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Oxidative Medicine and Cellular Longevity
Volume 2017 (2017), Article ID 8018197, 14 pages
https://doi.org/10.1155/2017/8018197
Review Article

Linking Cancer Cachexia-Induced Anabolic Resistance to Skeletal Muscle Oxidative Metabolism

1Department of Exercise Science, University of South Carolina, Rm. 405 Public Health Research Center, 921 Assembly Street, Columbia, SC 29208, USA
2Center for Colon Cancer Research, University of South Carolina, Rm. 614 Jones PSC Bldg, 712 Main Street, Columbia, SC 29208, USA

Correspondence should be addressed to James A. Carson; ude.cs.xobliam@jnosrac

Received 22 September 2017; Accepted 6 November 2017; Published 11 December 2017

Academic Editor: Giuseppe Filomeni

Copyright © 2017 Justin P. Hardee et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Cancer cachexia, a wasting syndrome characterized by skeletal muscle depletion, contributes to increased patient morbidity and mortality. While the intricate balance between protein synthesis and breakdown regulates skeletal muscle mass, the suppression of basal protein synthesis may not account for the severe wasting induced by cancer. Therefore, recent research has shifted to the regulation of “anabolic resistance,” which is the impaired ability of nutrition and exercise to stimulate protein synthesis. Emerging evidence suggests that oxidative metabolism can regulate both basal and induced muscle protein synthesis. While disrupted protein turnover and oxidative metabolism in cachectic muscle have been examined independently, evidence suggests a linkage between these processes for the regulation of cancer-induced wasting. The primary objective of this review is to highlight the connection between dysfunctional oxidative metabolism and cancer-induced anabolic resistance in skeletal muscle. First, we review oxidative metabolism regulation of muscle protein synthesis. Second, we describe cancer-induced alterations in the response to an anabolic stimulus. Finally, we review a role for exercise to inhibit cancer-induced anabolic suppression and mitochondrial dysfunction.