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 V˙O2max. 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.