Exercise-induced oxidative DNA damage and lymphocytopenia in sedentary young males.

UNLABELLED

Post high-intensity exercise lymphocytopenia is well documented, but its underlying mechanisms have not been fully elucidated. A possible mechanism is a reactive oxygen species-induced DNA damage after high-intensity exercise. Furthermore, lymphocyte apoptosis related to DNA damage might contribute to exercise-induced lymphocytopenia.

PURPOSE

This study examined lymphocytopenia, lymphocyte oxidative DNA damage, and apoptosis in young healthy sedentary males after acute high-intensity exercise.

METHOD

Fifteen subjects exercised on bicycle ergometers for 1 h at 75% of their VO2max. Venous blood samples were taken before exercise (PRE) and hourly after exercise until 4 h (P0-P4). Lymphocyte counts, oxidative DNA damage evaluated using the Comet assay with human 8-oxoguanine DNA glycosylase, and serum lipid peroxide (LPO) concentration were measured. Furthermore, lymphocyte superoxide, Fas receptor (CD95), and Annexin-V-positive lymphocyte apoptosis cells were measured in 10 subjects who exercised and gave blood samples as described above.

RESULTS

Lymphocyte counts became significantly lower than the PRE value (P < 0.05): 20.4% at P1, 24.3% at P2, and 16.3% at P3. Moreover, LPO significantly increased by P2 (P < 0.05): 1.6-fold. The % DNA in tail, indicating oxidative DNA damage, was significantly higher at P3 (54.3 +/- 12.8%) than at PRE (42.6 +/- 11.1%, P < 0.05). The lymphocyte superoxide level was significantly higher (51.3%) than the PRE value (P < 0.05). Neither CD95 nor Annexin-V-positive cells were significantly different than the PRE value.

CONCLUSION

Results of this study suggest that lymphocyte oxidative DNA damage can relate to lymphocytopenia, although DNA damage was not associated with apoptosis in healthy young sedentary males.