Posted on 3 Comments

A Guide to Endurance Training Methods

Previously, I have written about the three primary predictors of overall endurance performance which were VO2 max, functional threshold, and efficiency.   While each is important on its own, it is the interaction of all three (along with factor such as pacing, tactics, etc) that determine actual real-world performance.

Each is also developed in a different way.  So in this series I want to look at various methods of endurance training as they are commonly recommended or used by athletes to optimize and maximize performance.

Today I mainly want to introduce the topic by looking briefly at the major adaptations that occur in response to endurance training.  Since it will provide background to better understand why different methods of endurance training “work”, I will also delve into bit of molecular physiology regarding something called AMPk.

Today I want to mainly make some introductory comments, looking briefly at some of the major adaptations that occur in response to endurance training.  Also, since it gives some important background to understanding why different methods of endurance training work, I’m going to have to bore people with a bit of molecular physiology regarding something called AMPk.

Adaptations to Endurance Training

.There are a number of adaptations that occur with regular endurance training that work to improve performance. In no particular order these include (but are probably not limited to):

  1. Changes in heart function (notably an increase in how much blood is pumped per stroke)
  2. An increase in the oxygen carrying capacity of the blood (through both increased blood volume and increased hematocrit)
  3. An increase in capillarization around skeletal muscle
  4. Increases in both mitochondrial number and density
  5. Increases in levels of enzymes involved in energy production
  6. Increased buffering/utilization of acid byproducts

Now, something to keep in mind is that the above adaptations tend to not only occur at different rates (in terms of how long training needs to be carried out to generate/maximize them) but tend to be affected to a greater or lesser degree depending on the type of training that is done.  This is one of several reasons that the occasionally argued idea that there is a single optimal intensity for endurance training can’t be correct.  No single intensity or endurance training method can possibly stimulate or optimize all possible adaptations.

Practically speaking, endurance athletes use a variety of training zones (of varying intensity and duration combinations) to achieve different sets of adaptations as required by the specifics of their sport and their individual needs (e.g. to fix weak points that are limiting current performance).  Endurance, VO2 max, efficiency, lactate threshold, acid buffering can all be ‘targeted’ with specific combinations of intensity, duration and frequency.

Conceptually this is no different from strength athletes using a variety of training zones and intensities to achieve different things.  Extensive, moderate intensity methods may be used to generate hypertrophy which provides a base for increased strength gains through higher intensity “neural” training; heavy slow training may be combined with lighter speed/power work to generate still other adaptations.  At some point in the future I’m going to look at specificity vs. variety and discuss this in more detail.

It’s also worth noting that, at least in terms of the skeletal muscle adaptations (#4 an #5), which are what I’ll be focusing on in this series, there are differences in what types of training will preferentially impact on either Type I (slow-twitch) or Type II (fast-twitch) muscle fibers.

This is due to the physiological differences between the muscle fiber types. This is yet another reason that no single intensity can possibly be optimal since no single intensity can possibly generate maximal adaptations in both fibers.

I should make a quick comment about #6 since it’s phrased a bit oddly.  Many readers may have been exposed to the idea of lactic acid/lactate and its previous held role in terms of causing fatigue.  As is so often the case, things are turning out to be far more complicated and lactate/lactic acid per se appear to be, if anything, beneficial.  It’s certainly not the cause of fatigue during high intensity activities (some research suggests that lactate helps to buffer against fatigue).

However, and somewhat confusingly, it does look like acid (specifically H+) is a cause of fatigue.  It’s simply not coming from lactate production or dissociation of lactic acid into lactate and H+.  As it also turns out, one of the major determinants of how well the skeletal muscle can deal with this acid is…the size of the aerobic engine.  It’s turning out that mitochondria can metabolize the acid.  Simply put, the bigger your aerobic engine, the better your ‘anaerobic’ performance.

And with that out of the way, I want to get a bit molecular and talk about one of the major skeletal muscle ‘sensors’ that triggers endurance type adaptations.  While this may seem unnecessary detailed, it actually provides a basis for some of the different types of training I want to talk about.

AMPk: The Master Metabolic Regulator

.As I mentioned in the section above, today I’m going to focus primarily on the skeletal muscle adaptations that occur with regular endurance training so I want to look a little bit at what drives those adaptations (e.g. what the molecular stimulus actually is).  Now, as is always the case, there are a whole bunch of them.

Calcium levels in the skeletal muscle, fuel utilization (e.g. fatty acids and glycogen), and free radical production are all turning out to play a role in the stimulus that occurs from endurance training.  The last one is interesting as some studies are suggesting that high-dose antioxidant supplementation may actually impair some of the endurance adaptations that athletes are seeking.

However, one of the primary effectors of adaptation is something called AMPk (which stands for adenosine monophosphate kinase).

