Chao 2019 J Appl Physiol (1985)
Chao T, Burmeister DM, Corona BT, Greising SM (2019) Oxidative pathophysiology following volumetric muscle loss injury in a porcine model. J Appl Physiol (1985) 126:1541-49. |
Chao T, Burmeister DM, Corona BT, Greising SM (2019) J Appl Physiol (1985)
Abstract: Volumetric muscle loss (VML) occurs after severe orthopaedic trauma, and results in loss of muscle fibers and function which can leave patients permanently disabled. While animals models of VML are useful to test possible therapeutic strategies, the pathophysiological characteristics of remaining skeletal muscle and changes in metabolism are not thoroughly understood. Herein, alterations of neuromuscular function, muscle fiber morphology, myosin heavy chain (MyHC) expression, and myofiber mitochondrial respiration were evaluated in an adult Yorkshire swine VML injury model. VML injured animals showed reduced peak isometric strength (p<0.05) and a shift towards smaller muscle fibers independent of fiber type (p<0.001). The muscle remaining after VML had a greater distribution of type I fibers and lower distribution of type II fibers (p<0.001). Skeletal muscle mitochondrial state 2 and state 3, reflecting complex I respiration, increased after injury (p<0.05) with a consistent trend to display higher oxygen flux per mg of tissue. However, this was largely driven by increased mitochondrial content after VML which is associated with higher mitochondrial fission (FIS-1 protein levels). T This study demonstrates an underlying perturbation of oxidative metabolism within the remaining musculature following surgical creation of an isolated, sterile VML injury in a porcine model that may be influential to the development of insidious pathophysiology and regenerative and rehabilitative therapies. β’ Keywords: Mitochondrial Respiration, Myosin Heavy Chain, Orthopaedic, Skeletal Muscle Injury, Trauma β’ Bioblast editor: Plangger M
Labels: MiParea: Respiration
Pathology: Other
Organism: Pig Tissue;cell: Skeletal muscle Preparation: Permeabilized tissue
Coupling state: LEAK, OXPHOS, ET
Pathway: F, N, S, NS, ROX
HRR: Oxygraph-2k
Labels, 2019-04