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.
