Hypoxic exercise training reduces senescent T-lymphocyte subsets in blood

The integration and control of systemic immune responses depends on the regulated trafficking of T-lymphocytes. This study elucidates how various exercises regimens with/without hypoxia affect phenotypic characteristics of T-lymphocyte subsets in blood. Fifty sedentary males were randomly divided into five groups. Each group (n=10) received one of five interventions: normoxic (21%O₂) resting (N-C), hypoxic (15%O₂) resting (H-C), normoxic exercise (50%W_max under 21%O₂, N-T), hypoxic-relative exercise (50% maximal heart rate reserve under 15%O₂, H-RT), or hypoxic-absolute exercise (50%W_max under 15%O₂, H-AT) for 30min/day, 5days/week for 4weeks. Before the intervention, strenuous exercise up to exhaustion increased the mobilization of CD3, CD4, CD8, or CD8^bright lymphocytes expressing activated (CD11a) or senescent (KLRG1) molecules into the peripheral blood compartment. The H-AT for 4weeks up-regulated co-stimulatory molecule CD28 expression and was accompanied by depressed KLRG1 level on CD3, CD4, CD8, or CD8^bright lymphocytes at rest or following exercise. Simultaneously, this intervention increased interferon-γ (IFN-γ) level and unchanged interleukin-4 level, as well as, decreased myeloperoxidase (MPO) and interleukin-6 levels in plasma. However, no significant changes in resting and exercise-induced mobilizations of various T-lymphocyte subsets and productions of cytokines and MPO occurred following the N-C, H-C, N-T, and H-RT interventions. Therefore, we conclude that 4-week H-AT intervention reduced senescent T-lymphocyte subsets with increasing IFN-γ level in blood, which responses are accompanied by depressed oxidative stress and pro-inflammatory cytokine production. These findings can help to determine an effective hypoxic exercise regimen to minimize immune dysfunction by retarding T-lymphocyte senescence.