Aerobically trained older adults show impaired resting, but preserved exercise-induced circulating progenitor cell count, which was not improved by sprint interval training

接受过有氧训练的老年人静息状态下循环祖细胞数量受损,但运动诱导的循环祖细胞数量得以保留,而短跑间歇训练并未改善这一状况。

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Abstract

Older adults exhibit a reduced number and function of CD34 + circulating progenitor cells (CPC), a known risk factor for cardiovascular disease. Exercise promotes the mobilisation of CPCs from bone marrow, so whether ageing per se or physical inactivity in older age reduces CPCs is unknown. Thus, this study examined the effect of age on resting and exercise-induced changes in CPCs in aerobically trained adults and the effect of 8 weeks of sprint interval training (SIT) on resting and exercise-induced CPCs in older adults. Twelve young (22-34 years) and nine older (63-70 years) adults participated in the study. Blood was sampled pre and immediately post a graded exercise test to exhaustion in both groups. Older participants repeated the process after 8 weeks of SIT (3 × 20 s 'all-out' sprints, 2 × a week). Total CPCs (CD34(+)) and endothelial progenitor cells (EPCs: CD34(+)KDR(+)) were determined by flow cytometry. Older adults exhibited lower basal total CD34(+) CPCs (828 ± 314 vs. 1186 ± 272 cells·mL(-1), p = 0.0149) and CD34(+)KDR(+) EPCs (177 ± 128 vs. 335 ± 92 cells·mL(-1), p = 0.007) than younger adults. The maximal exercise test increased CPCs in young (CD34(+): p = 0.004; CD34(+)KDR(+): p = 0.017) and older adults (CD34(+): p < 0.001; CD34(+)KDR(+): p = 0.008), without difference between groups (p = 0.211). SIT did not alter resting or exercise-induced changes in CPCs in the older cohort (p > 0.232). This study suggests age per se does not impair exercise-induced CPC counts, but does lower resting CPC counts.

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