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Quindry, John C.; Broeder, Craig E.

Medicine & Science in Sports & Exercise: January 2004 - Volume 36 - Issue 1 - p 176
doi: 10.1249/01.MSS.0000106281.36268.4C
SPECIAL COMMUNICATIONS: Letters to the Editor-in-Chief

Department of Exercise and Sport Sciences and Physiology University of Florida Gainesville, FL

Biology Department Benedictine University Lisle, IL

Dear Editor-in-Chief:

In response to Mr. Peake’s concerns regarding our study, “The Effects of Acute Exercise on Neutrophils and Plasma Oxidative Stress,” our data provide evidence that blood oxidative stress is not significantly affected by superoxide leakage from respiring mitochondria within active skeletal muscle, as some have suggested. Further, our data include compelling evidence that neutrophilia during high-intensity exercise may impose an oxidative stress on the blood environment. Throughout the manuscript, care was taken to avoid statements of fact on this latter point. Clearly, nonneutrophilic oxidant sources cannot be ruled out as stated in our manuscript. Several discussion questions have been posed about our manuscript regarding the immune response, observed oxidative stress, and selection of references. These topics are addressed below.

Previous investigations involving nonmuscle-damaging exercise have found elevated neutrophil degranulation/demargination (7,9,11). These findings led to our investigation of high-intensity exercise-induced neutrophilia as a potential source for the commonly observed postexercise blood oxidative stress (1,7). We believe that the exercise performed in our study was insufficient to produce measurable muscle damage or evoke subsequent inflammation responses (8). Rather, the observed neutrophilia was caused by the humoral stress response to high-intensity exercise (6). Maximal-intensity exercise undoubtedly produced some cellular disruption to which primed/activated neutrophils could respond; granted this phenomenon may be below the sensitivity of current muscle damage measures. Thus, it is plausible that high-intensity exercise-induced neutrophilia may result in blood oxidative stress (7,9,11).

Explanations for the observed increase in neutrophil oxidative capacity 2 hours after maximal and high-intensity exercise are speculative. Nonetheless, several explanations were discussed including the involvement of a functionally different neutrophil subset. Incidentally, nuclear morphology was examined but was not different between time periods or trials. Future investigations could employ more specific means to identify functional characteristics of neutrophil subsets (e.g., cells capable of oxidative burst) after exercise.

Regarding our conclusion that maximal-intensity exercise resulted in an oxidative stress though lipid peroxidation markers were not changed, oxidative stress is defined as “a serious imbalance between production of ROS/RNS and antioxidant defense” (4). In light of the importance of ascorbic acid and uric acid as plasma antioxidants, significant decreases in these antioxidants do constitute an oxidative stress (3–5,10). Further, an important aspect of this investigation was integration of oxidant, antioxidant, and oxidant damage with respect to the pecking order of free radicals and antioxidants within biological fluids (2). In brief, the shift in redox balance favoring oxidants results in sequential depletion of water-soluble antioxidants and lipid-soluble antioxidants before lipid peroxidation (2,3).

Finally, the authors complied with the citation limitations of Medicine & Science in Sports & Exercise® and believe an adequate volume of pertinent research was referenced. No disrespect was intended by the omission previous and related scientific works, nor should it be implied—as an exhaustive survey of the scientific literature was not our aim. Moreover, study design, implementation, and manuscript preparation/submission spanned several years making inclusion of several citations highlighted by Mr. Peake impossible.

John C. Quindry

Craig E. Broeder

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