Oxidative damage to skeletal muscle following an acute bout of contractile claudication

The purpose of this study was to determine the extent and sources of oxidative stress within skeletal muscle following an acute bout of contractile claudication. Twenty-four hours after unilateral ligation of the femoral artery, rat hind limbs were stimulated in vivo for 30 min, and force production measured. One-hour post-stimulation, animals were sacrificed and soleus and gastrocnemius muscles removed. There was significant reduction in force in the control limb (sham ligated/stimulated (SS)), while force in the ligated limb (ligated/stimulated (LS)) was reduced by 72%. There was an increase in skeletal muscle lipid hydroperoxides (53 and 47%) and protein carbonyls (57 and 54%) in the soleus and gastrocnemius muscles, respectively, and the muscle wet/dry weight ratio was increased in the gastrocnemius muscles. Total glutathione (GHS) was reduced, while xanthine oxidase (XO) activity and neutrophil levels were increased, in LS compared to SS in both soleus and gastrocnemius muscles. These data suggest that an acute bout of contractile claudication causes significant oxidative damage and edema to skeletal muscle. This is associated with both an increase in the activity of the radical-producing enzyme xanthine oxidase and an increase in activated neutrophils.