Sleep serves biological functions that regulate reproductive health through the hypothalamic–pituitary–gonadal axis and metabolic systems, which ensure that the energetic cost of reproduction is satisfied. Disordered sleep arises from sleep loss, circadian misalignment, and/or disrupted sleep due to obstructive sleep apnea. These sleep disorders are widespread throughout the world, including both high- and low-income nations. Reproductive dysfunction—testosterone deficiency, impaired spermatogenesis, and ultimately, impaired fertility—can occur if disordered sleep is severe or prolonged. Improving sleep may therefore improve the reproductive health of populations. When epidemiological and interventional studies are considered collectively, lower sleep duration and sleep loss are associated with reduced fecundability and sperm count; lower morning, afternoon, and 24-hour testosterone; and higher afternoon, but not morning or 24-hour cortisol. These reciprocal hormonal changes imbalance anabolic–catabolic signaling toward a catabolic signaling state because testosterone and cortisol are the main anabolic and catabolic signals in humans, respectively. Rebalancing the catabolic signaling state mitigates the induction of insulin resistance from sleep loss. Obstructive sleep apnea is independently associated with lower testosterone, lower sperm quality, and male infertility. High-dose testosterone therapy acutely induces OSA, but the effects of more physiological dosing may be minimal or transient. Circadian misalignment, in the absence of sleep loss, has little effect on testosterone, semen parameters, or fertility. The laboratory evaluation of male hypogonadism in nightshift workers should be with respect to the sleep period since the 24-hour rhythm in testosterone is a consequence of sleep, not the central circadian pacemaker.