Exercise training decreases rat heart mitochondria free radical generation but does not prevent Ca2+-induced...

Area of Science:

• Cardiovascular Physiology
• Mitochondrial Biology
• Exercise Science

Background:

• Exercise confers cardioprotection against ischemia-reperfusion injury.
• This injury involves mitochondrial dysfunction, including reactive oxygen species (ROS) generation and calcium overload.
• Endurance exercise training (ET) may mitigate these effects.

Purpose of the Study:

• To investigate if mitochondria from endurance-trained rat hearts exhibit reduced ROS production and enhanced tolerance to calcium-induced dysfunction.
• To determine the specific mechanisms underlying exercise-induced changes in mitochondrial function.

Main Methods:

• Male Fischer 344 rats underwent 16 weeks of endurance exercise training (ET) or remained sedentary (Sed).
• Mitochondrial oxidative phosphorylation, hydrogen peroxide (H2O2) production, and permeability transition pore (PTP) opening were assessed.
• Assays were performed with and without calcium, and with rotenone to inhibit Complex 1.

Main Results:

• ET hearts showed significantly lower H2O2 production compared to Sed hearts, both in the absence and presence of calcium.
• Rotenone abolished the differences in H2O2 production between ET and Sed groups, implicating Complex 1.
• Exercise training did not alter Ca(2+)-induced decreases in respiratory function or PTP opening, indicating no improved tolerance to calcium overload.
• Catalase activity was increased in ET mitochondria.

Conclusions:

• Endurance exercise reduces myocardial mitochondrial ROS production, primarily through adaptations in Complex 1.
• Exercise training does not enhance mitochondrial tolerance to calcium overload.
• These findings highlight specific adaptations in mitochondrial ROS handling with endurance exercise.