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article and Chilvers' concern about our statistical analysis is unwarranted. JAMES H. ZAVECZ, PH.D. WILLIAM McD. ANDERSON, M.D. School of Medicine Louisiana State University Medical Center Shreveport, LA

1. Lagos N, Vergara J. Phosphoinositides in frog skeletal muscle: a quantitative analysis. Biochim Biophys Acta 1990; 1043:235-44.

THE EFFECT OF REPETITIVE EXERCISE ON AIRWAY TEMPERATURES

To the Editor: I read with great interest the recent article by Gilbert, Fouke, and McFadden (1) concerning airway heat flux and its role in altering airway responses during repetitivestimulation. Gilbert and colleagues compared changes in tracheal temperatures during repetitive bouts of exercise in seven asthmatic subjects. They reported that the decrease in FEY, after the first exercise period (24 ± 50/0) was significantly greater than that following the second period of exercise (5 ± 40/0). They also noted that during the second trial, less cooling developed in the trachea during inspiration and airstream temperatures in the trachea were warmer during expiration. The authors concluded that repetitive exercise performed over short intervals reduced the "essential thermal gradients" needed to produce obstruction (p. 826). However, for these conclusions to be valid, it is necessary to demonstrate that post-exercise lung function was significantly less impaired after the second exercisechallenge when compared with that which occurred after the first. Unfortunately, the data included in this article fail to show this convincingly. Thus, their conclusions concerning the relationship between tluctuations in airstream temperature and airflow limitation with repetitive exercise are not substantiated. It is essential to emphasize that the interpretation of their data is based on the assumption that each of the seven asthmatic subjects used in this study is refractory to a second bout of exercise. However, it has been reported that refractoriness in response to a repetitive exercise challenge occurs in only 50% of individuals who exhibit exercise- or hyperventilation-induced asthma (2-4). Thus, it would seem very important for the authors to document the existence of a refractory period in each of the seven subjects. In this regard it is important to note that on the average, subjects in this study started the second exercise period with a baseline FEY, that was markedly lower than that preceding their first exercise challenge (figure 3, p. 827). This mismatch in "baseline" lung function makes it impossible to conclude that any difference existed in the magnitude of airway obstruction observed after each of the two repetitive exercise challenges. Although the average FEY, returned to within 15% of the original baseline value, given the magnitude of variation, the individual data would likely show changes in baseline FEY, that were comparable to the maximum changes in FEY 1 recorded after the second exercise period. This analysis could be remedied by using the original baseline value to recalculate the percentage decrease in FEY, after the second trial, thus simulating the situation in which full recovery was allowed to occur. If this is done the percentage decrease in FEY 1 would be 19%, not the 5 ± 4% decrease reported by the authors. On the average, baseline FEY I decreased but the maximum fall in post-exercise FEY, remained unchanged. Thus, the "significantly smaller effect" seems to be an artifact of the shift in baseline FEY,. In summary, I do not believe that the authors have adequately demonstrated the existence of a refractory period in the group of asthmatics they studied, and with an alternative analysis of their data there is no change in FEY, with exercise. Without convincing documentation of significant changes in lung function following

repeated exercise, any discussion of the role of intrathoracic heat flux and its ability to alter responses to repetitive exercise seems inappropriate. ARTHUR N. FREED, PH.D. Assistant Professor of Environmental Health Sciences and Medicine The Johns Hopkins University Baltimore, MD

1. Gilbert lA, Fouke JM, McFadden ER Jr. The effect of repetitive exercise on airway temperatures. Am Rev Respir Dis 1990; 142:826-31. 2. Edmunds AT,Tooley M, Godfrey S. The refractory period after exerciseinduced asthma: its duration and relation to the severity of exercise. Am Rev Respir Dis 1978; 117:247-54. 3. Rakotosihanaka F, Melaman F, D'Athis P, Florentin D, Dessanges JF, Lockhart A. Refractoriness after hyperventilation-induced asthma. Bull Eur Physiopathol Respir 1986; 22:581-7. 4. Anderson SD. Exercise-induced asthma. The state of the art. Chest 1985; 87:19IS-5S.

From the Authors: We are afraid that we have difficulty comprehending Dr. Freed's concerns, as many of his comments simply do not stand up to analysis. Dr. Freed's statement that the interpretation of our data is based on an assumption that each of the subjects in our study is refractory to a second bout of exercise is untrue and appears to represent a misunderstanding of our efforts. The aim of our study is clearly stated in the last paragraph of the introduction (p. 826) and reiterated in the first paragraph of the discussion (p. 828).The word "refractory" does not appear in either place. We wanted to examine the effects of repetitive exercise on airway temperature and heat flux in asthmatics and relate that phenomenon to the changes in mechanics that developed. In no way did we predetermine how any of the dependent variables should behave. Instead, we gathered the necessary data using accepted scientific principles to assess the interrelationship among these indices. As it turns out, our subjects developed less obstruction in concert with less airway cooling and slower rewarming after the second challenge. Dr. Freed appears to have missed the point that each part of this relationship was determined prospectively and experimentally and was not based on any assumptions. The frequency with which a refractory period has been reported in the literature is irrelevant to our observations. Our data unequivocally show that the second exercise challenge produced less of a mechanical consequence than the first (figure 3). Hence, these findings speak for themselves and provide the very documentation of the existence of refractoriness that Dr. Freed requests. One only needs to look at figure 3 to see that the response to the second exercise trial differs markedly from that of the first. We are at a loss to understand how these data differ in substance from refractory periods reported in the literature (1-7). In the above context, Dr. Freed's suggestion that we biased our findings by using the wrong baseline value to make our comparisons is extremely difficult to accept. Furthermore, his comments that our subjects started the second exercise challenge with a "markedly lower" baseline FEY, is an exaggeration. Six of the seven participants had recovered to within 15% of their original baseline and one was at 20%. We would remind Dr. Freed of two phenomena. First, the data in figure 3 were purposefully displayed in absolute and not relative terms. Nothing is hidden and the reader has the opportunity of judging for him- or herself the effects of both challenges on lung function. Such an approach obviates the possibility of inadvertently misrepresenting the results by displaying percentage changes in the face of a shifting baseline. Our calculation of percentage changes in the text was for descriptive pur-

The effect of repetitive exercise on airway temperatures.

685 article and Chilvers' concern about our statistical analysis is unwarranted. JAMES H. ZAVECZ, PH.D. WILLIAM McD. ANDERSON, M.D. School of Medicin...
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