HR-training: can running too fast inhibit aerobic adaptations?

Those 'metabolic adaptions' as you call them are nothing but maintenence work. Define metabolic efficiency in a meaninful way. Now relate that to biomechnical efficiency. What do you get?

So you're saying that metabolic efficiency is determined by biomechanical efficiency, and hence a runner cannot become more metabolically efficient while simultaneously becoming less biomechanically efficient??

Or that a runner cannot become more mechanically efficient while simultaneously decreasing RE?

bad_stats wrote:

It's the word "either" that strikes me. He's saying that running too fast can hinder aerobic development. Is this true? Are certain adaptations inhibited when easy runs are done too quickly?

tl;dr: Yes, if you only do fast aerobic running, there are adaptations you will miss out on to some degree. Even if you provide adequate recovery.

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My current training "philosophy" is greatly influenced by Hadd, but I have to say that I do disagree (probably too harsh a term) with some things... so what I say is not purely from a "Hadd perspective," but from my perspective/interpretation.

Further, I'm going to assume that your base training is focusing on an eventual marathon, since that's largely what Hadd's writing was aimed at. (I'm just stating this in case we end up going back/forth on some things.)

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First, try not to think of discrete training zones as the be-all-end-all. Running effort spans a spectrum, and each of these "zones" on the spectrum are all connected in some way. Where you are on the spectrum will determine the amount and type of stimuli and adaptation, but just because you move from "Zone 2" to "Zone 3" doesn't mean adaptations from one are not found in the other.

What we're trying to do in the base phase is build a base on which to support our event-specific training. In this case, we want to extend our ability to run at a goal marathon pace (MP). Now, you could just go and do all of your runs at MP (hey, specificity, right?), but this has a few issues.

You can't spend as much time on your feet at MP in a given week as you can at an easier pace. You're going to be on your feet for, say, 3 hours in a marathon. It's much easier to give your body this specific metabolic and mechanical stress if you're out on an easy(ish) long run as opposed to just going and running a marathon. The former is a (short-term) repeatable stress, whereas the latter is not.

While both easy(ish) distance runs and MP runs provide aerobic adaptation (in addition to other adaptations), the former gives us a greater volume at aerobic efforts with less wear-and-tear and overall stress, while building us up to handle the stress our race and race-specific training will place on us. Most elite runners, such as Moses Mosop, spend 80% - 85% of their training time at sub MP effort.

Now just because you have all this easy(ish) distance running under your belt doesn't mean you're such an aerobic beast that you can go CRUSH a marathon. You need MP-specific training to get the most out of your race. The easy(ish) running is there to support this specific work... it's there to build on.

For the same reason, our fast/hard running in the base phase tends to be very short strides and hill sprints at first. We start at the opposite extreme (fast and short) to support future training that is fast and longer in duration, which provides event-specific support on the anaerobic/speed side of things.

bad_stats wrote:

You are saying that as long as you are getting adaquet recovery, running faster is better aerobically.

I wouldn't say this. As mentioned, the "aerobic benefit" between running at (for instance) 145 HR vs 160 HR is probably not quite enough to fuss over. The primary difference is the race specificity of training at 160 HR. Getting comfortable and efficient at running at MP is a primary benefit of training at 160 HR vs 145 HR. You *may* get a bigger "aerobic bang for your buck" training at 160 HR, but you can't spend as much time at 160HR as you can at 145HR, so the intensity vs. duration balances out to some degree when we only consider the aerobic part of the stimuli.

Remember, we're not only running at these slow aerobic speeds for the aerobic benefits.

train smart wrote:

The adaptions you need to improve are all skill based.

I disagree. Yes, developing skill is important, but it is not the only adaptation we seek. For instance, in the marathon, a major component is utilizing fuel efficiently. Yes, fuel utilization can be improved by running in a more (mechanically) efficient way, but there are further ways to improve. For instance, doing long runs in a glycogen depleted state helps to both increase the amount of glycogen we can store and how much we spare it.

train smart wrote:

So you think that more running will give you more mitochondria? But you have no actual evidence?

Actually, low muscle glycogen initiates the AMPK and MAPK pathways, which result in increased mitochondria. High volume running often results in low muscle glycogen.

Fast running results in low muscle glycogen a lot sooner than slow running does.

Bad Wigins wrote:

Fast running results in low muscle glycogen a lot sooner than slow running does.

But if you want to deplete primarily slow twitch muscle fibers, you have to go slow enough to avoid depleting the intermediate fibers. You cannot always run fast (of course). Muscle clycogen resynthesis of the type II fibers is slower than in type I fibers, hence you cannot train at faster paces that often, you know.

the haddite wrote:

bad_stats wrote:

It's the word "either" that strikes me. He's saying that running too fast can hinder aerobic development. Is this true? Are certain adaptations inhibited when easy runs are done too quickly?

tl;dr: Yes, if you only do fast aerobic running, there are adaptations you will miss out on to some degree. Even if you provide adequate recovery.

haddite, you have hit on the core question behind my original post: are there training adaptations that don't occur when you train at (date) marathon pace or above?

