Base Training Revisited

OVERVIEW
There has been a great deal of discussion on the forum regarding “base training”. In general, the training method is centred around the ideas that Hadd puts forward in a series of postings which are termed Hadd’s Approach to Distance Training. The approach is broken down into 6 sections.

The 6 sections that Hadd has posted can be broadly divided into two areas; the theory behind his training approach (sections 1-3) and putting that theory into practice (sections 4-6). Let’s deal with the theory first and run through some of the key points that Hadd makes in sections 1-3.

Section 1. Hadd opens by stating that in an optimally trained athlete there should be a fixed relationship between race distance and pace e.g. 5K @ 5:30 min/mile, 10k @ 5:45 min/mile, 1/2M @ 6:00 min/mile, marathon @ 6:15 min/mile. Hadd stresses that the pace per mile should decrease by a fixed amount as the distance doubles (15 sec/mile in the example above), but that the exact amount that pace slows (e.g. 15 sec, 12 sec or 17 sec / mile) doesn’t especially matter. If the pace-distance relationship isn’t fixed, then Hadd concludes that the individual is poorly trained from an aerobic standpoint and suggests that this is likely to be because of “low mileage background” and running “too fast”.

Section 2. Hadd states that the lack of a fixed relationship between race distance and pace is because “LT (lactate threshold) is not good enough (not a high enough percentage of your personal VO2max)”. Essentially, this means that you hit your lactate threshold at too low an intensity i.e. at a relatively low percentage of your maximal heart rate. Hadd further states that “Your LT is dependent on adaptations in your leg muscles caused by training” and that “these adaptations are intensity dependent (train too fast, they won’t happen)”.

Section 3. Hadd then relates a personal experience in which, following an injury, he begins training again, doing a lot of high intensity workouts. Following 3 months of this type of training Hadd describes having a very tough time trying to complete a 2 hour+ run at 8 min/mile pace and cites publications by Holloszy and specifically Dudley, to explain why, stating “all my training in the 3 months leading up to it had been relatively hard. I had not trained slow enough for my slow twitch fibres to become stimulated to build huge amounts of mitochondria.”

THEORY
At the core of Hadd’s theory underlying his training methods (as he states in section 2) is the belief that “Your LT is dependent on adaptations in your leg muscles caused by training” and that “these adaptations are intensity dependent (train too fast, they won’t happen)”. In section 3 he cites experimental studies performed by Holloszy and specifically Dudley in support of why training at too high an intensity is ineffective at raising lactate threshold. The experimental data is taken from studies conducted in rats and it’s worth noting that there are significant differences in the composition of rat and human muscle. However, for the purposes of this discussion we’ll put this issue to one side. In section 3 Hadd states:

“But what about intensity? Were mitochondria only created while running long and slow?
In 1982, a guy called Gary Dudley (Dudley et al., 1982) decided to explore this question. He had several groups of rats training five days/week (but only for 8 weeks). Like Holloszy, he also used a range of different training durations, from 5-90 mins per day. However UNLIKE Holloszy (whose rats all trained at the same pace) he also used a range of training intensities. Dudley's rats trained at either 100%, 85%, 70%, 50% or 40% VO2max. He also examined how different intensities and different durations affected different muscle types (fast twitch white, fast twitch red or "intermediate", and slow twitch).”

Hadd states that the following training intensities were used by Dudley et al., “100%, 85%, 70%, 50% or 40% VO2max”, actual training intensities were 116%, 105%, 94%, 83%, 73% and 62% VO2 max which were calculated from treadmill speeds of 60, 50, 40, 30, 20 and 10 metres/min (see Figure 4 in Dudley et al., 1982). Dudley et al., estimated these training intensities from the treadmill speeds by using the data contained within a paper by Shepherd and Gollnick (Shepherd and Gollnick, 1976). It’s also worth noting at this point that only treadmill speeds of 10-40 m/min were run continuously. At speeds of 10, 20, 30 and 40 m/min rats were exercised for 30, 60 or 90 minutes per day (with an additional group doing 15 min daily at 40 m/min) for 5 days per week for a total of 6 weeks. At the two higher speeds of 50 and 60 m/min the exercise bout was conducted as an “interval” session i.e. for the treadmill speed of 50 m/min, there was a 4.5 min run then 2.5 min rest and for the treadmill speed of 60 m/min, the session was a 2.5 min run followed by 4.5 min rest. At these two higher speeds the intervals were repeated 2, 4 or 6 times to produce a total “run” time of 9, 18 and 27 minutes for a treadmill speed of 50 m/min and 5, 10 and 15 minutes for a speed of 60 m/min. The groups doing the interval sessions were also exercised for 5 days per week for a total of 6 weeks.

