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LETTER TO THE EDITOR
The main purpose of this study was to investigate the effects of an 8-wk severe interval training program on the parameters of oxygen uptake kinetics, such as the oxygen deficit and the slow component, and their potential consequences on the time until exhaustion in a severe run performed at the same absolute velocity before and after training. Six endurance-trained runners performed, on a 400-m synthetic track, an incremental test and an all-out test, at 93% of the velocity at maximal oxygen consumption, to assess the time until exhaustion. These tests were carried out before and after 8 wk of a severe interval training program, which was composed of two sessions of interval training at 93% of the velocity at maximal oxygen consumption and three recovery sessions of continuous training at 60-70% of the velocity at maximal oxygen consumption per week. Neither the oxygen deficit nor the slow component were correlated with the time until exhaustion (r = -0.300, P = 0.24, n = 18 vs. r = -0.420, P = 0.09, n = 18, respectively). After training, the oxygen deficit significantly decreased (P = 0.02), and the slow component did not change (P = 0.44). Only three subjects greatly improved their time until exhaustion (by 10, 24, and 101%). The changes of oxygen deficit were significantly correlated with the changes of time until exhaustion (r = -0.911, P = 0.01, n = 6). It was concluded that the decrease of oxygen deficit was a potential factor for the increase of time until exhaustion in a severe run performed after a specific endurance-training program.
To the Editor: Demarle et al. (2) asserted that a decrease in oxygen deficit is related to an increase in time to exhaustion during a severe run, following training. The basis for this assertion would seem to be the finding of a significant correlation (r = -0.911, P = 0.01, n = 6) between the change in time to exhaustion and the change in oxygen deficit, from pre- to posttraining. The time to exhaustion was measured at the same absolute intensity, equivalent to the median velocity between the velocities at lactate threshold and maximal oxygen uptake in an incremental test before training.
Although individual data for the six subjects are not presented, an inspection of the graphically presented data indicate that, despite a decrease in oxygen deficit, training had no effect on time to exhaustion in one subject and that there was a decrease in time to exhaustion in two subjects. This might question the assertion that a decrease in oxygen deficit improves exercise tolerance.
In an additional subject, time to exhaustion was increased by 449 s (101%) following training, and oxygen deficit decreased by a value approaching 2 liters. The correlation coefficient should be used with caution in the occurrence of such an outlying value, which can exert a large effect on the strength of the correlation (1).
However, a potential factor, the precise functional significance of changes in oxygen deficit with training, with regard to exercise tolerance remains to be elucidated.
REFERENCES
E-mail: stuart.taylor{at}biro.org.uk
O2 [oxygen uptake] kinetics is important because it reduces the reliance on intramuscular energy stores and anaerobic glycolysis at the rest-exercise transition. One consequence of this behavior is that, after training, there will be a reduced perturbation of the intracellular milieu and a decreased reliance on intramuscular glycogen stores. This effect will increase endurance at all submaximal work rates, but will be most pronounced in the heavy intensity domain, where depletion of intramuscular glycogen stores is thought to cause fatigue." The goal of our work (3) was then to test this hypothesis. In this prospect, we studied the training effects on the oxygen deficit and other parameters related to the O2 kinetics, such as the O2 slow component, and their potential consequences on the time to exhaustion at a given supralactate threshold velocity (intermediate between lactate threshold and maximal oxygen consumption). Such an experiment was conducted in six regularly trained athletes who specialized in middle- and long-distance running.
After subjects completed training, the oxygen deficit significantly decreased (see the individual data in Table 1); however, this was not the case for the O2 slow component. The time to exhaustion remained statistically unchanged; only three subjects improved their performance (see the individual data in Table 1). This was clearly specified in our work. Keeping in mind the population tested (only 6 well-trained athletes, for which it seems difficult to observe large training effects) and the fitting-method used (only a single transition from rest to exercise), we are fully in accordance with the Dr. Taylor's remarks concerning the interpretation of the correlation coefficient that was found (r = -0.911, P 
0.01). That was why we qualified the decrease of oxygen deficit and other training effects, such as the attenuation of the O2 slow component (nonsignificant here), as "potential factors" of performance improvement at a given supralactate threshold work rate (2, 3, 5). In the same line of thinking, only the subjects who increased their velocity at lactate threshold (see the individual data in Table 1) improved their time to exhaustion (r = -0.877, P 0.01).
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To conclude, our work (3) should be considered as "a starting point" for future research concerning the multiple factors of performance improvement at such supralactate threshold work rates. By the way, recent works from our laboratory give ample food for thought that the decrease of oxygen deficit and the attenuation of the O2 slow component, which is strongly linked to the increase of velocity at lactate threshold (3-5), may be a partial determinant for the improvement of performance at such supralactate threshold work rates (1, 4, unpublished observations). This remains, however that may be, an interesting area for future experiments.
FOOTNOTES
E-mail: alexandredemarle{at}aol.com
REFERENCES
O2 slow component: physiological and functional significance. Med Sci Sports Exerc 26: 1354-1358, 1994.[ISI][Medline]
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