Short Title:American Journal of Physiology. Endocrinology and Metabolism
Year, Volume, Issue, Page(s):14, 307, 5, E462-E467
Study investigated the impact of severe burn injury on skeletal muscle mitochondrial function and coupling control in adult humans. Mitochondria are the cellular organelles responsible for almost all oxygen consumption in vivo. It was hypothesized that severe burn injury alters skeletal muscle mitochondrial function, favoring mitochondrial thermogenesis. This hypothesis offers a novel mechanistic explanation for the hypermetabolic response to severe thermal trauma. Leak, coupled, and uncoupled mitochondrial respiration was determined in permeabilized myoﬁber bundles obtained from quadriceps muscle biopsies collected on two separate occasions from 6 severely burned adults and 12 healthy adults (controls). Indirect calorimetry was used to estimate metabolic rate in burn patients. Results indicated that metabolic rate was signiﬁcantly greater than predicted values for burn patients at both time points. Skeletal muscle oxidative capacity, citrate synthase activity, a marker of mitochondrial abundance, and mitochondrial sensitivity to oligomycin were all lower in burn patients vs. controls at both time points. A greater proportion of maximal mitochondrial respiration was linked to thermogenesis in burn patients compared with controls. Increased metabolic rate in severely burned adults is accompanied by derangements in skeletal muscle mitochondrial function. Skeletal muscle mitochondria from burn victims are more uncoupled, indicating greater heat production within skeletal muscle. The ﬁndings suggest that skeletal muscle mitochondrial dysfunction contributes to increased metabolic rate in burn victims.