Cardiac mitochondrial respiratory function and oxidative stress: The role of exercise

Abstract

Investigations on the mechanisms capable of influencing heart mitochondrial function constitute a central contribution to the understanding of cardiac bioenergetics. In contrast to the conventional idea that reactive oxygen species (ROS) mostly act as a trigger for oxidative damage of biological structures, in low physiological concentrations they can regulate a variety of important molecular mechanisms, including those related to mitochondrial respiratory function. Among others, moderate physical exercise seems to be an important agent to induce cellular and mitochondrial environmental redox modifications and it is possible that these alterations could mediate cardiac mitochondrial respiration patterns. This brief review summarizes some current knowledge on mitochondrial respiratory pathways and focuses on data provided by studies dealing with exercise and cardiac respiratory mechanisms. It is emphasized the need of further experimental studies that analyze the association between physical exercise, particularly endurance training, and several mechanisms hypothetically related to the improvement of mitochondrial function, such as the overexpression of some important chaperone machinery and the up-regulation of both cellular and mitochondrial antioxidants. The influence of chronic moderate exercise on the functionality of some inner membrane components and on mitochondrial calcium loading capacity remains to be established.