Endogenous biological rhythms are commonplace throughout the natural world and can be broadly categorised as being ultradian (period <24-h), circadian (period of ~24-h), or infradian (period >24-h). Circadian rhythms have been studied in detail in mammalian species, including humans. These rhythms are driven by cell autonomous clocks found in the suprachiasmatic nuclei (SCN) of the hypothalamus and also throughout the rest of the body. Circadian clocks influence the bodys physiology via numerous output pathways. Within any given tissue, it is estimated that around 1020% of the transcriptome, proteome, and metabolome is under circadian control. Moreover, nearly half of all murine genes are circadian in at least one tissue. Circadian time is also communicated via regulation of signalling molecules (e.g. hormones) and behaviour. One key behaviour that exhibits circadian control is sleep. The regulation of sleep is described by a two-process model in which circadian regulation of sleep-arousal (process C) combines with a homeostatic measure of sleep pressure (process S) that increases during wakefulness and dissipates during sleep. Although clocks and sleep are sometimes studied separately, there are clear reciprocal links between these two aspects of physiology; sleep propensity exhibits a circadian rhythm and disruption of sleep duration or timing alters circadian rhythmicity. Some hormones (e.g. melatonin and cortisol) are well-known to exhibit robust daily rhythms with well-defined relationships to the sleepwake cycle. More recent research has clearly demonstrated widespread interactions between clocks, sleep, endocrinology, and physiology. One such example is the control of glucose homeostatis, which is controlled at multiple levels by circadian rhythms and is adversely effected by altered quantity and quality of sleep. This talk will explain why both circadian time and sleep history are important considerations in the study of endocrine function and broader physiology.