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Eleven days of moderate exercise and heat exposure induces acclimation without significant HSP70 and apoptosis responses of lymphocytes in college-aged males

机译:适度运动和热暴露的11天诱导了适应,而没有显着的HSP70显着增加,并且年龄大的男性没有淋巴细胞的凋亡反应

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The purpose of this study was to assess whether a lymphocyte heat shock response and altered heat tolerance to ex vivo heat shock is evident during acclimation. We aimed to use flow cytometry to assess the CD3+CD4+ T lymphocyte cell subset. We further aimed to induce acclimation using moderately stressful daily exercise-heat exposures to achieve acclimation. Eleven healthy males underwent 11?days of heat acclimation. Subjects walked for 90?min (50?±?8% VO2max) on a treadmill (3.5?mph, 5% grade), in an environmental chamber (33°C, 30–50% relative humidity). Rectal temperature (°C), heart rate (in beats per minute), rating of perceived exertion , thermal ratings, hydration state, and sweat rate were measured during exercise and recovery. On days?1, 4, 7, 10, and 11, peripheral blood mononuclear cells were isolated from pre- and post-exercise blood samples. Intracellular and surface HSP70 (SPA-820PE, Stressgen, Assay Designs), and annexin V (ab14085, Abcam Inc.), as a marker of early apoptosis, were measured on CD3+ and CD4+ (sc-70624, sc-70670, Santa Cruz Biotechnology) gated lymphocytes. On day?10, subjects experienced 28?h of sleep loss. Heat acclimation was verified with decreased post-exercise rectal temperature, heart rate, and increased sweat rate on day?11, versus day?1. Heat acclimation was achieved in the absence of significant changes in intracellular HSP70 mean fluorescence intensity and percent of HSP70+ lymphocytes during acclimation. Furthermore, there was no increased cellular heat tolerance during secondary ex vivo heat shock of the lymphocytes acquired from subjects during acclimation. There was no effect of a mild sleep loss on any variable. We conclude that our protocol successfully induced physiological acclimation without induction of cellular heat shock responses in lymphocytes and that added mild sleep loss is not sufficient to induce a heat shock response.
机译:这项研究的目的是评估在适应过程中淋巴细胞热休克反应和对体外热休克的耐热性是否改变。我们旨在使用流式细胞仪评估CD3 + CD4 + T淋巴细胞亚群。我们进一步的目标是使用中等压力的日常运动-热量暴露来诱导适应,以实现适应。 11名健康男性接受了11天的热适应。在环境室(33°C,相对湿度30–50%)中,受试者在跑步机(3.5英里每小时,5%坡度)上行走90分钟(50 VO±8%VO2max)。在运动和恢复期间,测量了直肠温度(°C),心率(每分钟心跳数),感觉到的劳累等级,热等级,水合状态和出汗率。在第1、4、7、10和11天,从运动前和运动后的血液样本中分离出外周血单核细胞。在CD3 +和CD4 +(sc-70624,sc-70670,Santa Cruz)上测定了细胞内和表面HSP70(SPA-820PE,Stressgen,Assay Designs)和膜联蛋白V(ab14085,Abcam Inc.)作为早期凋亡的标志物生物技术)门控淋巴细胞。在第10天,受试者经历了28小时的睡眠丧失。与第1天相比,第11天的运动后直肠温度,心率降低和出汗率增加证实了热适应。在驯化过程中,细胞内HSP70平均荧光强度和HSP70 +淋巴细胞百分比没有明显变化的情况下实现了热适应。此外,在适应过程中从受试者获得的淋巴细胞的二次离体热休克期间,细胞耐热性没有增加。轻度失眠对任何变量均无影响。我们得出的结论是,我们的方案成功诱导了生理适应,却没有诱导淋巴细胞中的细胞热休克反应,并且增加的轻度睡眠不足不足以诱导热休克反应。

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