In fact, other spectrophotometric works did show inhibition of complex I and complex IV, with or without a parallel decrease of citrate synthase activity, in vastus lateralis muscle of patients with sepsis, especially if L-CCG-l severe or prolonged. We then purposely studied patients with septic shock, usually on high dose of catecholamines, either on day one or seven. We performed subgroup analysis to select most severe cases and complemented biochemistry with histology, histochemistry and electron microscopy. Even so, all our efforts to detect signs of mitochondrial dysfunction were vain. Our present work differs from those reported above because it examined mitochondrial function in triceps brachii, and not in vastus lateralis, muscle. Muscles differ in their mitochondrial content or activity, susceptibility to oxidative damage and blood flow. As a consequence, sepsis may diversely affect different muscles, just as other systemic insults do. In animals, sepsis changes mitochondrial integrity, adenosine triphosphate levels and protein turnover in some muscle groups more than in others. In humans, it apparently affects mitochondrial morphology in liver but not in rectus abdominis, triggers mitochondrial biogenesis in rectus abdominis, but not in vastus lateralis, induces energy failure in vastus lateralis, but not in serratus anterior, muscle. Therefore discrepancy between present and past GI 254023X findings in skeletal muscle probably reflects compartmentalization of response to infection. However, we cannot exclude that it simply indicates that skeletal muscle mitochondrial biochemistry is not, at least constantly, altered during sepsis. Some aspects of this study deserve a comment. First, muscle biopsies were not immediately frozen in liquid nitrogen. We considered important to remove contaminants to measure ����pure���� skeletal muscle mitochondrial biochemistry. In retrospect, this was probably not a very relevant issue. In fact, results did not differ between samples processed as above and those snap-frozen. Moreover, changes in platelet mitochondrial biochemistry could be readily detected even if pellet preparation required approximately one hour. Second, we did not measure markers of apoptosis that, according to other authors, are associated with platelet mitochondrial dysfunction and thrombocytopenia.