Introduction/Purpose: The effect of a triathlon competition on death of neutrophils from elite athletes was investigated.
Methods: Blood was collected from 11 sedentary volunteers and 12 triathletes under rest and after a Half Ironman triathlon competition (2-km swimming, 80-km cycling, and 20-km running).
Results: The triathlon competition increased DNA fragmentation, phosphatidylserine externalization, and reactive oxygen species production in neutrophils when compared to the results at rest. The proportion of neutrophils with mitochondrial transmembrane depolarization was increased in the triathletes at rest and after competition as compared with sedentary volunteers. Plasma levels of thiobarbituric acid reactive substances were increased in triathletes after competition. Expression of bcl-xL (antiapoptotic) was decreased and that of bax (proapoptotic) was increased, whereas intracellular neutral lipid content was lowered in neutrophils after the triathlon. A positive correlation was found between the proportion of neutrophils with DNA fragmentation and the plasma free fatty acid levels (r = 0.688, P< 0.05), which was elevated by threefold after competition. Plasma levels of oleic, linoleic, and stearic acids were increased in triathletes after the competition when compared with sedentary volunteers. The plasma concentration of these three fatty acids, measured after the triathlon competition, was toxic for 3-h cultured neutrophils obtained from sedentary volunteers. The maximal tolerable (nontoxic) concentration of the fatty acids by 3-h cultured neutrophils was 100 μmol·L−1 for oleic and linoleic acids and 200μmol·L−1 for stearic acid.
Conclusion: The triathlon competition induced neutrophil death possibly by apoptosis as indicated by DNA fragmentation and phosphatidylserine externalization. The increase in plasma levels of oleic, linoleic, and stearic acids induced by the competition may be involved in the neutrophil death observed possibly by increasing the production of reactive oxygen species andby decreasing the accumulation of intracellular neutral lipid.
1Department of Physiology and Biophysics, Institute of Biomedical Sciences, University of São Paulo, BRAZIL; 2Farmoterapica, São Paulo, BRAZIL; and 3Post-Graduate Program in Physical Education, Biological Sciences and Health Center, Cruzeiro do Sul University, São Paulo, BRAZIL
Address for correspondence: Adriana Cristina Levada-Pires, Ph.D., Department of Physiology and Biophysics, Institute of Biomedical Sciences, Av. Prof Lineu Prestes, 1524, CEP 05508-900, University of São Paulo, SP, Brazil; E-mail: email@example.com.
Submitted for publication October 2007.
Accepted for publication February 2008.