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Heat and exercise acclimation increases intracellular levels of Hsp72 and inhibits exercise-induced increase in intracellular and plasma Hsp72 in humans

机译:热和运动适应增加人体内Hsp72的细胞内水平并抑制运动引起的人体内和血浆Hsp72的增加

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摘要

In order to verify the effects of heat and exercise acclimation (HA) on resting and exercise-induced expression of plasma and leukocyte heat shock protein 72 (Hsp72) in humans, nine healthy young male volunteers (25.0 ± 0.7 years; 80.5 ± 2.0 kg; 180 ± 2 cm, mean ± SE) exercised for 60 min in a hot, dry environment (40 ± 0°C and 45 ± 0% relative humidity) for 11 days. The protocol consisted of running on a treadmill using a controlled hyperthermia technique in which the work rate was adjusted to elevate the rectal temperature by 1°C in 30 min and maintain it elevated for another 30 min. Before and after the HA, the volunteers performed a heat stress test (HST) at 50% of their individual maximal power output for 90 min in the same environment. Blood was drawn before (REST), immediately after (POST) and 1 h after (1 h POST) HST, and plasma and leukocytes were separated and stored. Subjects showed expected adaptations to HA: reduced exercise rectal and mean skin temperatures and heart rate, and augmented sweat rate and exercise tolerance. In HST1, plasma Hsp72 increased from REST to POST and then returned to resting values 1 h POST (REST: 1.11 ± 0.07, POST: 1.48 ± 0.10, 1 h POST: 1.22 ± 0.11 ng mL−1; p < 0.05). In HST2, there was no change in plasma Hsp72 (REST: 0.94 ± 0.08, POST: 1.20 ± 0.15, 1 h POST: 1.17 ± 0.16 ng mL−1; p > 0.05). HA increased resting levels of intracellular Hsp72 (HST1: 1 ± 0.02 and HST2: 4.2 ± 1.2 density units, p < 0.05). Exercise-induced increased intracellular Hsp72 expression was observed on HST1 (HST1: REST, 1 ± 0.02 vs. POST, 2.9 ± 0.9 density units, mean ± SE, p < 0.05) but was inhibited on HST2 (HST2: REST, 4.2 ± 1.2 vs. POST, 4.4 ± 1.1 density units, p > 0.05). Regression analysis showed that the lower the pre-exercise expression of intracellular Hsp72, the higher the exercise-induced increase (R = −0.85, p < 0.05). In conclusion, HA increased resting leukocyte Hsp72 levels and inhibited exercise-induced expression. This intracellular adaptation probably induces thermotolerance. In addition, the non-increase in plasma Hsp72 after HA may be related to lower stress at the cellular level in the acclimated individuals.
机译:为了验证热量和运动适应(HA)对人休息和运动诱导的血浆和白细胞热休克蛋白72(Hsp72)表达的影响,共有9名健康的年轻男性志愿者(25.0±0.7岁; 80.5±2.0 kg) ; 180±2 cm,平均值±SE)在炎热干燥的环境(40±0°C和45±0%相对湿度)中锻炼60分钟,持续11天。该协议包括使用受控热疗技术在跑步机上跑步,其中将工作速率调整为在30分钟内将直肠温度升高1°C并保持另一个30分钟的升高温度。在HA之前和之后,志愿者在相同的环境下以其最大最大输出功率的50%进行热应力测试(HST)90分钟。在HST之前(REST),之后(POST)和之后1h(1h POST)抽血,分离并保存血浆和白细胞。受试者表现出对HA的预期适应性:降低运动直肠和平均皮肤温度和心率,并提高出汗率和运动耐力。在HST1中,血浆Hsp72从REST增加到POST,然后返回到静止值1小时POST(REST:1.11±±0.07,POST:1.48±±0.10,1h POST:1.22±±0.11 ng mL -1 ; p <0.05)。在HST2中,血浆Hsp72没有变化(REST:0.94±±0.08,POST:1.20±±0.15,1h POST:1.17±±0.16 ng mL -1 ; p> 0.05)。 HA增加了细胞内Hsp72的静息水平(HST1:1±±0.02密度单位和HST2:4.2±±1.2密度单位,p <0.05)。运动诱导的细胞内Hsp72表达在HST1上观察到(HST1:REST,1±0.02 vs. POST,2.9±0.9密度单位,平均值±SE,p <0.05),但在HST2上受到抑制(HST2:REST,4.2±1.2)与POST相比,密度单位为4.4±1.1,p,> 0.05。回归分析表明,细胞内Hsp72的运动前表达越低,运动引起的增加越多(R = -0.85,p <0.05)。总之,HA可增加静息白细胞Hsp72水平并抑制运动诱导的表达。这种细胞内适应可能诱导耐热性。另外,HA后血浆Hsp72的不增加可能与适应的个体在细胞水平上的较低应激有关。

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