Skeletal muscle electron transport chain dysfunction after sepsis in rats

The derangement in oxygen utilization occurring during sepsis is likely to be linked to impaired mitochondrial functioning. Skeletal muscle comprises 50%-60% of body cell mass and represents the largest organ potentially affected by systemic inflammation. Thus, we investigated whether sepsis induced by cecal ligation and puncture (CLP) modifies mitochondrial activity in respiratory and nonrespiratory skeletal muscle.

Wistar rats were subjected to CLP and at different times, diaphragm and quadriceps were removed for the determination of electron transfer chain activities and mitochondrial oxidative stress. In addition, we determined diaphragm contractile strength.

In the quadriceps, 12 h after CLP we demonstrated a significant diminution on complex II-III activity. At late times (48 h after CLP), we demonstrated a decrease in the activity of all electron transfer chain complexes, which seemed to be secondary to early oxidative stress and correlates with diaphragm contractile strength. Differently from diaphragm, electron transfer chain was not decreased after sepsis and even oxidative stress was not increased at all times tested.

Our results suggest that quadriceps mitochondria are more resistant to sepsis-induced dysfunction.