If I may; if you read the Noakes et al. works in this area thoroughly, they are really just presenting what has been self evident for a very long time, but wrapping it in different packaging. By that I mean, it has been clear for ages that the cause of \"fatigue\" for an effort of 10 sec in duration is different than the cause of \"fatigue\" in the marathon. Further, in some cases an athlete may fatigue due to glycogen depletion, or dehydration, or hyperthermia, or.... ad nauseum. The physiology of fatigue has been a complicated issue, and has been accepted as a complicated issue in the field of Exercise Physiology for decades, if not a century or more. It is fairly reminiscent of George Brooks, in the early 90\'s, \"proposing\" the Crossover Concept. Of course, it was self evident before that, that we oxidized primarily fat at low intensity, and at some point we \"cross over\" to oxidizing primarily carbohydrate. Anyone who was properly educated in Ex Phys was aware of this, but there wasn\'t a pretty graph with a nice caption...\"Crossover Concept\" to point to in the text books. So, Brooks did it, and now is cited in most undergrad texts. It was nothing new though.
Similarly, Noakes has simply taken a number of observations that have been well known (e.g. \"fatigue\" sometimes preceedes glycogen depletion, or intramuscular ATP never drops below 50%, or we do better when we are externally motivated by crowds or stimuli) and put them together using the terminology of a relatively new field, Dynamical Systems, to \"sex it up\". Honestly though, it doesn\'t mean anything new to training. It also doesn\'t mean that there is no lactate threshold, by conventional terms. Lactate still remains (almost) linear at low workloads, and at some point, increases exponentially. That point corresponds to a number of physiological processes (e.g. fast twitch fiber recruitment, acceleratted glycolysis) that negatively impact performance, or at least the ability to sustain performance for a prolonged period of time. Further, it is, again, self evident, that training increases the workload/pace at which this exponential increase in lactate occurs in an apples to apples comparison, hence corresponding to an increase in performance. Of course.... lactate does not cause fatigue per se in almost any context that has been identified to this point. BUT,.. lactate accumulation is associated (so, guilt by association applies here) with the workload that cannot be sustained for a prolonged period of time.
The primary problem with the \"lactate threshold\" concept lies is the definition, or lack of a consistent one thereof. There are a gazillion of them, but the fact remains, under an apples to apples comparison, it is a traininable characteristic, and very relevant to training for endurace events. Plotting a curve, regardless of the definition, it\'s a bit like Pornography, \"I know it when I see it.\" The fact remains, if you train your \"lactate threshold\" to a higher level, you will be a better marathoner, or likely 10k, or even 5k or miler, depending on the circumstances. Performance at efforts longer than 10 min are clearly impacted by lactate threshold, and for durations as long as the marathon, primarily impacted by the lactate threshold. So, don\'t take what Noakes has been writing to mean you shouldn\'t think about that type of training. That being said, the LT is not the only variable in the physiological side of the equation, and certainly there are other equations in the non-linear dynamics of performance.
Finally, don\'t take everything above to mean that I don\'t respect everything that Noakes is/has done. He is one of the most prolific scientists in the field and continuously pushes the field forward with his insighful work. That doesn\'t necessarily imply endorsement, but respect.
Steve