Abstract
In exercise-induced muscle damage, oxidative stress derived from the liberation of
reactive oxygen species (ROS) is assumed to be of etiological importance. Xanthine
oxidase (XO) located in capillary endothelium is one of the possible sources for ROS,
mainly investigated so far under conditions of ischemia/reperfusion. XO can be inhibited
by allopurinol. To investigate the contribution of XO for the oxidative stress-induced
development of muscle damage, mice were subjected to a single bout of exhaustive running
exercise. Another exercised group received allopurinol. The reduced form of glutathione
(GSH) was measured to estimate the amount of oxidative stress in soleus muscle, and
the same muscle was examined in the light and electron microscope at different periods
of time (0, 48, 96 h) after exercise. While exercise alone resulted in a marked reduction
of GSH indicative for oxidative stress, which only recovered at 96 h, the administration
of allopurinal to exercised animals induced a complete recovery already at 48 h after
exercise. Muscle damage was more pronounced in the exercised animals which had not
been treated with allopurinol. It is concluded that endothelium-derived ROS contribute
reasonably to oxidative stress to exercised muscle and to fiber and capillary damage.
Key words
Exercise - muscle damage - oxidative stress - xanthine oxidase - allopurinol
