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.
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T cells expressing CD57 and KLRG1 are more susceptible to H2O2-induced apoptosis than total lymphocytes and naive phenotype cells in vitro.
“T cells expressing cell-surface proteins associated with differentiation or “senescence” (e.g., CD57 and KLRG1) are more susceptible to H2O2 induced apoptosis than total lymphocytes (Wang and Lin 2010) and cells of a naïve phenotype (e.g., CD45RA + CCR7+) in vitro (Takahashi et al. 2005).”
From Is immunosenescence influenced by our lifetime “dose” of exercise? (2016) · cites this paper as Wang and Lin 2010
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- Authors
- Wang, J.-S., & Lin, C.-T.
- Affiliations
- Chang Gung University (TW)
- Corresponding author
- Wang, Jong-Shyan
- ORCID
- Wang, Jong-Shyan
- Venue
- European Journal of Applied Physiology
- Published
- 2009-10-09
- Volume
- 108
- Issue
- 2
- Pages
- 371-382
- ISSN
- 0020-9376 (ISSN-L)
- 1439-6319
- 1439-6327
- OpenAlex
- W2037197191
- Cited by
- 29
- References
- 36
- Citations by year
- 2025: 1 · 2024: 3 · 2021: 2 · 2020: 1 · 2018: 3 · 2017: 2 · 2016: 2 · 2015: 3 · 2014: 1 · 2013: 4 · 2012: 2
- FWCI
- 2.38
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- European Journal of Applied Physiology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Science Council
- Topics
- Health Sciences › Medicine › Rehabilitation › Exercise and Physiological Responses
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › High Altitude and Hypoxia
- Health Sciences › Medicine › Complementary and alternative medicine › Cardiovascular and exercise physiology
- Keywords
- systemic hypoxia, lymphocyte apoptosis, oxidative stress, moderate-intensity exercise, lymphocyte mobilization, replicative senescence, glutathione, hydrogen peroxide, mitochondrial membrane potential, caspase activation, poly(ADP-ribose) polymerase, phosphatidylserine exposure, CD57, L-selectin, CD11a, CD28
- MeSH terms
- Hypoxia, Antioxidants, Glutathione, Humans, Lymphocytes, Male, Phenotype, Poly(ADP-ribose) Polymerases, Apoptosis, Oxidative Stress, Caspase 3, Young Adult
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