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LETTER TO THE EDITOR
O2) kinetics following acute plasma volume expansion (APVE) in a previous study (6) is utterly without foundation.
In the study of Zavorsky et al. (6), "O2 kinetics" was not measured, presented, or discussed. In Fig. 4 of their paper, O2 data are shown at rest and at 1-min intervals during a 6.5-min bout of high-intensity exercise. The method of averaging the O2 data for each minute of exercise was not stated. However, what Dr. Zavorsky has failed to appreciate is that such data provide no information at all on the time course with which O2 adjusts following the onset of exercise (i.e., the "O2 kinetics"; compare Fig. 4 in Ref. 6 with Fig. 2 in Ref. 1). The procedures for the correct measurement and interpretation of the O2 response to exercise are not trivial; the time delays, time constants, and amplitudes of the various phases or components of the response require careful consideration (2). For example, in endurance-trained athletes, the time constant (
) describing the fundamental increase in O2 following an abrupt increase in work rate is 
10–15 s (3). This means that the physiologically relevant "phase II" component of the pulmonary O2 response will be complete within 60 s (i.e., 4·). Zavorsky et al. (6), therefore, did not present or analyze data within the relevant time frame or with an appropriate sampling frequency. We politely refer Dr. Zavorsky to a recently published textbook (2) that not only provides information on what O2 kinetics actually is but also provides guidance on how O2 kinetics data might be appropriately collected, analyzed, and interpreted.
It appears from his letter that Dr. Zavorsky is aggrieved that we chose not to reference his previous publications. However, these papers concerned the influence of APVE on red cell pulmonary transit time and arterial PO2 in endurance athletes with hypoxemia, and they were not relevant to our work. Dozens of previous studies have used similar procedures to ours in producing APVE, and we make no apology for referencing only those of direct relevance. In this regard, it is plain that Dr. Zavorsky has missed one of the main goals of our study (1), which was to elucidate the possible role of physiological plasma volume expansion in the speeding of O2 kinetics that occurs soon after the commencement of an endurance training program in previously sedentary subjects (4).
Finally, we made the point in our study that APVE might be hypothesized to affect maximal O2 and exercise tolerance differently depending on the aerobic fitness of the subjects. We would point out, however, that the data of Zavorsky et al. (6) can make no contribution to this debate. The exercise time in that study was fixed at 6.5 min (i.e., subjects did not exercise to exhaustion), and the authors therefore have no way of knowing whether maximal O2 and exercise tolerance was, or was not, influenced by APVE their subjects.
FOOTNOTES
Address for reprint requests and other correspondence: A. M. Jones, School of Sport and Health Sciences, Univ. of Exeter, Heavitree Rd., Exeter EX1 2LU, UK (e-mail: a.m.jones{at}exeter.ac.uk)
REFERENCES
O2 kinetics, O2, and performance during high-intensity cycle exercise. J Appl Physiol 101: 707–714, 2006.O2 kinetics. Med Sci Sports Exerc 36: 225–232, 2004.O2 kinetics at the onset of submaximal exercise. J Appl Physiol 79: 1914–1920, 1995.
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