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Editor,—I read with interest the leader by Veronique Billat entitled “V̇o2 slow component and performance in endurance sports”.1 Oxygen uptake kinetics in general, and the aetiology of the V̇o2 slow component phenomenon in particular, are certainly topics of great conceptual and practical importance. However, there were several points of contention within Dr Billat's article that should be brought to the attention of readers so that an informed and balanced debate can take place.
Dr Billat states that “A high range of work (rates) can be identified at which there is a sustained increase in blood lactate . . .with time. These responses decline back towards a baseline value.” These two sentences, which are applied to a description of the physiological responses to moderate intensity exercise, are clearly inconsistent. It is also stated that during moderate exercise “oxygen uptake stabilises at about 80% in high level marathon runners”. This suggests that V̇o2 will reach a steady state close to 80% V̇o2max irrespective of the absolute work rate within the moderate exercise intensity domain. However, it should be remembered that moderate intensity exercise is, by definition, any exercise that is performed below the lactate threshold. Therefore constant load moderate exercise can lead to the attainment of a steady state V̇o2 of between ∼10% and ∼80% V̇o2max depending on the absolute work rate and fitness of the individual subject.
In her article, Dr Billat appears to support the widely held view that the maximal lactate steady state velocity and the critical velocity (which, by the way, corresponds to the horizontal and not the vertical asymptote of the hyperbolic relation between velocity and time to exhaustion) represent the same physiological transition point. However, it is difficult to reconcile this viewpoint with Dr Billat's statements that when “the rate of appearance of blood lactate exceeds the rate of disappearance . . .V̇o2 reaches a steady state that is higher than the V̇o2 requirement” and “(time to exhaustion at) critical velocity is reduced to less than 30 minutes”. If Dr Billat believes that critical velocity occurs at a higher intensity than the maximal lactate steady state, then she should support this position with references. I am unaware of any studies that have compared the directly determined critical velocity and maximal lactate steady state in runners, and the more thorough studies in cycling suggest that the two may be viewed synonymously.2 Dr Billat also states that time to exhaustion is limited above the critical velocity “because of rapid glycogen depletion”. To my knowledge, there is no evidence to support this assertion, and it would be safe to say that fatigue at these exercise intensities may result from a number of different mechanisms.
On the mechanism for the V̇o2 slow component, Dr Billat states that this “ . . .is mainly due to the recruitment of fast fibre type II fibres (sic) with fatigue”. This is something of an oversimplification. Although it is true that the relative amplitude of the slow component is well correlated with the proportion of type II fibres in the vastus lateralis,3 a great deal of additional work must be carried out before the recruitment of type II fibres during heavy exercise can be unequivocally accepted as the mechanism for the slow component phenomenon. Dr Billat also states that the reduction in the slow component observed at the same absolute exercise intensity after endurance training occurs “ . . .because of an increase in the distribution of type I fibres”. Again, to my knowledge, there is no evidence that changes in the proportion of type I muscle fibres will occur as the result of a short term training programme. It is also difficult to understand Dr Billat's assertion that “ . . .the amplitude of the slow component is not linked to endurance at all”. It seems implausible that a phenomenon that is causing V̇o2 to rise inexorably towards its maximum, and that is generally associated with a profound and increasing metabolic acidosis, is not related to endurance exercise performance. Indeed, in her own article, Dr Billat reports that, after a training programme that reduced the slow component, the time to exhaustion at the high intensity training pace was doubled.
Of greatest concern to me is Dr Billat's statement that “ . . .fit endurance athletes . . .have no V̇o2 slow component”. In several years of work in this field, I have yet to observe a single person (elite, well trained, recreationally active, or sedentary) in whom a V̇o2 slow component has not been shown during high intensity treadmill running. Dr Billat's reports of minimal slow components in highly trained runners can be explained by methodological problems in her studies.4 The subjects in these studies were not exposed to “square wave” exercise functions as is conventional in the serious study of V̇o2 kinetics but, rather, the treadmill belt velocity was increased gradually until the subjects reached the required velocity (which was not appreciably greater than the critical velocity) before timing was started. The V̇o2 slow component was then defined simply as the difference in V̇o2 between the value at three minutes and the value at the end of exercise. Given the faster V̇o2 on-kinetics in fit subjects, the reduced slow component in subjects who are aerobically fit or who have a high proportion of type I muscle fibres,3 and the fact that the slow component typically emerges at two minutes into heavy treadmill exercise,5 it is possible that Dr Billat's methods lacked the sensitivity to detect the slow component.
Dr Billat's work in identifying the type of training session that maximises the time spent at V̇o2max may well be of some conceptual value. However, I feel that it should be acknowledged that there is no evidence that this type of training is more effective than other types in improving V̇o2max or any other physiological correlate of endurance performance.
In conclusion, Dr Billat's observations and ideas are interesting and deserving of further study but I feel strongly that they should not be presented as fact (as they were in her article) until they can be confirmed by other groups. An over-reliance on unpublished observations, unreferenced material, and uncorroborated studies in review articles is unscientific and potentially misleading.