In essence, AMPk is a cellular energy sensor, it reacts to changes in the energy state of the muscle cell and this has a number of effects.  For example, when AMPk is activated, the muscle will burn more fat for fuel, it will take up glucose from the blood stream, it will become more insulin sensitive.  It’s worth mentioning that AMPk activation also inhibits protein synthesis by inhibiting another molecular sensor called mTOR.   This explains a whole bunch of other things (such as why doing a lot of endurance training after you lift is a bad idea) which I’m not going to get into in this article.

Relevant to this article, AMPk activation is a big part of what stimulates mitochondrial biogenesis (that is, the creation of new mitochondria).  If you remember hearing about the couch potato rat that was turned into a marathon running rat, that was done by over-expressing AMPk in the skeletal muscle.

Mitochondria: The Powerhouse of the Cell

This is critically important to endurance performance (and, as it turns out, “anaerobic” performance) because mitochondria are where oxygen is processed.  And, as I mentioned above, mitochondria are also involved in buffering acid accumulation during higher intensity/anaerobic activities.

Improving mitochondrial function and building a bigger aerobic engine overall ends up impacting on performance in two ways:

  1. You can produce more power without producing acid in the first place
  2. When acid is produced, the body can metabolize it better

This explains why seemingly “anaerobic” sports end up doing a fair amount of basic endurance work.  Even in the 400m in track and field (an event lasting 45 seconds), the aerobic contribution is about 50% or so. By the time you get to the 800m, it’s even more significant.    At the mile mark and above, the primary energy system being used is the aerobic system. Athletes in the 400m do at least some amount of aerobic work during their training and it may make up 50% of the total training volume for an 800m runner.  Mind you this can depend on the athlete’s strengths and weaknesses.  A speed based runner may do a bit more endurance work while an endurance based runner may do a bit more speed work.

But beyond the 200m (sub 20 seconds), all runners will do at least some aerobic work.

What Activates AMPk?

So what, you ask, turns on AMPk?  Basically, AMPk is activated when the energy status of the cell is disrupted.  So under normal conditions, the body is using ATP for fuel but can make as much as it needs. When you start exercising, the body can’t make ATP quickly enough and you get an increase in something called ADP (adenosine diphosphate, it’s just ATP with a phosphate stripped off of it).  ADP is further metabolized to AMP (adenosine monophosphate which is ATP with both phosphates stripped off of it).

This shift in the ATP/AMP ratio is what turns on AMPk.  Basically the cell “senses” that its energy levels have been disrupted so it turns on other stuff to try and combat that.  And AMPk activation is a big part of “what happens”.   And when you activate AMPk along with doing a bunch of other stuff you get an adaptation.  Mitochondria proliferate, aerobic enzymes increase and endurance improves.

If you think about what’s happening, this should make sense.   Endurance is the ability to resist fatigue and improving endurance means that the body is better able to produce sufficient energy for exercise without fatiguing.  So the stimulus for improving endurance would logically be creating an imbalance between energy production and energy requirements.  This stresses the system metabolically such that it adapts for the future.

This also explains why training has to progress in either intensity, duration or both depending on what’s trying to be achieved.  At a fundamental level, an improvement in “endurance” means that the body has improved its ability to maintain ATP levels during exercise.  Eventually the same training load no longer stimulates AMPk and no further adaptations will occur.  So training has to increase in some form or fashion.

I’d mention in that context that AMPk can be activated by a number of different types of stimuli and this has relevance for the different successful methods of endurance training that have been used over the years.  Some research suggests that AMPk is only activated if a certain intensity of endurance training is surpassed.

However, even at lower intensities, long enough durations of training can still stimulate AMPk and adaptations to training.   Optimally activating AMPk in different muscle fibers may also require different combinations of intensity and duration.  Hence the need for endurance athletes to use multiple methods of endurance training to optimize performance.  No single method will be sufficient.

Pure Endurance Athletes vs. Athletes Who Need Endurance

Before getting into the methods, I want to make a point that I think some folks tend to miss or confuse.  And that’s that pure endurance athletes are a different animal with different goals and needs than other athletes who simply need some amount of endurance as part of their overall performance package.  This can describe team sports but some individual activities such as MMA or boxing have an endurance requirement for optimal performance.  It’s just not the primary goal.

Below I’ve reproduced what I call the adaptation continuum, showing the primary adaptations that certain sports require.

The Adaptation Continuum

For the pure endurance athlete, developing things like VO2 max, Lactate threshold and efficiency to the absolute maximum levels is going to be more or less the be-all, end-all of their training goals and this determines how they train.  Strength per se is rarely a massive determinant of overall performance although this depends on the sport (e.g. the start in rowing requires a good deal of strength to overcome inertia).

In contrast, athletes who need some degree or type of endurance as part of their overall performance won’t need nearly the development in those terms.  Aerobic endurance is certainly part of the overall package but it’s not the be-all, end-all of performance.