Hadd then states:

“The results were interesting and each fibre type responded differently:
Improvements in mitochondria in fast twitch white fibres began while running at 80% VO2max (but not slower, presumably because they were not recruited) and increased exponentially as the pace climbed to 100% VO2max.
However improvements in fast twitch red (intermediate) fibres maximised at sub-max paces (85% VO2max) and did not get better with increased speed.
And the best way to cause improvements in slow-twitch fibres was to run long and slow at 70% VO2max (adaptation began from as low as 50% VO2max pace). Faster was not better. Although Dudley found that 90 mins was not better than 60 mins, Holloszy had shown that 2hrs was definitely better than one hour (which ties in nicely with Lydiard-type training recommendations that one 2hr run was better than 2 x 60 mins — you have to admit that the guy had great intuition born of his experience trying out different training on himself).”

Hadd states that “improvements in fast twitch red (intermediate) fibres maximised at sub-max paces (85% VO2max) and did not get better with increased speed”, which agrees with the data presented in Figure 4 of the Dudley et al., paper. However, Hadd then states that “And the best way to cause improvements in slow-twitch fibres was to run long and slow at 70% VO2max (adaptation began from as low as 50% VO2max pace). Faster was not better.”. This statement is puzzling because the data illustrated in Figure 4 of Dudley et al., indicates that faster was better, at least up to 83% VO2 max. Indeed training at either 83% or 94% VO2 max appeared to be equally effective at elevating Cytochrome C concentration (and therefore mitochondrial density) in slow-twitch muscle fibres of the soleus. The reference that Hadd makes to 50% VO2 max is also puzzling because the lowest exercise intensity that was used in this study, a treadmill speed of 10 m/min, corresponds to 62% VO2 max (see Figure 4).

There’s no doubt that training at relatively low intensities e.g. 62% and 73% VO2 max does produce elevations in Cytochrome C and therefore mitochondrial density in slow-twitch fibres (Figure 4). Furthermore, there’s also no doubt that doing interval workouts at 105% and 116% of VO2 max will not maximise mitochondrial density in slow-twitch fibres (Figure 4). However, to state that “the best way to cause improvements in slow-twitch fibres was to run long and slow at 70% VO2max” , is a misrepresentation of the data as an exercise intensity of 83% or 94% VO2 max clearly produced the greatest elevations in mitochondrial density in slow-twitch fibres (see Figure 4). It’s also worth pointing out that in terms of elevating mitochondrial density, exercise intensities of 62% and 116% VO2 max were roughly equivalent as were exercise intensities of 73% and 105% (see Figure 4). So “long and slow” running was roughly equivalent to interval training in terms of elevating mitochondrial density in slow-twitch fibres.

Next Hadd moves on to offer an explanation of why a long, slow run, undertaken following 3 months of high intensity sessions, had caused him so much discomfort, stating:

”So, (some of you may be way ahead of me already). Why was my 8.00m/m run so difficult?
Well, all my training in the 3 months leading up to it had been relatively hard. I had not trained slow enough for my slow twitch fibres to become stimulated to build huge amounts of mitochondria. My fast twitch red were becoming okay (I was reasonably good for 3-6m fast), but I could not access those fast powerful fibres at 8.00m/m. The intensity was too low. I was being forced to use my slow-twitch fibres... and they were not trained for any kind of endurance, and certainly not 2hrs.”

