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Copyright ©The Author(s) 2016. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Orthop. Oct 18, 2016; 7(10): 628-637
Published online Oct 18, 2016. doi: 10.5312/wjo.v7.i10.628
Skeletal muscle mitochondrial health and spinal cord injury
Laura C O’Brien, Ashraf S Gorgey
Laura C O’Brien, Ashraf S Gorgey, Spinal Cord Injury and Disorders Service, Hunter Holmes McGuire VA Medical Center, Richmond, VA 23249, United States
Laura C O’Brien, Department of Physiology and Biophysics, Virginia Commonwealth University, Richmond, VA 23298, United States
Ashraf S Gorgey, Department of Physical Medicine and Rehabilitation, Virginia Commonwealth University, Richmond, VA 23298, United States
Author contributions: O’Brien LC and Gorgey AS wrote the paper.
Conflict-of-interest statement: The authors declare no conflict of interest.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Ashraf S Gorgey, MPT, PhD, FACSM, Chief of Spinal Cord Injury Research, Spinal Cord Injury and Disorders Service, Hunter Holmes McGuire VA Medical Center, 1201 Broad Rock Blvd, Richmond, VA 23249, United States. ashraf.gorgey@va.gov
Telephone: +1-804-6755000 Fax: +1-804-6755223
Received: May 5, 2016
Peer-review started: May 9, 2016
First decision: June 13, 2016
Revised: June 18, 2016
Accepted: August 15, 2016
Article in press: August 16, 2016
Published online: October 18, 2016
Abstract

Mitochondria are the main source of cellular energy production and are dynamic organelles that undergo biogenesis, remodeling, and degradation. Mitochondrial dysfunction is observed in a number of disease states including acute and chronic central or peripheral nervous system injury by traumatic brain injury, spinal cord injury (SCI), and neurodegenerative disease as well as in metabolic disturbances such as insulin resistance, type II diabetes and obesity. Mitochondrial dysfunction is most commonly observed in high energy requiring tissues like the brain and skeletal muscle. In persons with chronic SCI, changes to skeletal muscle may include remarkable atrophy and conversion of muscle fiber type from oxidative to fast glycolytic, combined with increased infiltration of intramuscular adipose tissue. These changes contribute to a proinflammatory environment, glucose intolerance and insulin resistance. The loss of metabolically active muscle combined with inactivity predisposes individuals with SCI to type II diabetes and obesity. The contribution of skeletal muscle mitochondrial density and electron transport chain activity to the development of the aforementioned comorbidities following SCI is unclear. A better understanding of the mechanisms involved in skeletal muscle mitochondrial dynamics is imperative to designing and testing effective treatments for this growing population. The current editorial will review ways to study mitochondrial function and the importance of improving skeletal muscle mitochondrial health in clinical populations with a special focus on chronic SCI.

Keywords: Mitochondria, Spinal cord injuries, Body composition, Diabetes mellitus, Obesity, Metabolism

Core tip: Mitochondria are the main source of cellular energy production and have decreased function in many disease states. After spinal cord injury (SCI) there is a dramatic deterioration of body composition including increased adipose tissue deposition, skeletal muscle atrophy and conversion from oxidative to glycolytic skeletal muscle fibers. These changes put persons with SCI at a high risk for developing cardiovascular disease and type II diabetes. How skeletal muscle mitochondrial function is impacted after human SCI has yet to be determined. The current editorial will discuss the importance of studying skeletal muscle mitochondrial function after SCI.