Reactive oxygen species and exercise on bone metabolism: friend or enemy?

Reactive oxygen species (ROS) are well recognised for playing a dual role as both deleterious and beneficial species. They are normally generated by tightly regulated enzymes. ROS overproduction arises either from mitochondrial electron transport chain or excessive stimulation of NAD(P)H resulting in oxidative stress, a deleterious process that can be an important mediator of damage to cell structures (lipids, membranes, proteins, and DNA). However, ROS could have a beneficial affect at low/moderate concentrations. Physiological roles in cellular responses to noxia have been reported, in defence against infectious agents, in the function of a number of cellular signalling pathways, and the induction of a mitogenic response. The role of ROS in bone metabolism is dual. It is a key modulator of bone cell function and also implicated in the pathophysiology of mineral tissues. Elevated production of ROS and/or depletion of antioxidants have also been observed in a variety of pathological conditions, including inflammatory joint diseases. Performing physical exercise is associated with numerous health benefits, playing a role especially in the prevention of bone loss. However, the production of ROS increases during demanding exercise. To explore this further, the aim of the present review was to examine bone remodelling in relation to oxidative stress and exercise.