Morton J P, Maclaren D P M, Cable N T, Campbell I T, Evans L, Bongers T, Griffiths R D, Kayani A C, McArdle A, Drust B
Research Institute for Sport and Exercise Sciences, Liverpool John Moores University, Liverpool, UK.
Acta Physiol (Oxf). 2007 Aug;190(4):319-27. doi: 10.1111/j.1748-1716.2007.01711.x. Epub 2007 May 3.
Exercise-associated hyperthermia is routinely cited as the signal responsible for inducing an increased production of heat shock proteins (HSPs) following exercise. This hypothesis, however, has not been tested in human skeletal muscle. The aim of the present study was to therefore investigate the role of increased muscle and core temperature in contributing to the exercise-induced production of the major HSP families in human skeletal muscle.
Seven physically active males underwent a passive heating protocol of 1 h duration during which the temperature of the core and vastus lateralis muscle were increased to similar levels to those typically occurring during moderately demanding aerobic exercise protocols. One limb was immersed in a tank containing water maintained at approximately 45 degrees C whilst the contra-lateral limb remained outside the tank and was not exposed to heat stress. Muscle biopsies were obtained from the vastus lateralis of both legs immediately prior to and at 48 h and 7 days post-heating.
The heating protocol induced significant increases (P < 0.05) in rectal (1.5 +/- 0.2 degrees C) and muscle temperature of the heated leg (3.6 +/- 0.5 degrees C). Muscle temperature of the non-heated limb showed no significant change (P > 0.05) following heating (pre: 36.1 +/- 0.5, post: 35.7 +/- 0.2 degrees C). Heating failed to induce a significant increase (P > 0.05) in muscle content of HSP70, HSC70, HSP60, HSP27, alphaB-crystallin, MnSOD protein content or in the activity of superoxide dismutase and catalase.
These data demonstrate that increases in both systemic and local muscle temperature per se do not appear to mediate the exercise-induced production of HSPs in human skeletal muscle and suggest that non-heat stress factors associated with contractile activity are of more importance in mediating this response.
运动相关体温过高通常被认为是运动后诱导热休克蛋白（HSPs）产生增加的信号。然而，这一假设尚未在人体骨骼肌中得到验证。因此，本研究的目的是探讨肌肉和核心体温升高在人体骨骼肌运动诱导主要HSP家族产生过程中的作用。
七名体力活跃的男性接受了为期1小时的被动加热方案，在此期间，核心体温和股外侧肌温度升高至与中等强度有氧运动方案中通常出现的水平相似。将一条腿浸入盛有保持在约45摄氏度水的水箱中，而对侧腿留在水箱外，不暴露于热应激。在加热前、加热后48小时和7天，从双腿的股外侧肌获取肌肉活检样本。
加热方案使直肠温度（1.5±0.2摄氏度）和受热腿的肌肉温度（3.6±0.5摄氏度）显著升高（P<0.05）。加热后，未受热肢体的肌肉温度无显著变化（P>0.05）（加热前：36.1±0.5，加热后：35.7±0.2摄氏度）。加热未能使HSP70、HSC70、HSP60、HSP27、αB-晶状体蛋白、MnSOD蛋白含量的肌肉含量或超氧化物歧化酶和过氧化氢酶的活性显著增加（P>0.05）。
这些数据表明，全身和局部肌肉温度的升高本身似乎并不能介导人体骨骼肌运动诱导的HSPs产生，并表明与收缩活动相关的非热应激因素在介导这一反应中更为重要。
