Today I want to continue by looking at some general concepts of endurance training methods…
Methods of Endurance Training Part 1
In Predictors of Endurance Performance, I talked a little bit about the three primary predictors of overall endurance performance which were VO2 max, functional threshold, and efficiency. Over the next two (or possibly more depending on how verbose I am) articles, I want to look at some of the actual methods of endurance training that are used commonly to improve endurance performance.
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.
In the next sets of article(s), I’ll look at the specific methods within the context of the information I’ve provided today.
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):
- Changes in heart function (notably an increase in how much blood is pumped per stroke)
- An increase in the oxygen carrying capacity of the blood (through both increased blood volume and increased hematocrit)
- An increase in capillarization around skeletal muscle
- Increases in both mitochondrial number and density
- Increases in levels of enzymes involved in energy production
- Increased buffering/utilization of acid
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 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 due to the physiological differences between the muscle fiber types. This is yet another reason that no single intensity can possibly be optimal. I’ll come back to this in more detail in the next parts of the article.
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 it’s 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 anti-oxidant 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). Now, I wrote an article about AMPk: The Master Metabolic Regulator several years ago and, since that time, research has simply continued to mount on the topic. For the details you can read the article, I’ll simply recap below.
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.
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. Having a bigger aerobic engine ends up having two impacts:
- You can produce more power without producing acid in the first place
- When acid is produced, the body can metabolize it better
Which is why even seemingly ‘anaerobic’ sports end up doing a fair amount of basic endurance work. Even in the 400m (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. Athletes in the 400m do a fair amount of aerobic work as part of their total training, it can comprise half or more of the total training volume for an 800m runner depending on their strengths and weaknesses. A speed based runner may do more endurance work; an endurance based runner does proportionally more speed work. But they all do a good bit of aerobic work. But I digress.
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).
And this shift in the ATP/AMP ratio is what turns on AMPk; basically the cell ‘senses’ that it’s energy levels have been disrupted so it turns on other stuff to try and combat that; 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; endurance improves.
If you think about what’s happening, this should make sense. Increasing endurance simply means that the body is better able to produce sufficient energy to keep continuing without fatigue. So the stimulus for this is related (at least partially) to an imbalance between energy production and energy requirements. The power output or endurance duration that had previously caused the energetic imbalance no longer does due to the adaptation.
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; this means that the same training load will no longer activate AMPk in the future and no further adaptations will be stimulated.
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. I’d note again that AMPk activation may also be different (or require different combinations of intensity and duration) for different fiber types, a topic I’ll come back to again in the next articles.
And with that I’ll bring Part 1 to a close. The final paragraph above is really sort of the take home message from all of this since it provides the major basis for what I’m going to talk about in the next part of the series which I’ll continue on Tuesday.