Repeated high-intensity Wingate cycle bouts influence markers of lymphocyte migration but not apoptosis
Repeated high-intensity Wingate cycle bouts influence markers of lymphocyte migration but not apoptosis
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DOI：
10.1139/h11-156
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发表时间：
2012-04-01
期刊：
影响因子：
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通讯作者：
Schafer, Mark A.
中科院分区：
文献类型：
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作者：
Friedman, Rachel A.;Navalta, James W.;Schafer, Mark A.
研究表明，在持续运动中淋巴细胞发生了显著变化，但很少有研究表明反复高强度运动的影响。本研究旨在检验反复间歇性发作对淋巴细胞亚群细胞计数、凋亡和迁移的影响。参与者（N = 8）在指定的恢复期（运动后过量耗氧量（EPOC））之前、之后和之后进行了一系列6次Wingate厌氧循环试验，以观察淋巴细胞的变化。评估淋巴细胞亚群（CD4+, CD4/CD45RA+, CD8+, CD8+/CD45RA+, CD19+）的凋亡（膜联蛋白V+）和细胞迁移（CX(3)CR1）。我们的研究结果表明，CD8+和CD8+/CD45RA+亚群受到重复Wingate循环方案的显著影响，细胞计数随着运动而增加，然后在EPOC终止时减少（p = 0.016）。运动后CD8+和CD8+/CD45RA+细胞的减少伴随着CX3CR1细胞迁移受体的显著变化（p = 0.019），但不伴有凋亡（p = 0.87）。这表明，在重复的高强度循环中，CD8+细胞的反应可能是由于细胞迁移而不是细胞死亡。
Studies have shown significant changes in lymphocytes during continuous exercise, but little has been shown on the effect of repeated high intensity bouts. This study was designed to examine the effect of repeated intermittent bouts on lymphocyte subset cell count, apoptosis, and migration. A series of 6 Wingate anaerobic cycle tests were performed by participants (N = 8) with blood samples attained before, immediately following, and after a designated recovery period (excess postexercise oxygen consumption (EPOC)) to observe lymphocyte changes. Lymphocyte subsets (CD4+, CD4/CD45RA+, CD8+, CD8+/CD45RA+, CD19+) were assessed for apoptosis (annexin V+) and cellular migration (CX(3)CR1). Our results indicate that the CD8+ and CD8+/CD45RA+ subsets were significantly influenced by the repetitive Wingate cycling protocol such that cell counts increased with exercise, and then decreased at EPOC termination (p = 0.016). The observed postexercise decrease in CD8+ and CD8+/CD45RA+ cells was accompanied by a significant change in the CX3CR1 cell migration receptor (p = 0.019), but not apoptosis (p = 0.87). This indicates that with repetitive high-intensity cycling, the response in CD8+ cells following the bout is likely due to cell migration rather than cell death.