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Lore of running

Table of Contents

Book notes for Lore of running by Tim Noakes

Part 1: Physiology and biochemistry of running

Chapter 1: Muscle structure and function

Tryglycerides are broken into free fatty acids and transported via the bloodstream to the mitochondria of the muscle, where they are used for energy. There are also droplets of fat (cellulite!) throughout the muscle cell, these can be used directly after been broken down, without needing to enter the bloodstream at all.

Noakes suggests that the differences between sprinters and distance runners is genetic. Sprinters have 26% type I (slow twitch) vs 80+ for distance runners. Huge difference. Interestingly, cyclists and swimmers are around 50% (around the same as mid-distance runners).He gives the classic example of west-african sprinters vs east african marathoners.

to check: does muscle fibre composition stay the same? can it change over lifetime? Training will target different types depending on if it is short/long-term, explosive or not, so training type II only might result in larger type II muscle cells, not more of them. Can you ever make more of them?

Interestingly, Noakes does not think that having a high % of type-I fibers is important for distance running, he instead thinks there is a selection effect: people with lots of type-II fast-twitch fibers run short-distance. People who are unable to run fast become marathon runners! He suggests that world-class marathoners actually have 40-60% of type-II fibers, like a cyclist. sub-2 mararthon not possible for a 20% type-II person!

eccentric contractions use fewer muscle fibers, so they put more (almost twice) force on each fiber, which is why they are more able to produce muscular damage (running downhill kills the quads, as they say).

Benefits of strength training seem unclear. adding strength training is good, but substituting it for running may not be helpful. Possible it does help for >5km distances though.

Chapter 2: Oxygen transport and running economy

Vo2max is the amount of oxygen used by the body when running to exhaustion for around 5-8 minutes.

It was thought that the limitation was the heart, that it would eventually get into oxygen debt, produce lactate, and slow down, which would then cause the other muscles to slow down due to lack of oxygen.

It turns out that the heart does not contract anaerobicly, so when entering oxygen debt you experience sharp pains as the heart is unable to contract fast enough.

Noakes then suggests that the brain (central governer) prevents you from getting to this point. When it feels the heart or brain is at risk of not getting enough oxygen, it limits muscle output to prevent damage. This is why we see muscle fatigue cause people to stop exercising, not heart pain.

tocheck: not 100% sure I understand what he is saying about the different models here, should revisit this section with other materials

Age affects vo2max, decline of about 9%/decade after 25, although might be possible to reduce to 5% by lifelong exercise (may be caused by less muscle mass and less efficient muscles – therefore less able to use oxygen)

vo2max can be changed, on average it can be increased by only 5-15% (although can be 0-60% at extremes). Of course running ability changes more than this with training (efficiency, fatigue resistance etc can change), but since the differences between elites and hobbies are >>15%, we can see that elites have genetic predisposition, not just training.

vo2max also drops around 10% for every 1000m above 1200m.

Normal men are 45-55 vo2max, (ml/kg/min). elites are high 60s to low 80s.

The real number we care about though is the speed at vo2max (J Daniels vVo2max thingy). This takes efficiency into account, since it is no use having 80 vo2max if you recorded that value at a very low speed due to being an inefficient runner!

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Last modified 2019-08-16 Fri 08:52. Contact