Holbrook Alexander K, Peterson Hunter D, Bianchi Samantha A, Macdonald Brad W, Bredahl Eric C, Belshan Michael, Siedlik Jacob A
Department of Medical Microbiology and Immunology, Creighton University, Omaha, Nebraska.
Department of Exercise Science and Pre-Health Professions, Creighton University, Omaha, Nebraska.
Physiol Rep. 2019 Sep;7(18):e14234. doi: 10.14814/phy2.14234.
Early studies in exercise immunology suggested acute bouts of exercise had an immunosuppressive effect in human subjects. However, recent data, show acute bouts of combined aerobic and resistance training increase both lymphocyte activation and proliferation. We quantified resistance exercise-induced changes in the activation state of CD4 T lymphocytes via surface protein expression and using a medically relevant model of infection (HIV-1). Using a randomized cross-over design, 10 untrained subjects completed a control and exercise session. The control session consisted of 30-min seated rest while the exercise session entailed 3 sets × 10 repetitions of back squat, leg press, and leg extensions at 70% 1-RM with 2-min rest between each set. Venous blood samples were obtained pre/post each session. CD4 T lymphocytes were isolated from whole blood by negative selection. Expression of activation markers (CD69 & CD25) in both nonstimulated and stimulated (costimulation through CD3 CD28) cells were assessed by flow cytometry. Resistance exercised-induced effects on intracellular activation was further evaluated via in vitro infection with HIV-1. Nonstimulated CD4 T lymphocytes obtained postexercise exhibited elevated CD25 expression following 24 h in culture. Enhanced HIV-1 replication was observed in cells obtained postexercise. Our results demonstrate that an acute bout of resistance exercise increases the activation state of CD4 T lymphocytes and results in a greater susceptibility to HIV-1 infection in vitro. These findings offer further evidence that exercise induces activation of T lymphocytes and provides a foundation for the use of medically relevant pathogens as indirect measures of intracellular activation.
运动免疫学的早期研究表明,急性运动发作对人体受试者具有免疫抑制作用。然而,最近的数据显示,急性有氧和阻力联合训练会增加淋巴细胞的激活和增殖。我们通过表面蛋白表达并使用医学相关的感染模型(HIV-1),对阻力运动引起的CD4 T淋巴细胞激活状态变化进行了量化。采用随机交叉设计,10名未经训练的受试者完成了一次对照和一次运动训练。对照训练包括30分钟的坐姿休息,而运动训练则包括3组,每组10次的后深蹲、腿举和腿伸展,强度为1-RM的70%,每组之间休息2分钟。在每次训练前后采集静脉血样。通过阴性选择从全血中分离出CD4 T淋巴细胞。通过流式细胞术评估未刺激和刺激(通过CD3 CD28共刺激)细胞中激活标志物(CD69和CD25)的表达。通过体外感染HIV-1进一步评估阻力运动对细胞内激活的影响。运动后获得的未刺激CD4 T淋巴细胞在培养24小时后显示CD25表达升高。在运动后获得的细胞中观察到HIV-1复制增强。我们的结果表明,急性阻力运动发作会增加CD4 T淋巴细胞的激活状态,并导致其在体外对HIV-1感染的易感性增加。这些发现提供了进一步的证据,证明运动可诱导T淋巴细胞激活,并为使用医学相关病原体作为细胞内激活的间接测量方法提供了基础。