SPECIAL COMMUNICATIONS: Letters to the Editor-in-Chief
I would like to generate some discussion on an article (7) that was recently published in the journal. I would like to pose the following questions regarding the rationale, results, and conclusions drawn in this study.
- Why should superoxide production by neutrophils and the inflammatory responses to muscle damage contribute to a substantial increase in overall oxidative stress within the body? Others have addressed this question with inconclusive findings (2–5). This previous work was not mentioned.
- Why should neutrophil activation increase at higher exercise intensities?
- Can the authors explain their conclusion that the exercise used in their study caused oxidative stress, when there was apparently no change in the plasma concentration of either malondialdehyde or lipid hydroperoxides?
- There was a small decline in the plasma concentration of ascorbic acid and uric acid after exercise. What significance do the authors attach to these responses? Other groups have also demonstrated changes in plasma ascorbic acid concentration in the absence of any alteration in markers of oxidative stress (1,5,8,9). Once again, this previous work was not mentioned.
- How can the mere presence of increased numbers of neutrophils in the circulation contribute to exercise-induced oxidative stress, if they are not activated?
- What mechanisms can the authors provide to account for the increase in the production of superoxide by neutrophils increased after exercise? Was it due to the presence of immature band neutrophils, which were measured, but not mentioned in the results? Why was there no change in plasma myeloperoxidase concentration, which is contrary to all previous work (6)?
Overall, I believe that a considerable amount of pertinent previous literature was overlooked, both before the beginning of the study, and also in the discussion. Had this literature been adequately reviewed before data collection, different research hypotheses may have been formulated, a better experimental design might have been implemented, and a more detailed and accurate discussion could have been generated.
1. Bergholm, R., S. Makimatilla, M. Valkonen, et al. Intense physical training decreases circulating antioxidants and endothelium-dependent vasodilatation in vivo. Atherosclerosis 145: 341–349, 1999.
2. Cannon, J. C., S. F. Orencole, R. A. Fielding, et al. Acute phase response in exercise: interaction of age and vitamin E on neutrophils and muscle enzyme release. Am J Physiol. 259: R1214–R1219, 1990.
3. König, D., K.-H. Wagner, I. Elmadfa, and A. Berg. Exercise and oxidative stress: significance of antioxidants with reference to inflammatory, muscular, and systemic stress. Exerc. Immunol. Rev. 7: 108–133, 2001.
4. Nieman, D. C., D. A. Henson, S. R. Mcanulty, et al. Influence of vitamin C supplementation on oxidative changes after an ultramarathon. J. Appl. Physiol. 92: 1970–1977, 2002.
5. Nieman, D. C., D. A. Henson, D. E. Butterworth, et al. Vitamin C does not alter the immune response to 2.5 hours of running. Int. J. Sports Nutr. 7: 173–184, 1997.
6. Peake, J. M. Exercise-induced alteration in neutrophil degranulation and respiratory burst activity: possible mechanisms of action Exerc. Immunol. Rev. 8: 49–100, 2002.
7. Quindry, J. C., W. L. Stone, J. King, and C. E. Broeder. The effects of acute exercise on neutrophils and plasma oxidative stress. Med. Sci. Sports Exerc. 35: 1139–1145, 2003.
8. Schroder, H., E. Navarro, A. Tramullas, et al. Nutrition antioxidant status and oxidative stress in professional basketball players: effects of a three compound antioxidative supplement. Int. J. Sports Med. 21: 146–500, 2000.
9. Viguie, C., B. Frei, M. K. Shigenega, et al. Antioxidant status and indexes of oxidative stress during consecutive days of exercise. J. Appl. Physiol. 75: 566–572, 1993.