Mitochondria in Exercise-Induced Oxidative Stress

Abstract

In recent years it has been suggested that reactive oxygen species (ROS) are involved in the damage to muscle and other tissues induced by acute exercise. Despite the small availability of direct evidence for ROS production during exercise, there is an abundance of literature providing indirect support that oxidative stress occurs during exercise. The electron transport associated with the mitochondrial respiratory chain is considered the major process leading to ROS production at rest and during exercise. It is widely assumed that during exercise the increased electron flow through the mitochondrial electron transport chain leads to an increased rate of ROS production. On the other hand, results obtained by in vitro experiments indicate that mitochondrial ROS production is lower in state 3 (ADP-stimulated) than in state 4 (basal) respiration. It is possible, however, that factors, such as temperature, that are modified in vivo during intense physical activity induce changes (uncoupling associated with loss of cytochrome oxidase activity) leading to increased ROS production. The mitochondrial respiratory chain could also be a potential source of ROS in tissues, such as liver, kidney and nonworking muscles, that during exercise undergo partial ischemia because of reduced blood supply. Sufficient oxygen is available to interact with the increasingly reduced respiratory chain and enhance the ROS generation. At the cessation of exercise, blood flow to hypoxic tissues resumes leading to their reoxygenation. This mimics the ischemia-reperfusion phenomenon, which is known to cause excessive production of free radicals. Apart from a theoretical rise in ROS, there is little evidence that exercise-induced oxidative stress is due to its increased mitochondrial generation. On the other hand, if mitochondrial production of ROS supplies a remarkable contribution to exercise-induced oxidative stress, mitochondria should be a primary target of oxidative damage. Unfortunately, there are controversial reports concerning the exercise effects on structural and functional characteristics of mitochondria. However, the isolation of mitochondrial fractions by differential centrifugation has shown that the amount of damaged mitochondria, recovered in the lightest fraction, is remarkably increased by long-lasting exercise.

3,4-Dihydroxycinnamic Acid Attenuates the Fatigue and Improves Exercise Tolerance in Rats

“…6,7,17,18) Thus a reduction in ROS production, and the more oxidative and less glycolytic glucose metabolism in the groups receiving 3,4-DA is consistent with a reduced production of lactate and with the attenuation of fatigue during the progressive exercise protocol used in this study.…”

Investigation of oxidative stress in blood, brain, kidney, and liver after oxime antidote HI-6 application in a mouse experimental model

“…It arises by lipoxidation of polyunsaturated lipids (Pryor and Stanley, 1975;Yin and Porter, 2005). In a healthy individual, there is a steady level of ROS generated by several enzymes, especially by the oxidative phosphorylation metabolic pathway in mitochondria (DiMeo and Venditti, 2001). HI-6 impact on physiological levels of TBARS probably relates to suppression of the basal metabolism.…”

Manipulation of systemic oxygen flux by acute exercise and normobaric hypoxia: implications for reactive oxygen species generation

“…In the present study, we suggest that either muscle mitochondria or extracellular leucocytes had a role to play in the generation of primary free radicals and lipid peroxidation during aerobic exercise. The mitochondrial electron transport chain within a muscle fibre has long been considered the major site of ROS (reactive oxygen species) production at rest and during exercise [23]. Studies on isolated mitochondria suggest that between 2-5 % of total electron flux through the cytochrome chain may undergo one electron univalent reduction with the formation of superoxide and H 2 O 2 [24,25].…”