Chen H W, Chen S C, Tsai J L, Yang R C
Department of Physiology, Graduate Institute of Medicine, Kaohsiung Medical University, Republic of China.
Kaohsiung J Med Sci. 1999 Oct;15(10):572-80.
The study was designed to investigate the role of hyperthermia in the tolerance of exercise in rats and the possible mechanism was examined. The hyperthermic pretreatment was performed using an electric pad on the anesthesized rats 24 hours before exercise. Rats were exercised passively in a motor-controlled round treadmill in high temperature environment (36-37 degrees C) until exhaustion. The capacity of tolerance was calculated. Lymphocytes and gastrocnemius muscle were collected from both groups. The changes in muscular morphology, mitochondria oxidative enzyme activity and induction of Hsp72 were investigated. The results revealed that experimental rats were more tolerant to exercise at high temperature than the control group; the duration time were 89 +/- 17.8 min and 63.1 +/- 7.3 min, respectively. Hsp72 was induced markedly in the experimental group, both in muscle and lymphocytes, indicating a heat shock response. There was no significant change in morphology of the mitochondria, 24 hours after hyperthermic treatment, as shown by histopathological and electromicroscopic investigation. However, the activity of mitochondrial enzymes increased significantly in experimental group before exercise: 84.6 +/- 6.3 and 345 +/- 15.4 (nmole cytochrome c/min/mg total protein) respectively of NADH-cytochome c reductase and succinate-cytochome c reductase activity in experimental group compared to 58.9 +/- 4.7 and 269.0 +/- 24.0 in control group (p < 0.05, by student t-test). It is concluded that hyperthermic treatment enhances muscular mitochondrial oxidative enzyme activity in rats, and results in increasing tolerance to exercise at high temperature. The heat shock response, most probably the inducible Hsp72, is a crucial factor in this effect.
本研究旨在探讨热疗在大鼠运动耐力中的作用，并对其可能的机制进行研究。在运动前24小时，使用电垫对麻醉后的大鼠进行热预处理。大鼠在高温环境（36 - 37摄氏度）下于电动控制的圆形跑步机上被动运动直至疲惫。计算耐受能力。收集两组的淋巴细胞和腓肠肌。研究肌肉形态、线粒体氧化酶活性的变化以及Hsp72的诱导情况。结果显示，实验组大鼠在高温下比对照组更耐受运动；持续时间分别为89±17.8分钟和63.1±7.3分钟。实验组肌肉和淋巴细胞中Hsp72均显著诱导，表明存在热休克反应。组织病理学和电子显微镜检查显示，热疗24小时后线粒体形态无显著变化。然而，实验组运动前线粒体酶活性显著增加：实验组NADH - 细胞色素c还原酶和琥珀酸 - 细胞色素c还原酶活性分别为84.6±6.3和345±15.4（纳米摩尔细胞色素c/分钟/毫克总蛋白），而对照组为58.9±4.7和269.0±24.0（学生t检验，p < 0.05）。结论是，热疗可增强大鼠肌肉线粒体氧化酶活性，并导致对高温运动的耐受性增加。热休克反应，很可能是可诱导的Hsp72，是此效应的关键因素。