Hadd states that “I had not trained slow enough for my slow twitch fibres to become stimulated to build huge amounts of mitochondria.”. Judging from the data in the Dudley et al., paper, the optimal pace for maximising mitochondrial density in slow-twitch fibres is in the region of 83% VO2 max (see above). So what does this equate to in terms of heart rate and pace? Swain and colleagues have shown that 83% VO2 max is roughly equivalent to 90% maximum heart rate (Swain et al., 1994), which typically translates into somewhere between 10k and half marathon race pace. It therefore seems that hard tempo runs are the optimal training sessions for maximising mitochondrial density in slow-twitch fibres, which were exactly the types of training session that Hadd incoporated into his training regimen in the 3 months prior to his 8 min/mile, long, slow run that had caused him so much difficulty. It’s also worth noting that when Hadd states “My fast twitch red were becoming okay (I was reasonably good for 3-6m fast), but I could not access those fast powerful fibres at 8.00m/m”, that this interpretation also diverges from the data in the Dudley et al. paper as it is clear that both fast-twitch red and slow-twitch fibres were recruited at low exercise intensities (62% and 73% VO2 max) and therefore both fast-twitch red and slow-twitch fibres are recruited during “long and slow” running.

So where does this leave us? Although Hadd’s interpretation of the Dudley et al. paper is flawed, and the susbsequent extrapolations he makes regarding training intensity and mitochondrial density are therefore at odds with the data this by no means indicates that base training is necessarily ineffective. For one thing, it is clear that training at lower intensities does elevate mitochondrial density in both slow-twitch and fast-twitch red (intermediate) fibres (but it will not maximise mitchondrial density). Furthermore, there are likely to be many other adaptations which take place in response to endurance training e.g. enhanced glycogen deposition, capillarisation, improved thermoregulation etc, which will all play a role in exercise performance. However, I do think that it is important that if one wishes to cite scientific data to support a particular theory (an approach to training in this case) that the data must be correctly interpreted and represented. In this particular instance Hadd has not correctly interpreted the data and it is certainly untrue that mitochondrial density will be maximised in any fibre type by “long and slow” running. So the bottom line with regard to Hadd’s theory that one should train at a low-intensity to maximise mitochondrial density in slow-twitch fibres is incorrect.

The next post will examine Sections 4-6 of Hadd’s training approach in which he puts his theory into practice.

Further Reading
It’s also worth looking at the following thread:
<a href=” http://www.runtexu.com/forum/forum/forum_posts.asp?TID=4487&PN=1
“>Analysis of Hadd’s Approach to training for a lively and informative debate surrounding Hadd’s methods.

References
Dudley GA, Abraham WM, Terjung RL. Influence of exercise intensity and duration on biochemical adaptations in skeletal muscle. J Appl Physiol. 1982 Oct;53(4):844-50.

Shepherd RE, Gollnick PD. Oxygen uptake of rats at different work intensities. Pflugers Arch. 1976 Apr 6;362(3):219-22.

Swain DP, Abernathy KS, Smith CS, Lee SJ, Bunn SA. Target heart rates for the development of cardiorespiratory fitness. Med Sci Sports Exerc. 1994 Jan;26(1):112-6

Sorry the link under further reading got messed up, should appear correctly below:

Analysis of Hadd’s Approach to training

Further apologies, the link to Hadd's postings is also messed up, here it is again:

Hadd’s Approach to Distance Training

Gosh!

Erm.... now could you please explain base training to me in words of one syllabub?!?!?!

:o~

right
do continue

Hippy Benzy! Hewwo!

hi sass
this is blimmin fascinating
CMON MARMITE, GET TYPING

He's gone to find a piece of toast!

MM - thanks for this - really interesting.

I always wondered if base training (among other training theories!) is seen to 'work' becuase for many people, it is the first time they've taken a structured and progressive approach to training.

right, going to read this again now ...

you could have a point there lizzy

Very good point.

Pwease could someone give me an overview? I just can't read it all.......

well, he hasnt finished yet
hes refuting the assumtion that long slow running makes you faster

this could however mean that my racing addiction might be helpful

Purple Sassie,
"now could you please explain base training to me in words of one syllabub?!?!?!"

- if you train slow all the time you will not get as fast as you would if you train fast some of the time.

Lizzy B, interesting point.

Hippo,
"hes refuting the assumtion that long slow running makes you faster". No I'm not! I'm refuting the claim that you can maximise mitochondrial density in slow-twitch muscle fibres via long, slow mileage.