Kisspeptin regulates reproduction by activating gonadotrophin-releasing hormone (GnRH) neurons through its receptor, Kiss1r. Previous evidence shows that the neuropeptide kisspeptin and Kiss1r have an important, previously-uncharacterised role in metabolic status, energy balance, and glucose homeostasis. Specifically, infertile kisspeptin receptor (Kiss1r) knockout (KO) mice have reduced energy expenditure. This important discovery advances our understanding of the interconnections between fertility, obesity and energy balance with important etiologic and therapeutic implications. For this study, we used Kiss1rKO and wild-type (WT) male mice to investigate the relationship between absent kisspeptin signalling and locomotor behaviour by allowing mice free access to running wheels. We examined the real-time characteristics of wheel running activity in mice over a 3-week period and its flow on effects on body weight. We used Lafayette Mouse Activity Wheel Chambers (23.5 cm × 35.3 cm; Model 80820; Lafayette Instrument, IN, USA) equipped with a 12.7 cm diameter exercise wheel with a 5.72 cm wide running surface (Model 80820RW, Lafayette). Each chamber was equipped to constantly record distance travelled (0.40 m/revolution) and speed (m/min). The Activity Wheel Monitoring (AWM) Software (Model 86065) was used to record all data sets. Our data show an 82% reduction in total distance travelled per 24 h in KO mice compared to WTs (WT, 4804 ± 632 m; KO, 871 ± 270 m; P<0.01). Moreover, the circadian pattern of wheel running activity (dark phase activity) clearly present in WT mice was severely diminished in KO mice. These experiments are ongoing but suggest that absent of kisspeptin signalling may act as a regulator of voluntary activity and patterns of locomotion behaviour, potentially involving circadian rhythm.