Many have commented sensibly on the need for recovery and hence the need for easy pace between hard or long efforts.

Some have also pointed out that the volume of training possible at an easy pace (E) is so much greated than at marathon-pace (M) or above that the greater time spent at E swamps the incrementally greater benefits at M or above.

I've never doubted either of these points. I started the thread because I was curious whether there is something additional happening at E-pace. For example (and I'm making this up) what if certain kinds of vacularization are inhibited by the lower pH's associated with faster paces.

I'm wondering if there are specific adaptations that occur primarily when training at E-pace. As Pete pointed out, Hadd certaily thought so and he cited animal studies to support this point. A decade later, do we still believe the animal studies he cited? For instance, I've read on these forums that mitrochondrial growth is better stimulated by higher intensities, which contracticts one of Hadd's claims.

I don't want any of this to be construed as an attack on Hadd's training philosophy. My take is that Hadd used these studies to motivate a training plan that was based on real-world coaching experience (I get the same feeling reading Lydiard). That said, if he's right and things happen at E-pace that don't happen (or happen much more slowly) at M-pace, then there have be specific physiological (or neurological) adaptations that occur as a result of the E-pace stimulus and I'm curious about what those adaptations are.

Bad Wigins wrote:

Fast running results in low muscle glycogen a lot sooner than slow running does.

I never said it didn't. My point was that running more will most likely increase mitochondria, in contrast to wait train_smart is claiming.

And as BadWigins noted, you can deplete glycogen in different fiber types, so training at all intensities along the spectrum is important (especially in the context of the marathon).

the haddite wrote:

So you're saying that metabolic efficiency is determined by biomechanical efficiency, and hence a runner cannot become more metabolically efficient while simultaneously becoming less biomechanically efficient??

Or that a runner cannot become more mechanically efficient while simultaneously decreasing RE?

Yes, determine by biomechanical efficiency. I assume you are refering to RER?

Think of it this way. Why would my RER be poor in the morning, but good in the afternoon? That is not a metabolic adaption, so much as a good warm up making me more efficient per se.

the haddite wrote:

train smart wrote:

The adaptions you need to improve are all skill based.

I disagree. Yes, developing skill is important, but it is not the only adaptation we seek. For instance, in the marathon, a major component is utilizing fuel efficiently. Yes, fuel utilization can be improved by running in a more (mechanically) efficient way, but there are further ways to improve. For instance, doing long runs in a glycogen depleted state helps to both increase the amount of glycogen we can store and how much we spare it.

Again this is neural, not metabolic. You have to learn the skill of running in a depleted state, controlled by neurotransmitters. So the concentration does not go down and force the pace to slow. It's easy to do this for a few minutes, but for an hour or more, that requires the adrenaline to be flowing just right.

And then you have to be able to run with efficiently at the start of a marathon with a full tank of glycogen and keep going as that fuel depletes. Both skills being equally important.

the haddite wrote:

train smart wrote:

So you think that more running will give you more mitochondria? But you have no actual evidence?

Actually, low muscle glycogen initiates the AMPK and MAPK pathways, which result in increased mitochondria. High volume running often results in low muscle glycogen.

Ah the mitochondrial biogenesis stuff. Good luck figuring that out with real numbers.

U.N.O. wrote:

Bad Wigins wrote:

Fast running results in low muscle glycogen a lot sooner than slow running does.

But if you want to deplete primarily slow twitch muscle fibers, you have to go slow enough to avoid depleting the intermediate fibers. You cannot always run fast (of course). Muscle clycogen resynthesis of the type II fibers is slower than in type I fibers, hence you cannot train at faster paces that often, you know.

This related to a point I'm confused about. I've heard of the 'size principle' that the size of fibers recruited increases with increasing power of the muscular contraction: to spring requires the large type II fibers, to run slowly we can get by with mostly type I fibers. Do you know if the smaller fibers actually shut off at higher running speeds or do they just become increasinly less relevant?

This relates to one of Hadd's claims that running too fast doesn't adaquetly train the smaller muscle fibers. The text of one of his old posts is pasted into this thread:

. I guess in one rat study the mitochondria seemed to in muscle fibers responded best in slow twitch at slow speeds, fast twitch at faster speeds.

Here's a quote from the link above:

'''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.

It seems paradoxical, that I can be okay at 7.00m/m, but not at 8.15m/m, but here is one example.

