Dent Jessica R, Fletcher Deborah K, McGuigan Michael R
Sports Performance Research Institute New Zealand, School of Sport and Recreation, Auckland University of Technology , Auckland, New Zealand.
J Sports Sci Med. 2012 Sep 1;11(3):363-70.
This review will focus on the proposed second mode of testosterone action (now termed non-genomic) that appears to occur independently of the traditional transcriptional mechanism in mammalian skeletal muscle cells which may enhance skeletal muscle contractile properties. This mechanism of testosterone action differs from the traditional pathway, originating at the cell membrane, having a rapid onset of action, requiring second messengers to execute its effects and is insensitive to inhibitors of traditional androgen receptor action, transcription and protein synthesis. Importantly, unlike the traditional action of testosterone in skeletal muscle, this non-genomic pathway is shown to have a direct acute effect on calcium-dependent components important for the contractile process. The changes within the contractile apparatus may enhance the ability of the muscle to produce explosive power during athletic performance. Rapid increases in Inositol triphosphate mass and calcium release from the sarcoplasmic reticulum have been reported in rodent skeletal muscle cells, and a rapid androgen (dihydrotestosterone)-induced increase in peak force production has been recorded in intact rodent skeletal muscle fibre bundles while showing increases in the activity of the Ras/MAP/ERK mediated pathway. Because the non-genomic action of testosterone is enhanced during increases in exposure to testosterone and is acute in its action, implications for athletic performance are likely greater in females than males due to natural fluctuations in circulating testosterone levels during the female menstrual cycle, reproductive pathology, and changes induced by hormonal contraceptive methods. Research should be undertaken in humans to confirm a pathway for non-genomic testosterone action in human skeletal muscle. Specifically, relationships between testosterone fluctuations and physiological changes within skeletal muscle cells and whole muscle exercise performance need to be examined. Key pointsNon-genomic calcium mediated events activated by testosterone have been identified in skeletal muscle cells.The non-genomic action originates at the cell membrane, is rapid in onset and is directed by second messengers' calcium and IP3.A possible action of non-genomic testosterone may be the initiation of a more efficient contraction through the mobilisation of calcium from the SR resulting in greater force production or velocity of contraction in fast twitch fibres.Physiologically, females with menstrual disorders that cause hyperandrogenism may have a performance advantage in events that require great force or power production.
本综述将聚焦于所提出的睾酮作用的第二种模式（现称为非基因组模式），这种模式似乎独立于哺乳动物骨骼肌细胞中的传统转录机制而发生，可能会增强骨骼肌的收缩特性。睾酮的这种作用机制不同于传统途径，它起始于细胞膜，作用起效迅速，需要第二信使来执行其效应，并且对传统雄激素受体作用、转录和蛋白质合成的抑制剂不敏感。重要的是，与睾酮在骨骼肌中的传统作用不同，这种非基因组途径对收缩过程中重要的钙依赖性成分具有直接的急性作用。收缩装置内的变化可能会增强肌肉在运动表现中产生爆发力的能力。啮齿动物骨骼肌细胞中已报道肌醇三磷酸量迅速增加以及肌浆网释放钙，并且在完整的啮齿动物骨骼肌纤维束中记录到雄激素（双氢睾酮）诱导的峰值力产生迅速增加，同时显示Ras/MAP/ERK介导途径的活性增加。由于在接触睾酮增加期间睾酮的非基因组作用会增强且作用具有急性特点，由于女性月经周期中循环睾酮水平的自然波动、生殖病理以及激素避孕方法引起的变化，其对运动表现的影响在女性中可能比男性更大。应该在人体中进行研究以证实睾酮在人体骨骼肌中的非基因组作用途径。具体而言，需要研究睾酮波动与骨骼肌细胞内生理变化以及全肌肉运动表现之间的关系。关键点在骨骼肌细胞中已确定由睾酮激活的非基因组钙介导事件。非基因组作用起始于细胞膜，起效迅速，由第二信使钙和肌醇三磷酸引导。非基因组睾酮的一种可能作用可能是通过从肌浆网动员钙来启动更有效的收缩，从而在快肌纤维中产生更大的力或收缩速度。从生理角度来看，患有导致雄激素过多的月经紊乱的女性在需要大力或产生力量的项目中可能具有表现优势。
