Background: Humans and mammals have sex-specific differences in cardiac electrophysiology, linked to the action of sex hormones in the cardiac muscle. These hormones can either increase or decrease the expression of ionic channels modulating the cardiac cycle through genomic and non-genomic interactions. Methods: Systematic search in PubMed, Medline and EMBASE including keywords pertaining to testosterone and QT interval. Included experimental studies, observation studies and case reports presenting the results of testosterone administration, excess or deficiency in humans and animals. Results: Testosterone has been shown to shorten the action potential duration, by enhancing the expression of K+ channels and downregulating ICaL increasing the repolarization reserve of the cardiac muscle. This increased repolarization reserve also protects the heart against the effects of QT prolonging drugs and arrhythmogenesis. This effect has been observed in both genders and animals. Conclusions: Testosterone deficient states can promote arrhythmogenesis. The evidence in this paper may be used to guide clinical consideration relating to testosterone levels and QT prolonging states and medications, such as increased clinical surveillance of patients in testosterone deficient states using ECG.