Citation

Porter C, Herndon DN, Sidossis LS, Børsheim E. Burns 2013; 39(6): 1039-1047.

Affiliation

Metabolism Unit, Shriners Hospitals for Children, Galveston, TX, United States; Department of Surgery, University of Texas Medical Branch, Galveston, TX, United States. Electronic address: cr2porte@utmb.edu.

Copyright

(Copyright © 2013, Elsevier Publishing)

DOI

10.1016/j.burns.2013.03.018

PMID

23664225

Abstract

Severe burns induce a pathophysiological response that affects almost every physiological system within the body. Inflammation, hypermetabolism, muscle wasting, and insulin resistance are all hallmarks of the pathophysiological response to severe burns, with perturbations in metabolism known to persist for several years post injury. Skeletal muscle is the principal depot of lean tissue within the body and as the primary site of peripheral glucose disposal, plays an important role in metabolic regulation. Following a large burn, skeletal muscle functions as and endogenous amino acid store, providing substrates for more pressing functions, such as the synthesis of acute phase proteins and the deposition of new skin. Subsequently, burn patients become cachectic, which is associated with poor outcomes in terms of metabolic health and functional capacity. While a loss of skeletal muscle contractile proteins per se will no doubt negatively impact functional capacity, detriments in skeletal muscle quality, i.e. a loss in mitochondrial number and/or function may be quantitatively just as important. The goal of this review article is to summarise the current understanding of the impact of thermal trauma on skeletal muscle mitochondrial content and function, to offer direction for future research concerning skeletal muscle mitochondrial function in patients with severe burns, and to renew interest in the role of these organelles in metabolic dysfunction following severe burns.

Language: en