Clonal expansion of T lymphocytes in response to antigenic stimulation is a fundamental process of adaptive immunity. As a consequence of clonal expansion, some T lymphocytes acquire a senescent phenotype, fail to replicate in response to further antigenic stimulation, and express the killer cell lectin-like receptor G1 (KLRG1) and/or CD57. Physical exercise elicits a mobilization of large numbers of T lymphocytes into the bloodstream from peripheral lymphoid compartments, but the frequency of senescent cells in the mobilized population is not known. Eight male runners (age: 29 ± 9 yr; maximal O₂uptake 62 ± 6 ml·kg⁻¹·min⁻¹) performed an intensive treadmill-running protocol at 80% maximal O₂uptake to volitional exhaustion. Blood lymphocytes isolated before, immediately after, and 1 h after exercise were assessed for cell surface expression of KLRG1, CD57, CD28, CD45RA, CD45RO, CD62L, and lymphocyte subset markers (CD3, CD4, CD8, CD56) by flow cytometry. The percentage of all CD3⁺T lymphocytes expressing KLRG1 and CD57 increased with exercise ( P < 0.01). The change in T-lymphocyte KLRG1 expression was attributed to both CD4⁺and CD8 bright T cells, with the relative change being greater for the CD8 bright population ( P < 0.01). Mobilized T-lymphocyte populations expressing KLRG1 and CD57 appeared to extravasate the peripheral blood compartment after 1 h of recovery. In conclusion, T lymphocytes with a senescent phenotype are mobilized and subsequently removed from the bloodstream in response to acute high-intensity exercise. This suggests that T lymphocytes contained within the peripheral lymphoid compartments that are mobilized by exercise are likely to be at a more advanced stage of biological aging and have a reduced capacity for clonal expansion than blood-resident T cells.

20 h after each bout. Six of the athletes completed a fourth bout. Left ventricular (LV) function was examined echocardiographically using two-dimensional M-mode, Doppler, and flow propagation velocity (Vp). Venous blood samples were analyzed for cardiac biomarkers including cardiac troponin T (cTnT). Results: Ejection fraction (EF) significantly decreased (P = 0.027) after the third exercise bout compared with baseline (mean ± SD: 56.3 ± 4.4 vs 51.3 ± 5.9%), accompanied by a nonsignificant decrease in systolic blood pressure/end systolic volume (SBP/ESV) ratio. A sustained depression in systolic function 20 h after bout 3 also persisted in the subset who completed a fourth bout, yet this did not reach clinical levels. Significant (P < 0.01) reductions in early to late diastolic filling (E:A) ratio pre-to post-bout 1 (mean ± SD: 1.9 ± 0.5 vs 1.4 ± 0.3) and pre- to post-bout 3(2.0 ± 0.5 vs 1.3 ± 0.4) normalized after each 20-h recovery period. A similar pattern of change was observed in Vp. Cardiac troponin T was elevated in four individuals 1 h after bout 1 (range: 0.013-0.125 μg·L−1) but was undetectable thereafter except in one athlete. Conclusion: Repeated bouts of prolonged exercise induce short-term reductions in diastolic filling and a cumulative decrease in systolic function, yet these alterations seem to have minimal clinical or functional impact. Elevated cTnT after the initial bout, but not thereafter, may represent an adaptive response to prolonged exercise....

Ageing is associated with an increased risk of developing noncommunicable diseases (NCDs), such as diabetes and cardiovascular disease (CVD). The increased risk can be attributable to increased prolonged exposure to oxidative stress. Often, CVD is preceded by endothelial dysfunction, which carries with it a proatherothrombotic phenotype. Endothelial senescence and reduced production and release of nitric oxide (NO) are associated with “vascular ageing” and are often accompanied by a reduced ability for the body to repair vascular damage, termed “reendothelialization.” Exercise has been repeatedly shown to confer protection against CVD and diabetes risk and incidence. Regular exercise promotes endothelial function and can prevent endothelial senescence, often through a reduction in oxidative stress. Recently, endothelial precursors, endothelial progenitor cells (EPC), have been shown to repair damaged endothelium, and reduced circulating number and/or function of these cells is associated with ageing. Exercise can modulate both number and function of these cells to promote endothelial homeostasis. In this review we look at the effects of advancing age on the endothelium and these endothelial precursors and how exercise appears to offset this “vascular ageing” process.