Heat exposure does not alter eccentric exercise-induced increases in mitochondrial calcium and respiratory dysfunction.

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.