In those non-endurance sports, you tend to see far more moderate/average values for VO2 max.  You also see a much more moderate level of strength compared to pure strength/power athletes.  Those mixed sports athletes are simply having to balance out the mixture of metabolic requirements of strength, power, endurance, etc. for their sport.

Excluding the Middle

I mention this because you’ll often see these truly silly arguments along the lines of “Look at marathon runners, they are small and weak, why would a [insert non-running athlete here] every do steady state cardio like that?”

And the answer is that they wouldn’t, or at least not to that extreme.  But that doesn’t mean that you throw out the baby with the bathwater and NEVER do continuous aerobic work or apply the methodologies used to improve endurance to those sports.

Because where the marathoner might need a 2.5 hour run once/week and 120 miles per week total to perform optimally, a non-marathon athlete who needs endurance might only be doing 30 minutes of continuous running/aerobic work a few times per week to develop some basic endurance or what have you.

But people love to play a game of excluding the middle with stuff like this: either an athlete is running 120 miles per week or NEVER doing aerobic steady state work.  They can’t even imagine a third option.  Not only is it a logical fallacy to exclude the middle, it ignores how real-world athletes actually train.

My point being that the methods used by the pure endurance athletes can still have some application to the non-pure endurance athletes.  They simply aren’t used to nearly the same extent or degree since they don’t make up the entirety of the performance structure.  But the methods can still be useful when applied within some reasonable level.

And with that out of the way, let me look at the first and arguably most common method of developing endurance which is the Miles Build Champions method.

Read Endurance Training Method 1: Miles Build Champions

Similar Posts:

Facebook Comments

3 thoughts on “A Guide to Endurance Training Methods

  1. Why do you keep speaking about “acid”? Lactate can not exist as an acid at the ph of blood. Instead it is the Lactate Ions that may be troubling. Moreover, there is a growing body of evidence to show its the hydrogen ions making the contribution to fatigue.

  2. I mention that specifically in later parts of the series. This was an introduction and I didn’t want to get into details. And the H+ accumulation still doesn’t come from lactate. See Robergs paper

    Am J Physiol Regul Integr Comp Physiol. 2004 Sep;287(3):R502-16.
    Biochemistry of exercise-induced metabolic acidosis.

    Robergs RA, Ghiasvand F, Parker D.

    Exercise Science Program, Department of Physical Performance and Development, Johnson Center, Rm. B143, The University of New Mexico, Albuquerque, NM 87131-1258, USA.

    Comment in:

    * Am J Physiol Regul Integr Comp Physiol. 2005 Sep;289(3):R891-4; author reply R904-910.
    * Am J Physiol Regul Integr Comp Physiol. 2005 Sep;289(3):R895-901; author reply R904-910.
    * Am J Physiol Regul Integr Comp Physiol. 2005 Sep;289(3):R902-3; author reply R904-910.
    * Am J Physiol Regul Integr Comp Physiol. 2006 Jul;291(1):R235-7; author reply R238-9.

    The development of acidosis during intense exercise has traditionally been explained by the increased production of lactic acid, causing the release of a proton and the formation of the acid salt sodium lactate. On the basis of this explanation, if the rate of lactate production is high enough, the cellular proton buffering capacity can be exceeded, resulting in a decrease in cellular pH. These biochemical events have been termed lactic acidosis. The lactic acidosis of exercise has been a classic explanation of the biochemistry of acidosis for more than 80 years. This belief has led to the interpretation that lactate production causes acidosis and, in turn, that increased lactate production is one of the several causes of muscle fatigue during intense exercise. This review presents clear evidence that there is no biochemical support for lactate production causing acidosis. Lactate production retards, not causes, acidosis. Similarly, there is a wealth of research evidence to show that acidosis is caused by reactions other than lactate production. Every time ATP is broken down to ADP and P(i), a proton is released. When the ATP demand of muscle contraction is met by mitochondrial respiration, there is no proton accumulation in the cell, as protons are used by the mitochondria for oxidative phosphorylation and to maintain the proton gradient in the intermembranous space. It is only when the exercise intensity increases beyond steady state that there is a need for greater reliance on ATP regeneration from glycolysis and the phosphagen system. The ATP that is supplied from these nonmitochondrial sources and is eventually used to fuel muscle contraction increases proton release and causes the acidosis of intense exercise. Lactate production increases under these cellular conditions to prevent pyruvate accumulation and supply the NAD(+) needed for phase 2 of glycolysis. Thus increased lactate production coincides with cellular acidosis and remains a good indirect marker for cell metabolic conditions that induce metabolic acidosis. If muscle did not produce lactate, acidosis and muscle fatigue would occur more quickly and exercise performance would be severely impaired.

  3. tolearn about basic of cricket endurance

Comments are closed.