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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. |