I was okay if I ran hard enough to force my body to recruit my fast twitch red fibres (and as long

as they had enough glycogen). Like most distance runners I have relatively few fast twitch white

fibres, so they were little help, and in all my 3 months of training my slow twitch were being bypassed

on every training run. (Or rather, recruited, but swamped/overworked). The intensity of

each training run was too high for them to be stimulated optimally to best create mitochondria in

themselves (and thus improve). So when I ran at a pace that I was forced to access ONLY them,

I was sunk.

Read more:

http://www.letsrun.com/forum/flat_read.php?thread=5606203#ixzz3s3JN4y9R

''''

bad_stats wrote:

This related to a point I'm confused about. I've heard of the 'size principle' that the size of fibers recruited increases with increasing power of the muscular contraction: to spring requires the large type II fibers, to run slowly we can get by with mostly type I fibers. Do you know if the smaller fibers actually shut off at higher running speeds or do they just become increasinly less relevant?

From

:

"RECRUITMENT OF MUSCLE FIBERS

Muscles produce force by recruiting motor units (a group of muscle fibers innervated by a motor neuron) along a gradient. During voluntary isometric and concentric contractions, the orderly pattern of recruitment is controlled by the size of the motor unit, a condition known as the size principle (Henneman, et al., 1974). Small motor units, which contain slow-twitch muscle fibers, have the lowest firing threshold and are recruited first. Demands for larger forces are met by the recruitment of increasingly larger motor units. The largest motor units that contain the fast-twitch B fibers have the highest threshold and are recruited last.

No matter what the workout intensity, slow-twitch motor units are recruited first. If the workout intensity is low, these motor units may be the only ones that are recruited. If the workout intensity is high, such as when lifting heavy weights or per- forming intervals on the track, slow- twitch motor units are recruited first, followed by fast-twitch A and fast- twitch B, if needed.

There is some evidence to suggest that the size principle could be altered or even reversed during certain types of movements-specifically those that contain an eccentric (muscle lengthening) component-such that fast-twitch motor units are recruited before slow- twitch motor units (Denier van der Gon, et al., 1985; Grimby & Hannerz, 1977; Nardone, et al., 1989; Smith, et al., 1980; Ter Haar Romeny, et al., 1982). It is possible that a preferential recruitment of fast-twitch motor units, if it exists, is influenced by the speed of the eccentric contraction, and can only occur using moderate to fast speeds (Karp, 1997; Nardone, et al., 1989)."

bad_stats wrote:I'm wondering if there are specific adaptations that occur primarily when training at E-pace.

Our skeletal muscles are composed of two types: type I and type II; slow twitch and fast twitch, respectively. The latter can be subdivided into type IIa and type IIb. Type I fibers are the first to be recruited, but as we increase the intensity of our exercise type IIa fibers will be recruited and at yet higher intensities we will recruit type IIb fibers.

Here is a (simplified) breakdown of fiber and energy types used in common zone systems:

Zone 1 (recovery) -- type I -- fat

Zone 2 (majority of Hadd running) -- type I -- fat/carb

Zone 3 (includes MP, but usually sub LT) -- type I / IIa -- fat/carb

:: higher zones from here, but not as important for our purposes

The closer we get to 100% VO2 max, the more we rely on carbohydrates as our major energy substrates. As we go beyond 100% VO2 max, we cannot generate ATP via aerobic glycolysis, so we shift to generating ATP via anaerobic mechanisms.

Type I fibers have the greatest mitochondrial density. They tend to utilize fat.

Type IIa fibers have lower mitochondrial density. They tend to utilize glucose.

Type IIb fibers have very low mitochondrial density. They utilize glucose and ATP stored in the fibers themselves. (Think instant anaerobic energy.)

As we can see, there are different metabolic responses and fiber type recruitment patterns at different points on our training-intensity-spectrum.

Further, we can see that training at this "Hadd pace" stimulates type I fibers to the largest degree, stimulate mitochondrial growth and function, and improve our ability to utilize fat as an energy substrate. The better we can utilize fat as an energy source, the more we improve our ability to reserve glycogen for higher intensities.

If you care about lactate clearance, type I fibers are also responsible for this to a large degree.

This is a good question, and it's been obscured by a lot of irrelevant noise in this discussion. The answer is no. HADD was very wrong about this.

I don't mean to suggest that his training didn't work, but that if it did, it wasn't for the reasons he explained. There's nothing strange about that, of course. Training is more an art than a science.

HADD's conclusion that running too fast prevents aerobic development is absolutely wrong. He based his conclusion on 1982 study with rats, and he misinterpreted the article, which actually showed that higher intensity leads to greater mitochondiral development than low or medium intensity exercise. Just the opposite of what HADD argued.

What did malmo say back in 2003?

He was sick of people "blathering on about mitochondria"

And he was right. If there is one area of running physiology where people have no clue what they are talking about but pretend they do, it's mitochondria.