Erschienen in:
01.01.2010 | Original Article
Systemic hypoxia promotes lymphocyte apoptosis induced by oxidative stress during moderate exercise
verfasst von:
Jong-Shyan Wang, Chia-Te Lin
Erschienen in:
European Journal of Applied Physiology
|
Ausgabe 2/2010
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Abstract
Blood undergoes oxidative stress during severe hypoxia or intense exercise. Excessive exposure to oxidative stress induces replicative senescence and apoptosis of lymphocytes. This study determines how various exercises with/without hypoxia affect lymphocyte subset mobilization and oxidative stress-induced lymphocyte apoptosis. Eighteen sedentary males randomly engaged in two normoxic exercise bouts [severe exercise (SE) (up to VO2max) and moderate-intensity exercise (ME) (50%VO2max) while exposed to 21%O2], two hypoxic exercise bouts (ME while exposed to 12%O2 and 15%O2) and two hypoxic resting conditions (resting while exposed to 12%O2 and 15%O2) in a normobaric hypoxia chamber. Under normoxic conditions, SE but not ME (1) increased the percentages of senescent (CD28− and CD57+)/activated (CD62L− and CD11a+)-form lymphocytes mobilized into the peripheral blood compartment; (2) decreased the levels of surface thiol and intracellular total (t-GSH) and reduced-form glutathione (r-GSH) of lymphocytes in blood; and (3) further enhanced the extents of H2O2-induced mitochondria trans-membrane potential diminishing, caspases 3/8/9 activation, poly(ADP-ribose) polymerase cleavage and phosphotidyl serine exposure in blood lymphocytes. However, no significant change occurred in the subset mobilization, antioxidant levels or apoptosis of lymphocytes following exposure to either 12%O2 or 15%O2. Although both 12%O2 and 15%O2 ME increased the mobilization of senescent/activated-form lymphocytes, only 12%O2 ME enhanced H2O2-induced lymphocyte thiol, t-GSH and r-GSH consumption and apoptotic responses. Therefore, we conclude that the 12%O2 exposure increases the mobilization of senescent/activated-form lymphocytes into the peripheral blood compartment and simultaneously enhances oxidative stress-induced lymphocyte apoptosis by diminishing cellular antioxidant levels during exercise.