In my book I explore the numerous successful applications of the ‘Lydiard System’, using recent exercise physiology findings to explain how this heavily endurance-weighted philosophy was so successful, and still is, over 50 years down the track.
After over two years of combing through the literature, and grilling New Zealand Olympic medallists and their coaches about the ways they trained under Arthur Lydiard, I came out with a relatively simple way of getting his message across to the modern audience in current ‘physiology-speak’, based on the differing muscle fibre types and their respective dominant energy systems. ‘Critics’ on Amazon.com were mostly well-pleased with my efforts, giving the book a 5-star rating for months on end, but there’s always someone who likes to rain on the parade. Eventually he emerged.
One outspoken online critic informed the world-at-large that the simple “cardiovascular-anaerobic” concept I was using was now very outdated, and then went to some trouble to heavily slate the book, giving it a two-star rating. To be truthful, although the most basic concept in my book was based on the aerobic / anaerobic model, I had not even yet heard of a ‘cardiovascular / anaerobic’ model. Not in years of reading and perusing the literature and well-authored books, had I heard this odd juxtaposition of terms.
I was less-perturbed when the critic stated that my book “could possibly be useful for a track athlete, but as I am just a fun-runner, it’s of no use to me”, or words to that effect. Considering that the serious track coach or athlete was exactly whom the book was written for, no wonder the fellow felt neglected. Anyhow, the ancient Roman running philosopher Gluteus Maximus stated “There is no such thing as a memorial to a serial critic”.
Critics can be handy sometimes. At other times they can throw the baby out with the bath-water. Is there anything to my critic’s comments that changes the way we should train for peak events in middle and longer distances? No; after looking at this question in some detail, I conclude that it’s “much ado about nothing”, or “much ado about a little thing that won’t change your training one iota”.
In my book I did state quite emphatically that exercise physiology is still an infant science, with no definitive areas of black and white; only many shades of gray, from predominantly very light gray, to predominantly very dark grey. Since 1924, the Nobel-prize winning work of scientists A.V.Hill, A.Bock, and D.B.Dill has been foundational to all current understanding of the processes that govern maximal performance, to this day. It was these pioneering scientists who first floated the aerobic/anaerobic model, but popular science being the way it is, not ALL of what they postulated was picked up on or understood by the world at large. In effect, it seems that what they were saying has been considerably dumbed down over the years, and never effectively explored in detail.
THIS is what my erstwhile critic has been prattling on about. He’s in extremely good company, namely that of Dr Tim Noakes, author of the fabulous ‘Lore of Running’. Dr Noakes wrote an article that was published in the year 2000 in a Scandinavian Sports Science Journal* that pointed out that there’s quite a bit more to factors that limit performance than just the aerobic / anaerobic process in the working muscle.
The currently very accepted model is that limitations in cardiovascular output AND oxygen uptake dictate ultimate performance outcomes in events that last longer than 90s. But what Dr Noakes further points out, very logically in my mind, is that the heart is itself is the MOST IMPORTANT working muscle, and in itself is subject to fatigue. To save you wading through quite a few pages of supportive data, the central axiom Dr Noakes proposes is very simple; too simple, perhaps. Noakes says ” a more rigorous analysis indicates that the first organ to be affected by anaerobiosis during maximal exercise would likely be the heart, not the skeletal muscles.”
The very first people who noted this ‘cart and horse’ problem were…scientists A.V.Hill, A.Bock, and D.B.Dill, in 1924!! Old science can be good science, even if it is nearly 90 years old. They weren’t given the Nobel prize for nothing! And their full work has been misinterpreted ever since, it seems!
There are other models of why fatigue occurs in maximal exercise; these are
(a) The cardiovascular/anaerobic model ( as just discussed)
(b) The energy supply/ energy depletion model
(c) The muscle recruitment (central nervous system fatigue) muscle power model
(d) The biomechanical model
(e) The psychological/motivational model
There are a number of nuisance facts that have been ignored in the ‘Cardiovascular/Anaerobic ‘ model, and the elephant in the room could be this: according to Noakes, who really has written THE book on the subject, “no study as yet has definitely established the presence of either anaerobiosis, hypoxia or ischemia in skeletal muscle during maximal exercise” (!!!).
( However, acidosis in the skeletal muscles’ blood supply has been routinely demonstrated for many years, and when the pH of the bloodstream gets above 4mmol/litre on average, it is held that more fast twitch fibre involvement with anaerobic glycolysis is starting to occur. We also have a shift in measureable blood gases as more CO2 gets blown off with increased metabolism of carbohydrates. These aspects of the aerobic / anaerobic model have not been disproven, although how we’d burrow deep into the muscle tissues and demonstrate hypoxia, ischaemia, or anaerobiosis at a microscopic level, I wouldn’t know. When muscles are pumping maximally, it’s a bit hard to keep a testing needle in the one spot.)
There are other demonstrated problems with maximal exercise fatigue in conditions of heat or high altitude, and in chronically ill people who have heart and lung diseases, without evidence of skeletal muscle anaerobiosis , hypoxia, or ischaemia. It’d be commonsense to suggest that ALL these models all contribute to fatigue, and this should be obvious.
Why there has to be one particular model or another that overrides all the rest is merely a complication that serves no purpose except to make training theory more difficult by far than it needs to be for the average athlete and coach. Does it really matter if the inability to run faster up the finishing straight is caused by one or the other? All we need to know is that all these limiting factors are present, and that at the end of the day, no matter their definition, we know that there are useful zones of training that build us up, and there are some high intensities that have to be monitored extremely carefully.
As Noakes does say in his article, the cardiovascular /anaerobic model has the major deficiency that when taken to logical conclusions means that we’re looking at the wrong organ/s in fatigue at maximal exertion; the muscle most concerned with ‘anaerobiosis’ in running is not the skeletal muscle in the leg, but the cardiac muscle. The brain too relies on good circulation and high glucose fuel content to function efficiently under stress, so there’s another organ to consider in the whole picture! Noakes has for some time proposed an ‘as yet unknown’ central governor that oversees fatigue response. I would suggest that it has been known for some time, and it is called the central nervous system, which is constantly monitoring blood gases, blood acid, and blood alkali levels, in every organ involved, and has the power to selectively shut down our physiology if it feels that the intensity is unsafe for the survival of the organism.
Given this is a shift in our common understanding, I’d say it still doesn’t change the application of training theory much, if at all. If anything, we should shift more in the direction of gently exercising the heart for prolonged periods. The essential facts of aerobic exercise and capillarization, mitochondrial proliferation, increased work capacity of the heart and skeletal muscles, skeletal muscle acidosis, etc, are not disproved in any way, and still apply. The major shift is that fatigue may occur in the cardiac muscle before the legs, and the sensory brain will steer us away from cardiac ischemia and slow us down in the legs by reducing power output. That’s why we feel it in the legs; maybe the neuro-motor power drives have been selectively switched off and made inaccessible… but this will give physiologists still something more to discuss while the rest of us who coach or compete will just have to get on with it as usual, looking at systems which have always worked, and applying them as sensibly as possible. That’s the ART of coaching; interpreting what the body is telling us, with the knowledge we have gained to date.
* Scand J Med Sci Sports 2000:10:123-145