Department of Physiological and Medical Sciences, The Jerzy Kukuczka Academy of Physical Education, Katowice, Poland.
J Physiol Pharmacol. 2013 Oct;64(5):639-47.
The aim of the study was to assess the effects of a combination of anabolic-androgenic steroid abuse and endurance training during adolescence on selected aspects of oxidative stress and antioxidant defenses in various striated muscle types. The effects were studied of testosterone propionate (TP) treatment (8 and 80 mg/kg/week, for 6 weeks), given alone or in combination with moderate-intensity endurance training, starting at adolescence, on thiobarbituric acid-reactive substances and heat shock protein 72 (Hsp72) contents, and androgen receptorm(AR) mRNA level in the heart left ventricle, soleus and extensor digitorum longus of male Wistar rats. TP treatment alone markedly elevated thiobarbituric acid-reactive substances only in the left ventricle and soleus; this effect was but marginally enhanced by endurance training. The training alone markedly elevated Hsp72 content in all muscles studied. TP treatment alone dose-dependently upregulated Hsp72, while the lower TP dose slightly curtailed the effect of the training. Low-dose TP treatment alone elevated, whereas high-dose TP treatment alone lowered androgen receptor mRNA level in the soleus and extensor digitorum longus. Endurance training alone elevated AR mRNA in all muscles studied, whereas TP treatment dose-dependently counteracted this effect. Exercise-associated rise in body temperature was significantly less in the TP-treated rats. We came to the conclusion that chronic suprapharmacological TP treatment might exert a protective effect on muscle cell proteins in adolescent sedentary rats, but it markedly enhanced lipid peroxidation. These effects were unlikely to result from an androgen receptor-mediated genomic action of testosterone. Exercise-related heat stress, and not oxidative stress, was mainly responsible for Hsp72 upregulation in striated muscles of chronic TP-treated endurance-trained adolescent male rats.
本研究旨在评估青春期滥用合成代谢雄激素类固醇和耐力训练对不同横纹肌类型氧化应激和抗氧化防御的某些方面的影响。研究了丙酸睾酮(TP)(8 和 80 mg/kg/周,6 周)单独或与中等强度耐力训练联合治疗对雄性 Wistar 大鼠心脏左心室、比目鱼肌和伸趾长肌的丙二醛反应物质和热休克蛋白 72(Hsp72)含量以及雄激素受体(AR)mRNA 水平的影响。TP 单独治疗仅显著增加左心室和比目鱼肌的丙二醛反应物质;耐力训练仅适度增强这种作用。单独训练显著增加了所有研究肌肉中的 Hsp72 含量。TP 单独治疗呈剂量依赖性地上调 Hsp72,而较低的 TP 剂量略微减弱了训练的作用。单独低剂量 TP 治疗可上调,而高剂量 TP 治疗可下调比目鱼肌和伸趾长肌中的雄激素受体 mRNA 水平。单独的耐力训练可上调所有研究肌肉中的 AR mRNA,而 TP 治疗呈剂量依赖性地拮抗这种作用。TP 治疗组大鼠的体温升高幅度明显低于单独运动组。我们得出结论,慢性超生理剂量的 TP 治疗可能对青春期久坐不动的大鼠的肌肉细胞蛋白有保护作用,但它显著增强了脂质过氧化。这些作用不太可能是由睾酮的雄激素受体介导的基因组作用引起的。与运动相关的热应激,而不是氧化应激,主要负责慢性 TP 治疗的耐力训练的青春期雄性大鼠横纹肌中 Hsp72 的上调。