increase in VO2 max as well.)  Of course, Dr Lagakos is basing his findings partly on studies with mice.  We haven’t had a study that shows this phenomenon of increased mitochondria in us that I know of, and we are obviously not mice, but it would sure explain some of the unique attributes of fat-adaptation.  Mark Sisson, a leader in the paleo community, wrote a wonderful article about mitochondria that speculates on this as well, but I encourage you to read it at this link because it goes into a lot more detail about what mitochondria actually do and how we can maximize them through exercise and diet, and his recommendations are pretty much along the same lines.  He even implies that healthy mitochondria can have an anti-inflammatory effect, which is one of the surprise side-effects that continuously pops up on ketogenic diet forums on the web.

It gets even more intriguing though, as Dr Lagakos also points toward two somewhat recent studies showing no loss of peak explosive power in well-trained athletes who switch to LCHF. The interesting thing here in the first study is that the gymnasts being tested lost body weight but lost no power, which improved their body composition with no sacrifice.  This would be valuable in most sports. The other study though, covered a broad range of tests of peak power: handgrip, vertical jump, max bench, back squat, max rep bench press power output, and the Wingate, which is the one that makes me drool the most. (Here's a video of the Wingate.  Damn that looks hard.)  There are of course theories about why these positive results might go against the standard thinking:  the weight loss from the diet might have made these athletes seem more powerful in comparison, or that eating extra protein might have had a “trickle charger” effect by forming sufficient glucose through gluconeogenesis, which could explain why I feel as I claimed above, better than ever at high intensities.  Also based on study design we could guess that peak power isn't diminished with LCHF "given enough recovery time" but more science will need to be done to get a full explanation. This concept intrigues me only because my schedule doesn’t allow for me to train as often as I would like, which would actually contribute to this effect for me and could be diminished in a more hard-core athlete.  I am certainly not needing to manage cumulative fatigue the way I did under my traditional training regimen twenty years ago as I am getting plenty of time to recover between workouts, even though it is not necessarily because I want it that way.

Hey, making a comeback at age 40 just requires a little extra rest, ya know?!

One thing that is clear though is that well-trained athletes seem to be able to flip the metabolic switch more quickly, which might have something to do with these studies of short duration showing improvements that imply successful fat-adaptation, and this is probably because someone who is in shape is much less likely to have developed a high level of insulin resistance to overcome. (The majority of studies on the ketogenic diet focus on weight loss and thus have subjects who are obese.)  Again, more research needs to be done with well trained athletes who are fat adapted for long periods of time to answer these questions.

The point is that increased mitochondria might be just as valuable as capillarity, even though it is typically accepted that in regard to vo2max, supply (capillarity) is considered more important than utilization (mitochondrial density.)  Of course, once again, when we get into the question of whether VO2 max is an important indicator of success in elite swimming.  A better formula for success might be: Technical efficiency and speed at the intensity as close as you can possibly hold to your VO2 max, for the specific distance of your intended race without the negative impact of lactate clearance not keeping up with production. VO2 max is really only a small part of that equation.  Again, more detail on that later.

Next we get into specificity.  Hold on to your helmets.