The skeleton has protective, mechanical, and metabolic roles. Bone should be strong to prevent fractures, but also light, enabling movement in a gravitational environment. Bone remodelling, the cellular machinery responsible for bone integrity and strength, is a finely balanced process responsive to mechanical loads and hormonal changes. As bone remodelling requires energy, it has been hypothesised that hormones produced by bone (osteokines) have endocrine-like effects beyond the skeleton. Exercise is a non-pharmacological intervention that improves bone and muscle health simultaneously, reducing the risk of osteoporosis and sarcopenia, as well as improving glucose disposal, thereby reducing the risk of type 2 diabetes. As such, exercise can be used as a tool to uncover the interactions between bone and muscle, as well as the mechanisms involved in this crosstalk. Indeed, it has been reported that the circulating levels of some osteokines, such as osteocalcin, RANKL/OPG, and lipocalin-2 (LCN2), are not only related to improved muscle strength, insulin sensitivity, and glucose control, but also have a direct effect on these measures. The aim of this presentation is to present recent data on the role of osteokines in muscle and glucose regulation. A better understanding of the mechanisms underlying the interactions between exercise, osteokines, and muscle glucose regulation may provide new pharmacological and non-pharmacological avenues to prevent and manage diseases such as type 2 diabetes and sarcopenia.