Effect of castration on mouse skeletal muscle oxidative capacity

Abstract

Low testosterone is often observed in male patients with cancer, COPD and HIV, and associated with impaired oxidative metabolism in skeletal muscle. Although testosterone has well described effects on muscle mass, less is known about the effect of testosterone on muscle's metabolic capacity. The purpose of this study was to determine if oxidative capacity is reduced in wasting skeletal muscle due to castration and if anabolic steroid (ND) administration can rescue this capacity. 8‐week male C57BL/6 mice were placed into three treatment groups: sham castration (CON, n = 6), castration (CAS, n = 6), and castration with ND administration (n = 6). Gastrocnemius (GAS) muscle succinate dehydrogenase (SDH) activity and PGC‐1 expression were examined. Castrated GAS muscle increased the percentage of low SDH activity fibers (78.2±1.5% vs. 84.5±1.1%, p < .05) and decreased the incidence of high SDH activity fibers (5.0±0.6% vs. 1.3±0.2%, p < .05) compared to CON. ND administration significantly attenuated these changes. PGC‐1 mRNA expression decreased 54% with castration (p = .029), but increased 141% with ND administration (p = .036). These data indicate testosterone availability may regulate oxidative capacity in mouse hindlimb muscle. This study was funded by NIH Grant 5R03AR051434‐02.