title: Systemic hypoxia promotes lymphocyte apoptosis induced by oxidative stress during moderate exercise.
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 VO(2max)) and moderate-intensity exercise (ME) (50%VO(2max)) while exposed to 21%O(2)], two hypoxic exercise bouts (ME while exposed to 12%O(2) and 15%O(2)) and two hypoxic resting conditions (resting while exposed to 12%O(2) and 15%O(2)) 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 H(2)O(2)-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%O(2) or 15%O(2). Although both 12%O(2) and 15%O(2) ME increased the mobilization of senescent/activated-form lymphocytes, only 12%O(2) ME enhanced H(2)O(2)-induced lymphocyte thiol, t-GSH and r-GSH consumption and apoptotic responses. Therefore, we conclude that the 12%O(2) 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.
authors.affiliation: Graduate Institute of Rehabilitation Science, Center for Healthy Aging Research, Chang Gung University, 259 Wen-Hwa 1st Road, Kwei-Shan, Tao-Yuan, 333, Taiwan. s5492@mail.cgu.edu.tw
authors.forename: Jong-Shyan
authors.initials: JS
authors.lastname: Wang
authors.forename: Chia-Te
authors.initials: CT
authors.lastname: Lin
mesh_terms: D000975:Antioxidants / Q000378:metabolism; D017209:Apoptosis / Q000502:physiology*; D053148:Caspase 3 / Q000378:metabolism; D005978:Glutathione / Q000097:blood / Q000378:metabolism; D006801:Humans; D000860:Hypoxia / Q000276:immunology* / Q000378:metabolism; D008214:Lymphocytes / Q000378:metabolism*; D008297:Male; D018384:Oxidative Stress / Q000502:physiology*; D010641:Phenotype; D011065:Poly(ADP-ribose) Polymerases / Q000378:metabolism; D055815:Young Adult
chemical_list: D000975:Antioxidants; D011065:Poly(ADP-ribose) Polymerases; D053148:Caspase 3; D005978:Glutathione