Exercise, Health and Performance Research Group, Faculty of Health Science, University of Sydney, Sydney, Australia.
Eur J Appl Physiol. 2011 Nov;111(11):2813-21. doi: 10.1007/s00421-011-1913-4. Epub 2011 Mar 18.
Eccentric exercise can lead to muscle damage including dramatic changes to mitochondrial calcium content (MCC) and impaired respiratory function. Heat acclimation can create a cross-tolerance to a number of stresses including eccentric exercise but little is known about any protection to mitochondria. We hypothesised that intermittent heat exposure will lead to improved control of MCC and to preserved mitochondrial function following eccentric exercise. Sprague-Dawley rats were exposed to 3 weeks of intermittent heat exposure (36°C, 40% relative humidity, 6 h/day, 5 days a week) or kept in cool conditions (20°C). Animals were then assigned to a control or exercise group (-14°C decline treadmill exercise for 90 min). MCC, mitochondrial respiration and mitochondrial permeability transition pore opening (mPTP) were measured in mitochondria isolated from the red quadriceps in animals killed immediately, 2 h and 48 h post-exercise. Results showed that heat exposure was associated with lower plasma creatine kinase levels (p < 0.05) post-exercise suggesting lower levels of muscle damage. There was a significant (~500%) rise in MCC (p < 0.001) and a reduction in mitochondrial respiratory control ratio (p < 0.001) 48 h post-exercise. mPTP displayed increased (p < 0.05) sensitivity to calcium immediately and 48 h post-exercise. Thus, decline running led to significant impairment of mitochondria respiration and calcium loading which was more pronounced 48 h post-exercise compared with earlier time points. MCC levels and mitochondrial function were not altered by heat exposure. In conclusion, intermittent heat exposure does not appear to provide protection against mitochondrial dysfunction resulting from eccentric exercise.
离心运动可导致肌肉损伤，包括线粒体钙含量（MCC）的显著变化和呼吸功能受损。热适应可以产生对多种应激的交叉耐受，包括离心运动，但对线粒体的任何保护作用知之甚少。我们假设间歇性热暴露将导致 MCC 的更好控制，并在离心运动后保持线粒体功能。将 Sprague-Dawley 大鼠暴露于 3 周的间歇性热暴露（36°C，40%相对湿度，6 小时/天，每周 5 天）或保持在凉爽条件（20°C）下。然后，将动物分配到对照组或运动组（-14°C 下降跑步机运动 90 分钟）。在运动后立即、2 小时和 48 小时处死动物，测量从红色四头肌中分离的线粒体中的 MCC、线粒体呼吸和线粒体通透性转换孔开放（mPTP）。结果表明，热暴露与运动后较低的血浆肌酸激酶水平（p<0.05）相关，表明肌肉损伤水平较低。MCC 显著升高（p<0.001），线粒体呼吸控制比降低（p<0.001）48 小时后运动。mPTP 对钙的敏感性立即和 48 小时后运动增加（p<0.05）。因此，下降跑步导致线粒体呼吸和钙负荷的显著损伤，与早期时间点相比，48 小时后更为明显。热暴露并未改变 MCC 水平和线粒体功能。总之，间歇性热暴露似乎不能提供对离心运动引起的线粒体功能障碍的保护。
