Muscle Cellular and Molecular Physiology (MCMP) and Applied Sport and Exercise Science (ASEP) Research Groups, Department of Sport and Exercise Sciences, Institute of Sport and Physical Activity Research (ISPAR), University of Bedfordshire, Polhill Campus, Polhill Avenue, Bedford, Bedfordshire MK41 9EA, UK.
Amino Acids. 2012 Nov;43(5):1933-44. doi: 10.1007/s00726-012-1265-3. Epub 2012 Mar 23.
HSP72 is rapidly expressed in response to a variety of stressors in vitro and in vivo (including hypoxia). This project sought a hypoxic stimulus to elicit increases in HSP72 and HSP32 in attempts to confer protection to the sub-maximal aerobic exercise-induced disturbances to redox balance. Eight healthy recreationally active male subjects were exposed to five consecutive days of once-daily hypoxia (2,980 m, 75 min). Seven days prior to the hypoxic acclimation period, subjects performed 60 min of cycling on a cycle ergometer (exercise bout 1-EXB1), and this exercise bout was repeated 1 day post-cessation of the hypoxic period (exercise bout 2-EXB2). Blood samples were taken immediately pre- and post-exercise and 1, 4 and 8 h post-exercise for HSP72 and immediately pre, post and 1 h post-exercise for HSP32, TBARS and glutathione [reduced (GSH), oxidised (GSSG) and total (TGSH)], with additional blood samples obtained immediately pre-day 1 and post-day 5 of the hypoxic acclimation period for the same indices. Monocyte-expressed HSP32 and HSP72 were analysed by flow cytometry, with measures of oxidative stress accessed by commercially available kits. There were significant increases in HSP72 (P < 0.001), HSP32 (P = 0.03), GSSG (t = 9.5, P < 0.001) and TBARS (t = 5.6, P = 0.001) in response to the 5-day hypoxic intervention, whereas no significant changes were observed for GSH (P = 0.22) and TGSH (P = 0.25). Exercise-induced significant increases in HSP72 (P < 0.001) and HSP32 (P = 0.003) post-exercise in EXB1; this response was absent for HSP72 (P ≥ 0.79) and HSP32 (P ≥ 0.99) post-EXB2. The hypoxia-mediated increased bio-available HSP32 and HSP72 and favourable alterations in glutathione redox, prior to exercise commencing in EXB2 compared to EXB1, may acquiesce the disturbances to redox balance encountered during the second physiologically identical exercise bout.
热休克蛋白 72(HSP72)在体外和体内(包括缺氧)对各种应激迅速表达。本项目试图寻找一种缺氧刺激,以增加 HSP72 和 HSP32,从而为亚最大有氧运动引起的氧化还原平衡紊乱提供保护。8 名健康的业余男性参与者接受了连续 5 天的每日一次缺氧(2980 米,75 分钟)。在缺氧适应期之前的 7 天,受试者在自行车功率计上进行 60 分钟的骑行(运动 1 次-EXB1),并且在缺氧期结束后 1 天重复该运动(运动 2 次-EXB2)。在运动前、运动后即刻和运动后 1、4 和 8 小时采集血液样本,用于 HSP72;在运动前、运动后即刻和运动后 1 小时采集血液样本,用于 HSP32、TBARS 和谷胱甘肽[还原(GSH)、氧化(GSSG)和总(TGSH)],并在缺氧适应期的第 1 天和第 5 天立即采集更多血液样本,用于检测相同的指标。通过流式细胞术分析单核细胞表达的 HSP32 和 HSP72,并使用市售试剂盒评估氧化应激指标。5 天的缺氧干预后,HSP72(P<0.001)、HSP32(P=0.03)、GSSG(t=9.5,P<0.001)和 TBARS(t=5.6,P=0.001)显著增加,而 GSH(P=0.22)和 TGSH(P=0.25)没有显著变化。EXB1 运动后 HSP72(P<0.001)和 HSP32(P=0.003)显著增加;而 EXB2 运动后 HSP72(P≥0.79)和 HSP32(P≥0.99)没有增加。与 EXB1 相比,EXB2 中运动前缺氧引起的生物可利用 HSP32 和 HSP72 增加以及谷胱甘肽氧化还原的有利变化可能会减轻第二次生理上相同的运动时遇到的氧化还原平衡紊乱。