Department of Exercise Science, University of South Carolina, Rm. 405 Public Health Research Center, 921 Assembly Street, Columbia, SC 29208, USA.
Center for Colon Cancer Research, University of South Carolina, Rm. 614 Jones PSC Bldg, 712 Main Street, Columbia, SC 29208, USA.
Oxid Med Cell Longev. 2017;2017:8018197. doi: 10.1155/2017/8018197. Epub 2017 Dec 11.
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.
癌症恶病质是一种以骨骼肌耗竭为特征的消耗综合征，导致患者发病率和死亡率增加。虽然蛋白质合成和分解之间的复杂平衡调节骨骼肌质量，但基础蛋白合成的抑制可能不能解释癌症引起的严重消耗。因此，最近的研究转向了对“合成代谢抵抗”的调节，即营养和运动刺激蛋白质合成的能力受损。新出现的证据表明，氧化代谢可以调节基础和诱导的肌肉蛋白质合成。虽然已经独立研究了恶病质肌肉中蛋白质周转率和氧化代谢的紊乱，但有证据表明这些过程之间存在联系，以调节癌症引起的消耗。本综述的主要目的是强调功能失调的氧化代谢与骨骼肌中癌症引起的合成代谢抵抗之间的联系。首先，我们回顾了氧化代谢对肌肉蛋白质合成的调节。其次，我们描述了癌症引起的对合成代谢刺激的反应改变。最后，我们回顾了运动抑制癌症引起的合成代谢抑制和线粒体功能障碍的作用。
