What is the purpose of training? Is it for fun? Is it to test yourself? Is it to cause adaptations that make you better? Something else altogether?
I think all of these things are potentially valid, but in my opinion what training actually involves is a person attempting to cause an adaptation (or set of adaptations) to occur in order to become better able to achieve specific goals. A focus on fun and tests doesn’t necessarily achieve this, and as as tempting as they may be I don’t think this is what training is for. But, ultimately, it does depend on what your goals are; and please note that I didn’t say to completely exclude these.
So what if your goal is to become a better runner?
If you want to win races, and to get fast over certain distances, always training for fun or treating every training session as a test is quite simply a mistake; this would be a case where you either need to change your training or re-evaluate your goals.
If the above-mentioned “get faster over certain distances” is your goal, then specific adaptations that allow the human body to do this are what we want to result from our training.
I think one of the most important adaptations to seek as an endurance athlete that would aid this goal would be mitochondrial biogenesis, which can be mediated by a protein called PGC-1α — a key regulator of energy metabolism. Our mitochondria are the part of our cells that generate most of the energy, so it should make sense that we want lots of mitochondria that function well in order to be a good endurance athlete. Increasing PGC-1α, then, would be a goal that one should probably have as an endurance athlete, and so training in a way that best does this might be a good idea!
One of the things that I’ve recently learned exhibits control over PGC-1α in skeletal muscle, is testosterone.
In this study, wherein some rats were fed exogenous testosterone, there were significant increases in their skeletal muscle PGC-1α. The level of increase here would likely only be seen if one were supplementing with exogenous testosterone, since the rats doing so had ~12-fold increase in serum testosterone vs. the control; but this at least demonstrates a potential link between testosterone levels and PGC-1α (and so mitochondrial biogenesis) in skeletal muscle.
PGC-1α itself also increases angiogenesis (the development of new blood vessels) and fat oxidation — so it does more than simply increase mitochondria. Both of these factors would also be helpful for improving performance.
The fact that PGC-1α is affected by testosterone should make us think twice about whether we want to engage in training that has a robust and prolonged stress response involved with it, which may negatively impact testosterone. This goes back to my original point of matching our training up with our goals.
So perhaps simply running as much as possible as fast as possible for as long as possible might not be the best way to train. We can negatively affect our testosterone production by waking up early to run (ie sleeping less), running too much or, more simply put, experiencing chronic stress. In doing these things we are potentially stopping one of the adaptations we want to be happening in the first place as a result of our training.
So if we want to actually benefit from our training and propel ourselves toward our goals, how should we go about doing so? I believe the method that makes the most sense is to reduce or remove the junk middle-ground training and train either at a high- or low-intensity.
High volume training, at a low intensity which can be sustained for long periods of time has lots of benefits, one of which is increasing mitochondrial biogenesis.
High intensity training induces metabolic stress, and also increases mitochondrial biogenesis through AMPK which is an enzyme that becomes more active when there is low energy levels within the cell, and subsequently activates PGC-1α. This happens especially so when in a glycogen-depleted state. This especially makes sense when we think of metabolic stress as a state wherein we don’t have enough energy as we need for whatever we are doing, and high intensity exercise is the “whatever we are doing” and the lack of glycogen (stored carbohydrate) is the “don’t have enough energy.”
Middle ground training is not as intense as high-intensity training (because high-intensity is done at a level beyond which is sustainable for time), and not as long-duration as low intensity high volume training, so although it will still obviously have some of the effects mentioned above, it is not going to give you the biggest return on investment. As fun as a tempo run may be, it should have a specific place in training in relation to your goals (race) and should probably not make up a large part of training.
This is a training model that I have mentioned before referred to as polarised training, which was looked at in this paper where they tested a group of well-trained athletes who were randomised into groups of either high intensity interval training (HIIT), high-volume low-intensity training (HVT), lactate threshold (THR) or polarised (POL). Here is a description of the intervention:
The HVT included three blocks each lasting 3 weeks: 2 weeks of high-volume training followed by 1 week of recovery. The two high volume weeks each included six training sessions with three 90 min LOW sessions, two 150–240 min LOW sessions (according to the training mode: running, cycling, or roller skiing) and one 60 min LT session using different types of interval training (e.g., 5 × 7 min with 2 min recovery, 3 × 15 min with 3 min recovery). The recovery week included three training sessions with two 90 min LOW sessions and one 150–180 min LOW session.
The THR included three blocks, each lasting 3 weeks: 2 weeks of high volume and intensity training followed by 1 week of recovery. The two high volume and intensity weeks each included six training sessions with two 60 min interval sessions at the LT (5 × 6 min and 2 min recovery in the first block, 6 × 7 min in the second block and 6 × 8 min in the last block), one 90 min LT session with longer intervals (3 × 15 min with 3 min active recovery in the first block and 3 × 20 min for the remaining two blocks), one 75 min session with varying changes in intensity (“fartlek”) (intensities resulting in a blood lactate of 1.5–5 mmol·L−1) and two 90 min LOW sessions. The recovery week included one 60 min LOW session and two 60 min LT interval sessions (5 × 6 min with 2 min of active recovery).
The HIIT included two interval blocks of 16 days with one adaptation week prior to and one recovery week after each block. The adaptation week included two 60 min HIIT sessions, three 90 min LOW sessions, one 120 min LOW session and 1 day of recovery. The condensed 16 day interval block included 12 HIIT sessions within 15 days, integrating four blocks of three HIIT sessions for three consecutive days followed by 1 day of recovery. The recovery week contained four LOW sessions of 90 min and 3 days without any training. All of the HIIT sessions included a 20 min warm-up at 75% of HRpeak, 4 × 4 min at 90–95% of HRpeak with 3 min active recovery and a 15 min cool-down at 75% HRpeak based on the protocol proposed earlier. The LOW sessions lasted 90–150 min depending on the training mode (running vs. cycling) at an intensity resulting blood lactate of <2 mmol·L−1.
The POL included three blocks, each lasting 3 weeks: 2 weeks of high volume and intensity training followed by 1 week of recovery. The high volume and intensity week included six sessions with two 60 min HIIT sessions, two 150–240 min long duration LOW sessions (duration according to training mode: cycling, running or roller skiing), which included six to eight maximal sprints of 5 s separated by at least 20 min, and two 90 min LOW sessions. The recovery week included one 60 min HIIT session, one 120–180 min LOW session and one 90 min LOW session.
The study was meant to assess specific “key endurance parameters” over 9 weeks. These parameters included submaximal and peak VO2 (VO2submax and VO2peak) and HR (HRsubmax and HRpeak), as well as time to exhaustion (TTE) and velocity/power. At the end of the 9 week period, it seemed that polarised training demonstrated “the greatest increase in VO2peak , time to exhaustion (during a specific protocol) and peak velocity/power.”
It would seem that a training model that includes the best of both worlds (and eliminates what interferes) makes sense both intuitively and in light of evidence. Polarised training allows one to use both high intensity training and high volume training (mentioned above to both induce mitochondrial biogenesis through different mechanisms) separately and effectively without running the risk of overtraining. I would, however, plan my own training quite a bit differently than was done in the above paper, which will likely be discussed in the future.