Kregel K C, Moseley P L
Department of Exercise Science, University of Iowa, Iowa City 52242, USA.
J Appl Physiol (1985). 1996 Feb;80(2):547-51. doi: 10.1152/jappl.1996.80.2.547.
Previous reports have suggested that the heat shock response to passive heating may be blunted by aging. However, during exertional heating, factors in addition to elevated temperature may amplify the degree of stress compared with hyperthermia alone. The purpose of this study was to compare the pattern of accumulation of the highly inducible 72-kDa heat shock protein (HSP72) in liver tissue of mature (12-mo-old) and senescent (24-mo-old) male Fischer 344 rats after either passive or exertional heat stress. A euthermic control group was exposed to an ambient temperature (Ta) of 25 degrees C for 4.5 h. A passive heating (heat) group was exposed to an Ta of 42 degrees C until colonic temperature (Tco) reached 41 degrees C. An exertional heating (exercise) group performed intermittent moderate-intensity treadmill exercise (similar absolute intensities for the two age groups) at an Ta of 32 degrees C until Tco reached 41 degrees C. Heating rates were similar in the heat and exercise groups (approximately 0.08 degrees C/min). Rats in both the heat and exercise groups were maintained at a Tco of 41 degrees C for an additional 30 min and subsequently returned to an Ta of 25 degrees C for 3 h. Liver HSP72 accumulation was increased in mature rats after both the heat (+192% vs. control) and exercise (+292%) protocols. In contrast, the senescent rats demonstrated no significant increase in inducible HSP70 with heating but a large increase with exercise (+232%; P < 0.01 compared with control and heat groups). These data suggest that the blunted heat shock protein response to heating observed with aging is not a result of the inability to produce inducible HSP72 because older rats had an robust response to exertional hyperthermia.
先前的报告表明，衰老可能会削弱对被动加热的热休克反应。然而，在运动性加热过程中，与单纯热疗相比，除温度升高外的其他因素可能会加剧应激程度。本研究的目的是比较成熟（12月龄）和衰老（24月龄）雄性Fischer 344大鼠在被动或运动性热应激后肝脏组织中高度可诱导的72 kDa热休克蛋白（HSP72）的积累模式。一个体温正常的对照组在25摄氏度的环境温度（Ta）下暴露4.5小时。一个被动加热（热）组暴露于42摄氏度的Ta下，直到结肠温度（Tco）达到41摄氏度。一个运动性加热（运动）组在32摄氏度的Ta下进行间歇性中等强度跑步机运动（两个年龄组的绝对强度相似），直到Tco达到41摄氏度。热组和运动组的加热速率相似（约0.08摄氏度/分钟）。热组和运动组的大鼠在Tco为41摄氏度的情况下再维持30分钟，随后回到25摄氏度的Ta下3小时。在热（与对照组相比增加192%）和运动（增加292%）方案后，成熟大鼠肝脏中的HSP72积累增加。相比之下，衰老大鼠在加热时可诱导的HSP70没有显著增加，但在运动时大幅增加（增加232%；与对照组和热组相比，P<0.01）。这些数据表明，衰老时观察到的对加热的热休克蛋白反应减弱并非由于无法产生可诱导的HSP72，因为老年大鼠对运动性热疗有强烈反应。
